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How to find sequencing data of a specific drosophila strain
I'm trying to correct low coverage parts of an assembly of these PacBio reads with Illumina data. According to PacBio they "have sequenced adult males from a subline of the ISO1 (y; cn, bw, sp) strain of D. melanogaster.  This is the same stock used in the official BDGP reference assemblies since the first genome sequence release in 2000."
Unfortunately the Illumina data sequenced by the same guys (also  ISO1 (y; cn, bw, sp) but 2057) "revealed significant differences" to the official reference strain. Something I found out as well.
Now I'm trying to find Illumina data for the reference strain at NCBI, but I'm pretty lost. There seem to be dozens of different strains and I can't figure out which one is the reference strain, mostly because I'm completely unfamiliar with the biological nomenclature like ISO1, (y; cn, bw, sp) and 2057 or D8, D20-C2, mbn2 and so on.
So I guess my question is: What strain exactly is the drosophila melanogaster reference strain used in BDGP and how do I find SRA data of this strain on NCBI?

As described in File S1 of Gutzwiller et al (2015) the relationship between the sub-strain of the ISO1 reference strain used by BDGP for the original Drosophila genome proejct, and the sub-strain in the Bloomington Drosophila Stock Center is complicated:

"We investigated the cause of the discrepancy of Wolbachia sequences in the Berkeley Drosophila Genome Project (BDGP) and Bloomington Drosophila Stock Center (BDSC) ISO1 genomic data by first establishing the provenance of these lineages. As documented in the BDSC database, the BDSC ISO1 sub-strain was donated directly to the stock center by Jim Kenni- son in 1994. The ISO1 sub-strain used by the BDGP was obtained from Gerry Rubin’s lab in the late 1990’s (Roger Hoskins, personal communication). The Rubin lab ISO1 sub-strain was obtained in the mid-1990s from Jim Kennison via at least one intermediate lab (Todd Laverty, personal communication). Thus, in contrast to naive assumptions, the ISO1 sub-strain at the Bloomington Drosophila Stock Center is neither a direct descendant nor progenitor of the ISO1 sub-strain used in the D. melanogaster genome project, and these two sub-strains have had independent trajectories since at least 1994."

The PacBio dataset you refer to was generated using the BDGP sub-strain. The Illumina data you refer to was generated using the BDSC sub-strain and is available here: https://www.ncbi.nlm.nih.gov/sra/ERX645969[accn]

Yes, but I'm looking for Illumina data for the BDGP sub-strain. It is exactly the problem that one of the data sets is BDGP and the other BDSC. Otherwise great background information!

As far as I know, there is no public Illumina DNA-seq data from the BDGP sub-strain of ISO1.


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Cooperative Enzyme Question
I'm currently studying for the MCATs. After doing some biochemistry practice questions, I came upon a question that I believe may be incorrectly posed. I was wondering if I'm correct in saying this or not.
The question is: " A certain cooperative enzyme has four subunits, two of which are bound to substrate. Which of the following statements can be made?"
The correct answer is "The affinity of the enzyme for the substrate is greater than with one substrate bound."
My confusion lies in the fact that the question never specified whether this cooperative enzyme had a positive or negative Hill coefficient. When approaching future questions like this, should I assume a positive Hill coefficient?

You need to rephrase your question. This list cannot give advice on interpreting examination questions, or whether questions are ambiguous. Only questions about biology are valid. We can answer questions about the binding of substrates to enzymes showing positive or negative cooperativity or whether such enzymes exist. These might be a way of establishing whether or not you are correct. Then you can draw your own conclusions about the academic level at which the question is pitched and your best examination strategy.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

sort: votes


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Does increasing contractility increase LV ESP?
I see many PV diagrams showing a negligible difference in the ESP when contractility increases. I'm wondering why this is the case, because if more blood is being pumped out into the aorta, the MAP should increase, which should subsequently increase the ESP.

LV, ESP, MAP, PV? Well I do know what ESP means — Extra-sensory perception, which is presumably what is needed to understand the question.

LV = left ventricle, ESP = end systolic pressure, MAP = mean arterial pressure, PV = pressure-volume

Then edit the question to make it intelligible, especially the title. You might also give an example (with source) of the type of diagram you are referring to. The purpose of comments is to suggest improvements or clarification of questions, not for a dialogue.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Which one is better to use for water stress experiment GWAS or RNASeq?
This is my first time in this area of research. I am working on 95 varieties of bambara groundnut. I have done the agromorphological characterization of these varieties as well as the genetic diversity using DArT markers. Based on the charaterization result, i have selected 10 varieties to be subjected to water stress with the objective of identifying genes that are responsible for tolerance in this plant. My challenge now is:
1. bambara groundnut does not have a reference genome, so will i be able to use GWAS in getting these genes from the result of the DArTSeq.
2. Bearing in mind that the whole 95 varieties characterized were not subjected to water stress, do i need to set up another experiment entirely for the water stress and go ahead to make use of RNASeq to get the genes?
3. It is obvious that some genes will be upregulated and some will be downregulated, how do i identify these genes and how do i know if they are expressed at the onset of stress, during, or after stress?
4. when is the appropriate time to take my samples, i was considering taking at 50% flowering stage. Is this good?
Any help and insightful articles will be greatly appreciated.

The choice of the experiment to do depends on the question you are trying to ask. RNAseq will give you a direct readout of gene expression which you can relate to a particular condition. GWAS is more difficult to interpret.

bambara groundnut does not have a reference genome

This is your biggest problem if you want to do any sequencing based analysis. Neither GWAS nor RNAseq data analysis are possible without a reference genome (or at least transcriptome).
Depending on the availability, quality & similarity of reference genomes from related species it may however be possible to construct a reference transcriptome for your species from RNA sequencing data you get from RNAseq experiments. I'm whether it's feasible (or indeed possible) to try the same with genome sequencing data, since with only 10 individuals/strains you may only be able to get huge linkage groups for GWAS analysis.
Either way I'd highly recommend you to talk with someone (i.e. from your institute) who has experience in doing RNAseq or GWAS on plants, when planning this. (The experience with platns important, mammalian/model system genomes are much better studied and generally have less genome duplications, so analysis of plant data comes with its own set of baggage)

Bearing in mind that the whole 95 varieties characterized were not subjected to water stress, do i need to set up another experiment entirely for the water stress and go ahead to make use of RNASeq to get the genes?

If you want to use RNAseq to find genes that are differentially expressed between states of water stress and no water stressin the same plant/species you will need to compare samples taken from corresponding conditions. This is only possible with RNAseq data.
Another approach could be to do some other experiments to determine which plants show a phenotype when exposed to water stress, and then look for correlations of this phenotype with (sequence) isoforms variants [GWAS like approach, possible with RNAseq or genomic sequencng data] or with expression levels of certain genes [again only possible with RNAseq data]. In thsi approach you need to be aware that your sequencing data either represents the ground state of all plants (no stress) or a potentially stressed state and missing one of these may mean that you can't find genes that change expression levels based on stress.

It is obvious that some genes will be upregulated and some will be downregulated, how do i identify these genes and how do i know if they are expressed at the onset of stress, during, or after stress?

First, while most analysis tools will always give you some values for up- or downregulation, that does definitely not mean that these values are always meaningful. Only proper statistical testing can tell you which up/downregulation is somewhat reliable (it still wont tell you if its biologically meaningful) and depending on the quality of your data and the actual biological differences you may not be able to find anything.
Secondly, if you care about the timepoint of expression for specfic genes, you will need to some time series experiments. (Doing that for the whole RNAseq/GWAS would be very expensive, so ideally you first identify some candidate genes and then study their specific expression profiles with easier methods).

when is the appropriate time to take my samples, i was considering taking at 50% flowering stage.

If you are not an  expert on the species you#re working with, I'd again highly recomment you to speak with someone who is.

Many thanks, these points are highly insightful for me a start, i will discuss with someone that have experience to see what can be done. Thank you so much.


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Do all tumour variants affect the disease pathway
I have analysed some lung tumour samples for somatic variants which generated a list of genes affected by those variants. I tried to analyse KEGG pathways to see what could they disrupt. However, many of the affected genes cause neurological diseases and some cause congenital structural defects. I believe these genes would not be expressed given the location of the tumour. I suppose they will be inaccessible so they would not affect the individual. Is it true or there's something else going on?

Biology is complicated. It's hard to say without looking at the list of genes. Or indeed, even with the list of genes.
What you are calling a "disease pathway" might instead just be a list of parts that cause cancer when they are broken. There is no guarantee that that list of parts is complete. But as you seem to guess it is hard to conclusively demonstrate causality without either experiments or corroborating information (such as finding genes previously known to cause cancer). For example, this page writes:

A recent study published in Nature Genetics, for example, found 10 new variants associated with lung cancer, and studies published in Nature and Nature Genetics found 72 new variants associated with breast cancer.

In the case of breast cancer, 10 of the risk variants are associated specifically with the risk of developing estrogen receptor-negative disease, which tends to have a poor prognosis and for which few genetic influences were previously known.

So only 10/72 of their variants fit into a clear mechanism! This is pretty standard in the field, is my understanding.
Some people have tried to increase their power in GWAS to detect functional associations by leveraging biological associations between genes, for example protein-protein interactions.
While this type of analysis is convenient for variant interpretation, its actual truth is difficult to interpret (for me at least). But it might provide some path forward.
Update
As an aside: you should be able to directly check the expression of genes. You don't have to guess/doubt that the genes are expressed. There are anatomical atlases of gene expression, though in cancerous dysregulation some additional genes may also be expressed. Alternately, you could just directly measure expression, assuming that you still have samples.

Is this what you're thinking of?  They write they have a package including networks for small cell lung cancer available for download, though I was getting a "page can't be found" just now.

@MikeSerfas I wasn't thinking of that specifically, more reflecting that this is a generic method that people use for association results when there isn't a clear pathway. However, that ref does seem pretty relevant to the asker. I do see that they include a ZIP archive of matlab code, which I was able to download (proprietary, so possibly not too useful): https://www.nature.com/articles/nmeth.2651#Sec24


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Inheritance likelihood of SNVs vs InDels
Suppose you have identified a couple of variants in a tumour sample. One of them is a deletion and the other is an SNV in the same gene. You have a familial history of prostate cancer and other cancers. The germline testing results are several weeks away but in the meantime how would you decide which one of them is inherited and which is somatic. They both could be somatic or inherited but for sake of curiosity let's consider they are different.

I don’t understand the question - are you asking whether there is a difference whether SNPs or indels occur on germline or somatic cells?

Welcome to Biology.SE. Thank you for taking the [tour], please also go through the [help] pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, your question: 1) isn't clear, 2) is overly broad, and 3) shows no evidence of prior research. Details: 2) among other things you haven't specified what gene(s) you are interested in. 3) you haven't said where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please note all of these are reasons for down-voting and closure.


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MLE estimation with Mk model in ape or phangorn?
When doing MLE with the R package ape or phangorn, is it possible to set the substitution model to Mk? If so, how does one do this?

I'm voting to close this question as off-topic because this belongs on Bioinformatics SE

SE Biology has an established question tag for bioinformatics, so that property alone should not be reason for closing the question as off-topic.

When u have a Stack Exchange website solely dedicated to bioinformatics work, I would suggest that you ask your question there.

I will do that. The existence of the Bioinformatics SE does not make this question off topic, however.

From reading though the documentation, the Mk model does not appear available.
Although the JC69 model is, which this source describes as a slightly less generalized form as Mk.  The JC69 model still assumes equal substitution rates and equal base frequencies.  To use the JC69 model in phangorn set the model to "JC" and in ape set the model to "JC69".

Of course this will not work if you have more than 4 discrete states - JC69 is a DNA model of sequence evolution. Look into using a program which isn't R. RAxML, IQ-TREE, MrBayes all allow Mk.

The R package diversitree has a large range of models including functions to optimise under Mk. Perhaps have a look at that.


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Is there a measure for degree of reticulation in a phylogenetic network?
When working with phylogenetic networks, how does one talk about reticulate (i.e., web-like) the branches are? Is there a standard measure of this?

biostars.org may have some phd students that deal with that alot.


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What are the methods for detecting anagenetic versus cladogenetic change?
I'm new to the study of phylogenetics and am wondering if there are ways of identifying evolutionary changes that associate with cladogenetic events versus those that arise via anagenesis.

This is thorny, but also depends on exactly what you're asking. What sort of evolutionary changes/traits are you interested in?

Additionally, are you interested in studying anagenetic change within the context of phylogenetic inference, or within the context of trait evolution along an inferred phylogeny?

I'm interested in the evolution of a multistate trait along an inferred phylogeny. I want to know if there is any reason to think that the trait changes are associated with cladogenesis (i.e., took place around the time of cladogenetic events).

If you're interesting in connecting traits to rates of speciation and extinction, then this paper might offer some leads. I'm not sure about how one would go about it for a particular node or set of nodes, but perhaps methods based on stochastic mapping could be helpful?

Thank you! That article was very helpful.


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What plant is this? (Found in Southwest Germany in June)
The picture was taken in Southwest Germany in June, and they covered the ground of a garden we were at...

Undoubtedly a Sedum, but someone with local expertise will have to give the species.  Wikipedia states there are several common species in Europe (https://en.wikipedia.org/wiki/Sedum).

I am almost sure this is Sedum reflexum (aka S. rupestre), in English prickmadam or crooked yellow stonecrop and in German Felsen-Mauerpfeffer. It usually grows at rocky or stony ground, not full of grass.
Distinctive features are the pointed leaves, which are not as round as in S. album and also the bended stem (flower stalks are always bend, hence the name reflexum). Its' flowers should be yellow.
These features can be seen well at the botanical drawing below (from wikipedia commons).

The reason I'm not completely sure is that in garden (and on roofs) exotic sedums are often planted.


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What do Caucasians see in their peripheral vision, and how is their visual field?
I am an Asian who has no idea how much of their nose Caucasians (especially for those with extremely deep-set eyes, very prominent and low brow ridges, and high noses like Brian Shimansky or Rishi Idnani) can see. I also wonder if they are distracted by their nose.
Also, what are their visual fields (nasal, upward, and downward) in degrees?
These articles have made me think of this question: http://pizzawithrice.blogspot.com/2012/08/wondering-about-white-people-visual.html?m=1
https://www.quora.com/Not-to-be-racist-but-why-do-Asians-have-smaller-eyes-and-does-it-affect-their-vision (comment of 3rd answer by Dale Thomas: "I did always want to ask. Do Caucasian men see their eyebrows and forehead? Is there any impact on vision?")

I think we only needed to see the face from the picture!

Speak for yourself @Remi.b. Haha!

There is quite a diversity of noses among caucasians too. As a caucasian with a somewhat similar nose than the guy on the picture (but not as extreme), I can say that I am able to see the "bulgy part" of my nose if I cross my eyes. If I point my eyes toward the right and close my right eye (and vice-versa on the left), I can see a fair part of my nose. If my right eye is left open, the I can barely notice the presence of my nose. I have never felt like my nose was a distraction in my visual field, no $\ddot \smile$

@Remi.b Do you see your entire nose or just most of it? If your nose is shined on, such as by sunlight or overhead halogen lights, does it become more noticeable?

No, I don't think I can see my entire nose although that depends upon when you define being the start of the nose. There is no particular lighting that makes my nose more noticeable in my field of vision. I suspect that you can also see some of your nose as you cross your eyes (at least the tip) but it does not bother you at all. It is the same, it really never bothers me in any way.

@Remi.b I define the start of nose as the bridge of nose (glabella). Do you see your nose bridge? Where it meets the eyebrows? What about your eyebrows? Also, the horizontal skin below/behind your eyebrows (top of eye socket/bottom of brow ridge)?

I can almost see my nose bridge but not quite.

If I look up my vision is just barely obscured by my brows, particularly if scrunched up


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Gypsy Moth Caterpillar Behavior
I have recently done a fair amount of online research about gypsy moth caterpillars and sources I looked at say that older caterpillars feed on the trees primarily during the night and drop down and hide in dark sheltered areas during the day.
I work for someone who had a severe gypsy moth infestation last year and we tied burlap around several isolated trees to see if we could reduce the damage. At the height of the infestation we noticed that there were, at any given time during the day, 20-40 caterpillars circling the base of the burlap and sometimes successfully crawling over it. It looked like they were actively trying to climb up into the trees during the day, which seems to contradict everything I've read.
Can anyone offer any insight into this behavior?


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Hamilton's rule: When to change the equation?
So, in class, my teacher gave two examples of using hamilton's rule. Let b= 4 and c=2.5.
The first was whether altruism would evolve between two diploid full siblings given these values. Since r=1/2, the equation was (0.5)(4)-2.5.
The second question was the same but from a daughter to her mother. He used (1/2)(4)- (1/2)(2.5).
I was confused as to why the teacher outlined this difference. I know that it has to do with the asymmetrical and symmetrical relatedness concept but don't know the details.
Would it continue to apply to grandparents and aunts/uncles as well?


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Difference between reciprocal inhibition and regular muscle movement?
I was looking into a condition I have, anterior pelvic tilt, quite a bit. I ran into a website describing part of the issue as reciprocal inhibition. This was my confusion:
Reciprocal inhibition, defined by just about everyone, is the relaxation of muscles antagonistic to muscles currently contracting, and vice versa. How is this different from regular muscular flex? When we flex a muscle, don't the antagonistic muscles relax to compensate, same as in reciprocal inhibition? Thanks.

What is the difference between reciprocal inhibition and regular muscle movement?

Reciprocal inhibition is part of regular muscle movement. It is controlled by the stretch reflex controlled by the muscle spindle. It's an important part of a functioning muscle and spinal cord, and not pathologic at all. However, this same reflex, in an excessively tight muscle on one end of a joint, would cause an excessively loose muscle on another end of a joint.
Here is an image showing this reflex, from Brust Practice of Neural Science, Chapter 6.

I can't give you any medical advice on this site, so I can't put that in context, but I think that answers your biology question.

Ok, thanks! I just had the thought that the process is in fact pathologic because it was described in correlation with anterior pelvic tilt. Thanks for clearing it up.

@EthanD. Glad to help! If this cleared up your question, you should mark it as the answer by clicking on the gray checkmark. See someone answers


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Human genome, chromosomes
I have a very basic question, but it seems the hardest to me.
So we have 46 chromosomes (23, 2 copies of each). Do all chromosomes have the same DNA? If so, does it mean that in different cells with different functions some genes are expressed and some aren't? Also, if each chromosome has different lets say "fragment" of the genome, how is the genome interconnected?

Welcome to SE Biology. Please take the time to read the tour and, especially how to ask questions here. One key point is that you are expected to research  questions before asking. What texts have you consulted. Have you looked at pictures of human chromosomes and observed whether they are of similar size, for example? Try searching NCBI bookshelf, e.g. Molecular Biology of the Cell

Do all chromosomes have the same DNA?

No.  Not any more than each chapter of a book has the same words in the same order.

If so, does it mean that in different cells with different functions
  some genes are expressed and some aren't?

Yes.  In general, all cells in your body have all the same DNA; what makes your retina cells function differently from your pancreatic beta cells is which genes they express.  Like if every chef in a restaurant had the same recipe book which had every recipe the restaurant can make, but the pastry chef only makes pastries.

Also, if each chromosome has different lets say "fragment" of the
  genome, how is the genome interconnected?

The genome is not physically connected except for all the genes on a chromosome being physically connected.  But a gene product from one  chromosome might control expression of another gene by physically binding to the DNA close to it, which can affect its expression.  But most gene-gene interactions are really protein-protein interactions.  (Or in some cases, RNA interacting with RNA)

Well used analogies and nice short answers to simple, broad intro questions! +1


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What is titratable acid? Why is ammonium not titratable acid?
What exactly do we mean when we use term titratable acid in renal physiology? Why is ammonium not considered a titratable acid?

Ammonium is an ion. Ammonia is a base, not an acid. As far as I am aware this is true even in the kidney.

@David check this out: https://chem.libretexts.org/Bookshelves/Physical_and_Theoretical_Chemistry_Textbook_Maps/Supplemental_Modules_(Physical_and_Theoretical_Chemistry)/Equilibria/Acid-Base_Equilibria/1._Theories_of_Acids_and_Bases

Titratable acidity is a total amount of acid in the solution as determined by the titration using a standard solution of sodium hydroxide (titrant). In other words, it is the maximal capacity of the solution to "neutralise" base solution.
H$^+$ produced from CO$_2$ and H$_2$O is actively transported into the distal tubular lumen.
Titratable acidity is the amount of the H+ which is buffered by bases present in the tubular lumen. Mostly by phosphate (the highest concentration).
When the urinary pH change other molecules can gain the ability to buffer H$^+$.  For example creatinine (pKa about 5.0) or ketoacids (pKa about 4.8)  may contribute to the titratable acidity.
Standard measurement of the titratable acidity with the standard solution of sodium hydroxide spans pH range up to 7.4. Therefore:

Ammonium is not measured as part of the titratable acidity because the high pK of ammonium means no H$^+$ is removed from NH4$^+$ during titration to a pH of 7.4.

Source

I am answering more to the second part of your question as to why Ammonium is not considered a titrable acid.
The pKa of Ammonium is approximately 9.25.
By definition the titrable acidity of a solution is the amount of base (NaOH) that is required to neutralize the solution. On being neutralised the pH of the solution becomes 7 (neutral pH). For neutralisation to happen, the hydrogen ion(H+) from the acid should react with the hydroxyl ion (OH-) of the base to form water (H2O). For this to happen, the acid should be in its dissociated form.
However the pKa of Ammonium is higher than the neutral pH. It would mean that at a pH of 7 (which is the end point of titration) Ammonium ion still retains its hydrogen ion (H+), thus its contribution to the titrable acidity of the solution is minimal, if any.
This is why Ammonium is not considered a titrable acid


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Is it possible to guide animals to a new breeding ground?
(This is a question for a book I'm working on.)
One of the threats to some animal species is the disappearance of breeding grounds (because of the spreading human population, or for example because of ship routes).
Hypothetically: would it be possible to encourage a species to breed on another place? Has that ever been tried? What do animals do naturally - do they seek another location, or rather keep trying?

Hello and welcome to Biology.SE! I suggest you to take the tour to learn about this site and earn yourself your first badge. Also, can you provide a practical example of "breeding ground"?

"Breeding ground" - I'm sorry English is not my native language and I'm by no means a scientist. I mean the place where animals go to mate / spawn (f.ex. certain eels in the Sargasso Sea, if I'm not mistaken).

One example where it has been tried is with whooping cranes: http://operationmigration.org/

The problem that you mention deals primarily with habitat fragmentation, which has a great impact on species conservation. A fragmented habitat will impair migration and can result in inbreeding depression. This has been dealt with wildlife crossing in various sites in the world.


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Lac Operon and Arabinose Operon
In the lower concentration of glucose, what among lactose and arabinose, when both are present in the growth medium, is more likely to be utilized by E. coli?

It's been done.
Both are expressed.
I remember reading about lactose as a special case. The lac operon is not induced directly by lactose, but a different enzyme present in small concentration converts lactose to allolactose, and the allolactose induces the lac operon.
I vaguely remember reading an explanation, that at low lactose concentrations a fraction of cells would randomly get enough lactose to convert to allolactose to induce the lac operon. Then those cells would transport lactose. This would reduce the lactose concentration in the medium so that other cells would not start using lactose. A fraction of the population would use it up, while the rest concentrated on other energy sources. It would be less efficient for the whole population to gear up to use lactose and then use it up fast.
I don't remember where I saw that story and I don't know whether it's been refuted.


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Please help me identify this plant
I got a plant from friend but neither he nor I know what it is. Could anyone help me identify this? Google reverse image search could only find aloe vera and other green plants that are obviously not this species. In addition, it looks like it is dying so any help on caring it is appreciated as well.

It's some kind of succulent and it looks reasonably healthy.  Don't water it more than once a month.

Please add your location.

I would argue that house plants identification are off-topic here and such questions should rather be asked on gardening.SE.

Looks like a cultivar of Crassula ovata or Jade Plant.  A little searching will reveal that there are many out there.  Yours looks a lot like a cultivar humorously called "ET's Fingers".  Search for "crassula ovata ets fingers jade" and you'll see many images.  I won't link to any since they aren't my pictures and the sites may not be available in the future.


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Cleaning out Agar from Autoclave Reservoir
I have a Tuttnauer EZ10 autoclave where the previous user poured m-Endo Agar into the reservoir. Using vinegar, we've been able to remove most of it, but there is a thin film of purple residue coating the interior walls. To get the autoclave safely working again, would you recommend I 1) pour water in and do a steam cycle, or 2) buy the Tuttnauer Chamber Brite and use it?
P.S. I can't make an agar, autoclave, reservoir, maintenance, or cleaning tag, so would someone please make those too?
Thanks in Advance!

Did any get down in the water drain pipe?

Hi CKM, yes it's in there too. What next steps would you recommend?
We have got the agar out of the interior walls of the central chamber, but you can see the agar residue in the water reservoir container. Some vinegar we poured into that chamber has gotten a majority of it in the water reservoir, but we are interested in getting it as clean as possible before use.
And thank you so much for taking the time to help use resolve this issue!

So I had a floor-standing Hayama HV-50 autoclave when this happened, so I'm not sure how different the process must be, just to preface. We had to actually lock-out/tag-out our device, take the side covers off and disassemble the copper drain piping. Then we took what was essentially a plumbing snake and snaked the agar out of the drain pipe. Running a hot cycle and things like chemicals and boiling water didn't work well for us because down in the piping, the contact surface area at any given time is the thin diameter of the pipe. You could have 8+ inches of agar noodle in there.

It might be prudent to just get field service done on your device so you don't inadvertently void the warranty or permanently damage the device.

Hi CKM, sorry for the late response, thank you for your advice and suggestions! We'll look into doing field service like you recommended. Have a great day!


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Glycogen replenishment after exercise
In the body, the liver holds between 90-110 grams of glycogen in storage, while skeletal muscle storage makes up another 400 grams.
If a person exercises and depletes both stores, when a carbohydrate source is consumed, which of the stores is replenished first?

What makes you believe it is one or the other.

I did read that "Your muscles are the secondary storage facility, filling up only when the liver has reached its storage capacity". Is this true? So the muscles will only take in carbohydrates when the liver is full?


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If I expose a bowl of curd to sunlight,then will the bacteria undergo mutation?
Since bacteria undergo mutation while exposed to the sunlight, if a bowl of curd is exposed to sunlight, will the bacteria undergo mutation?

Mutations happen all the time. It does not take sunlight for mutations to happen, whether in bacteria or in eukaryotes. It mainly just take DNA replication for mutations to happen.

Spontaneous mutations occur in all cells (more frequently in bacterial cells) whenever DNA replicates.
No matter the location of the curd, bacterias from that enviroment will have muattions because they replicate.
 UV rays from the sunlight will also cause some mutations and extensive DNA damage in some bacterias that will eventually die, while others will get mutations that aren't as harmful for the cell.
Human cells, compared to bacterias have proof-reading and safety-check mechanisms that prevent mutated cells (UV damage, normal replication, viruses, etc) from spreading around-cancer.


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How does the order of the pairs of cross-links in DNA determine the arrangement of the amino acids?
Quoting Richard Feynman from Chapter 3 of his book Six Easy Pieces, when he talks about DNA:

Attached to each sugar along the line, and linking the two chains together, are certain parts of cross-links. However, they are not all of the same kind; there are four kinds, called adenine, thymine, cytosine, and guanine, but let us call them A, B, C, and D.
...
Next comes the question, precisely how does the order of the A, B, C, D units determine the arrangement of the amino acids in the protein? This is the central unsolved problem in biology today.

Feynman taught his lectures during 1961-1963. Do we now know how does the order of adenine, thymine, cytosine and guanine affect the order of the amino acids in the DNA?

I have found that starting with a relatively accessible and reliable source like Khan Academy is very helpful to learn about an unfamiliar area. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

Yes, it was solved in the early 1960s, starting about 1961.  See Wikipedia's Genetic Code - History, and perhaps "Establishing the Triplet Nature of the Genetic Code".


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What was the cause of some egg-laying animals evolution to animal-laying?
Is there a specific reason for this evolution? Are no egg-laying animals more complex beings so their embryonic  development requires more time and better nutrition conditions?

Oviparity to viviparity (and vice versa and middle ground with ovoviparity) has evolved a number of times. Is there a specific lineage you have in mind when asking this question?

Wikipedia > viviparity#evolution will probably give some useful information

No I think that first appeared oviparity an then viviparity.


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Limitations of the Self-Incompatibility Mechanism in Plants
For a given plant species, how many types of S-loci exists to prevent self-pollination? I would like to know how often a plant stops fertilization process by other plants, thinking the pollens belong to itself due to limitations of SSI/GSI.

The answer is going to vary dramatically depending on the species.
Have you checked wikipedia?

An examples suffices.

I think you mean to ask how many self-incompatibility alleles generally segregate in natural populations? (@tyersome gives a reasonable answer). I cannot tell if you instead mean how many different S-locus systems (mechanisms) exist. I am happy to provide an alternative answer if you clarify.

Herrera, Sara et al. 2018 suggest that there are at least 33 S-alleles in apricot.
I believe some species of Brassica have at least 60 S-alleles identified.
However, there are dominance relationships among these alleles, so I don't think you can directly extrapolate from the number alleles to to the rate at which non-self pollen will be excluded.  The frequencies of the different alleles within a population will clearly also affect this calculation.
In addition, different individuals with the same S-alleles are more likely to be closely related, so I would hesitate to classify this as a limitation of the system.
Ref: Herrera, Sara et al. “Identification of Self-Incompatibility Alleles by Specific PCR Analysis and S-RNase Sequencing in Apricot.” International journal of molecular sciences vol. 19,11 3612. 15 Nov. 2018, doi:10.3390/ijms19113612


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Do the organisms within a lichen communicate with each other?
So you've got your fungus and your algae (or cyanobacteria) (and the multitude of other variations and additions to this two-species symbiosis that lichens present). Do the species that comprise the lichen communicate with each other via chemical or electrical signalling? For instance, could an algal cell "tell" the fungus that it's diseased, thus triggering the allocation of more resources toward pathogen resistance?
And if there is no communication, how have lichens been so successful?

Communication definitely happens, but I don't know of any research into response to disease.
One example are molecules known as lectins that help the fungal partner recognize the correct photobiont (algal or cyanobacterial) symbiont.
Another example are the physical connections between fungal hyphae and photobiont known as haustoria that appear to help the fungus extract sugars from the photobiont.
You should find this review by Piercey-Normore & Athukorala 2017 a helpful place to begin learning more.
Ref: Piercey-Normore, M. D., & Athukorala, S. N. (2017). Interface between fungi and green algae in lichen associations. Botany, 95(10), 1005-1014.

Please expand your answer. Provide a quote, image, or some other useful summary item from the article you link to to demonstrate how it answers the OP's question. Also, due to concerns about links dying, please provide the citation of the article directly into your answer for future reference. (The citation is easily found by typing he paper title into Google Scholar and selecting the citation button (shown as a ") below the search result).

@theforestecologist: Is that more along the lines of what is expected?

@theforestecologist:  Great, thanks for the feedback!


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How are new antigens recognised by the body?
I understand that non-self cells are engulfed by APCs, and are recognised by Helper T cells for the cell-mediated response to occur, but the Helper T cell must have the specific binding for such an interaction to occur surely? How are such new binding sites available in naive Helper T cells for the recognition of the antigen to occur?

Helper T cell (CD4+) with it's T cell receptors (TCRs) can only recognize an antigen when it is complexed with major histocompatibility complex (MHC class II) molecules on the surface of other cells. T cell receptor binds to the MHC-antigen complex.
This guy explains it very well https://youtu.be/TadJkUCJLHo
references:
https://www.sciencedirect.com/topics/neuroscience/mhc-class-ii


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What is the relationship between cell size and metabolism?
What effect does a bigger cell have on its metabolic activity? I understand that bigger cells need more energy, but surely smaller cells may have high metabolic rates too due to their efficiency?


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Is evolution a means to an end?
In "The Red Queen", Matt Ridley frequently argues that evolution is a means to an end, without providing much explanation for such a big statement.
Is this a fact in biology? Do species mutate their genes so they can reach an optimum state, like the coelacanth fish that (allegedly) remained unchanged for the last 300 hundred million years?

The universe does not know neither care. It does not aim. There is no intention in evolving.

This is a good question to ponder but the answer is straightforward and is so very old and tiring to expound on. Evolution is not teleological. Case closed. This is discussed and answered everywhere on the internet. I vote to close, as duplicate of this and this and this and so many more.

Possible duplicate of Why do some bad traits evolve, and good ones don't?

It's been a decade since I read "The Red Queen" and I don't recall Ridley making any such suggestion. Could you quote some of the material that makes you think this?

@CharlesE.Grant in my 2003 copy published by Harper Perennial, at page 31: "[The coelacanth] has stayed the same - a design that persists without innovation, like a Volkswagen beetle. Evolving is not a goal but a means to solving a problem"

Good question--I think the first point to address is "a means to an end" seems to imply willful action. That is, evolution (according to Ridley) would be a conscious effort by a species to optimize the gene pool for survival of future generations; a rationalization for each species to mutate and diverge.
This is not the case, for a couple of reasons. First, evolution is largely due to environmental factors that exert much more control over the genetic drift of a species than any internal (i.e. willful) factors, such as sexual selection. Additionally, optimal performance is often sacrificed for the sake of reproduction (peacocks, now functionally flightless). All sexual selection happens in the context of the organism's environment--phentoypes can change, but if there's only one food source on your island, it's the limiting factor and will exert strong evolutionary pressure to maintain certain traits.
Second, no evolutionary trait is guaranteed to push the species towards a so-called optima. The influence of sexual selection on populations has left many species (again I lean on peacocks as an example) expending energy on developing traits that do not make them more viable or "optimized" as an organism, but instead make them more desirable mates and thus more likely to reproduce and pass on their genetic material. Peacocks could be much more resilient to predators without all that extra plumage, but they've traded off flight for mating success.
Finally, as an aside, evolution happens on such a large timescale that individual populations would barely be able to change their genetic makeup in the course of a single lifetime. This point is not as robust, but if general societal consensus was driving evolution, there would be extinct species littering the corners of the planet. Ridley seems to have missed the mark a little--nobody is doing anything to cause evolution; evolution happens to you over many years of mutations and environmental pressures.

In a comment I ask you for specific passages that give you this impression (since when I read The Red Queen I came away with the opposite impression). You provided the following quote.

in my 2003 copy published by Harper Perennial, at page 31: "[The
  coelacanth] has stayed the same - a design that persists without
  innovation, like a Volkswagen beetle. Evolving is not a goal but a
  means to solving a problem"

OK, that does make me wince a little. "means to solving a problem" does sound a little anthropomorphic to me. I think he may be trying to address the notion that evolution is some sort of metaphysical process driving towards greater complexity or sophistication. Or to put it another way he's arguing that there is no arrow of "progress" associated with evolution. Organisms that are not equipped to deal with their environment die out. Organisms that are well equipped to deal with their environment may persist with relatively little change for millions of years (at least as long as their environment doesn't change).

To quote a writer, We are trying to unravel the mighty Infinite using a language which was designed to tell one another where the fresh fruit was.

"Do species mutate their genes so they can reach an optimum state". No, for several reasons.
Species do not mutate their genes. Individuals suffer mutations.
Many species are in an environment that changes as fast as they can evolve, because of geophysical change, or other species including H.Sapiens. In these cases there is no optimal state to reach.
Evolution often means speciation, not genetic drift within one species.
Adaption often occurs by combining traits already in the gene pool, rather than by new mutations, which are rarely beneficial.


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Have there been multiple aboriginal species of dogs?
In "Variation under Domestication", Darwin writes that:

I may here state, that, looking to the domestic dogs of the whole world, I have, after a laborious collection of all known facts, come to the conclusion that several wild species of Canidae have been tamed, and that their blood, in some cases mingled together, flows in the veins of our domestic breeds.

From this, I understand that several species of dogs evolved independently and half-civilised man tamed them later on, but I want to confirm this. Does Darwin argue that there have been multiple species of beings that resemble the shape of what we now call "dogs", or that there has been one meta-species of aboriginal dogs, which branched off into several wild varieties?

Are you asking what actually happened, or what Darwin thought happened?

Both, I guess. It'd be interesting to know what he thought back then and clear that up with the knowledge we have today.

Most likely we should interpret Darwin as meaning the latter.  Animals that arrived at the shape of wild dogs via substantially different evolutionary routes (that is, via convergent evolution starting with distinct, non-interbreedable species) would be unable to interbreed.

That's one of — quite a few, we have to say — the mistakes Darwin made in his edition from 1859 (I have to confess that this is the only edition I've read, and I reckon this is the only edition anyone should read). This mistake is even more contrasting if you realize that he failed to apply the very same reasoning he had made just a few pages earlier, when discussing variation in pigeons: he explained that, even if counterintuitive, all different pigeons with all different features descend from the same wild species. Then, when he talks about dogs a few pages later, he incomprehensibly makes the same mistake he had just accused his readers of commiting.
Darwin is not the only one: Lorenz made the same unfounded claim, namely that the domestic dog would have two different origins, one from Canis lupus and another one from Canis latrans. We have to agree that Lorenz was way more bold than Darwin when it comes to making unfounded claims.
The fact is that, today, we're pretty sure (the scientific and statistical meaning of sure is being used here) that all domestic dogs (Canis lupus), from the chihuahua to the german shepherd, descend from a population of wolves (also Canis lupus) from east Asia.
Here is a Nature paper from Peter Savolainen, one of the best researchers on this subject: Wang, G., Zhai, W., Yang, H. et al. Out of southern East Asia: the natural history of domestic dogs across the world. Cell Res 26, 21–33 (2016) doi:10.1038/cr.2015.147

My understanding is that two domestication events from two separate populations of wolves is the current theory? obviously the products of those two domestication events (coming from the same species as they did) would have been compatible for breeding so would have become completely intermixed by now.


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NADP and NADPH in in vitro metabolisme test
I did an in vitro metabolism test using chicken liver S9 as the source of the enzyme. I did two different of method experiment. one was using NADP and second was using NADPH as the co-factor. my compound was fipronil, and I expect it to be metabolised become Fipronil sulfone (through oxidation reaction). The results, when I use NADP, fipronil sulfone formed was very low concentration, but in contrast, when using NADPH, I got high amount of fipronil sulfone.
what is the different using NADP and NADPH in this experiment?
Thank you for sharing the informatio.
Kind regards
Alex

Your question is unclear. What do you mean by an "in vitro metabolism test"? What is chicken liver S9? What enzyme are you assaying? What is your assay? Fipronil is hardly a compound that the average user of this site will have heard of — I had to Google for it. If you want us to help you, you should write down the equation of this reaction, showing what you expect to happen. At the moment you seem to be telling us that you are assaying an oxidation reaction but you only get results with a reducing cofactor. You are obviously doing something wrong. We need more information to help you.

Are you sure your question is accurate?
NADP in solution does not exist... it can either be NADPH which is the reduced form (has gained an electron in the form of a H atom and now has the potential to give that electron to another molecule in the solution) or NADP+ which is the oxidised form (has lost an electron in the form of H atom and now has the potential to gain an electron from the solution).
In your experiment, Fiprinol to Fiprinol Sulfone is an oxidation reaction, so the enzyme catalyses the removal of an electron from Fipronol, and it does that with the help of NADP+, which is missing an electron itself and therefore takes it from Fiprinol (oxidises it) to give a high Fiprinol Sulfone yield.

This is really a comment rather than an answer. You are explaining what the reaction is but not why his assay isn't working, which was his (unanswerable) question.


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Turbulence in blood
Turbulence in blood flow is known to indicate diseased or obstructed arteries. Techniques to measure turbulence in blood flow are mostly based on turbulence kinetic energy measurments using MRI [e.g., Ha H et al., PLOS ONE 11(3), (2016) (1)].
Are there any other well known techniques to measure turbulent blood flow, besides those based on MRI?
(1) https://doi.org/10.1371/journal.pone.0151540

Whatever constricts an orifice, whatever dilates a cavity, whatever establishes an orifice or cavity where none shall be, will disturb the even flow of blood and produce vibrations and a murmur.
—Samuel Jones Gee (1839–1911)

Turbulent blood flow is classically detected by auscultation (listening). Turbulent flow across the valves of the heart causes murmurs. A certain amount of external pressure applied to a brachial artery allows turbulent flow, which you can hear, which is how you measure blood pressure. Carotid bruit's are a sound produced by turbulence in the carotid artery.  You can reference any physical examination textbook, e.g., Bate's for information on this method of detecting turbulent flow. There's an NCBI books Clinical Methods textbook that you can search for turbulence.
Turbulence can also be detected by one of a variety of ultrasound methods. The specific measurements taken using these methods are typically anatomic measurements (e.g., thickness of a tissue, distance across a valve), peak flow, overall direction of flow, and gradient measurements, since those are the markers that have been used to characterize disease and/or outcomes. However they can detect turbulence. Quantitative measurements of turbulence just aren't used experimentally.


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Looking to identify this species
I found a rather strange invertebrate...something... outside my home this evening, and I have no idea what it might be. It looks kind of like a small brown lobster, without the claws. I think it has 8 legs, making it an arthropod(?), but if I've misidentified that, please correct the tags. It's 4 or 5 inches long, head to tail. It was found in south-eastern Massachusetts. Potential nearby habitats are open grassy fields, a forest, and a cranberry bog, if that helps.

The picture is kinda fuzzy, I think the video is better.
Any ideas?

Don't know for sure, but crayfish seems plausible to me.

Welcome to Biology.SE! I suggest you to take the tour to learn more about this site and earn yourself your first badge. Have a nice stay!

@mgkrebbs crayfish is what other people elsewhere are suggesting as well. It was pretty cool, I'd never seen one before.

Yep, it's a crayfish ... given the locality and assuming it's native to the area, we're looking at a member of the family Cambaridae, which has dozens of genera and hundreds of species north of Mexico (and requires that you have a "first-form male" for genus level identification: see How to Know the Freshwater Crustaceans, if you can find a copy).


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False positives in TAP - MS experiments
Is anyone aware of a website where they show common false positives often found when doing a TAP-MS experiment to find protein-protein interaction experiments?
Particularly the Acs1 protein (Acetyl-CoA synthetase) seems to be a protein I often see in a TAP-MS experiment so I am starting to think it is a false positives but I can't seem to find a good paper or website where it is mentioned as a commonly found false positive interacting protein.
Any insights will be helpful.
Thanks.

The common repository for affinity purification (CRAPome) contains the results from many tandem affinity experiments and scores them based on their presence in control purifications.
The database can be found here. I did a very quick and dirty comparison of the frequency that human ACSL_1 (Uniprot ID; P33121) and GAPDH were detected in control purifications. The graphs shows that ACSL_1 is not a frequent contaminant (detected in less than 5% of GFP control purifications) whereas GAPDH is frequently detected in control affinity purifications.

You can submit your tandem affinity experiments to the CRAPome and it will  provide quality scores for your hits. It's very well thought out and not difficult to use. You might want to try it if you're still .


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What bee do I have nesting in my front yard
Can someone help identify this bee? Its living in a hole between a boulder and a retaining wall. Our tree that is above it is now bleeding sap so I'm worried about the tree. Pest control wont come because they think it's a honeybee but I doubt that's what it is. I don't hear buzzing and one bee leaves at a time. They are not aggressive. The abdomen is black with yellow stripes.

Hello and welcome to Biology.SE! Take the tour to learn about this site and earn yourself your first badge. Also, can you specify where are you located in the world, what tree is that and the size of the bee?

I wouldn't worry about the bee with regards to the health of your tree.


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loops in neuron synapses
If we see at the connectome of c.elegans, it is easy to find "loops", in the simplest case, a neuron that synapses to another and this one backward to the first.
By example, neuron RIAR has 13 synapses to SMDVL (pre-synaptic is RIAR, post-synaptic is SMDVL) and this one has 8 synapses backward to RIAR (pre is SMDVL, post is RIAR).
Which is the scientific term to denote theses structures? Moreover, main hypothesis about its purpose?

"Recurrent" might be the term you are looking for, i.e.:
running or turning back in a direction opposite to a former course —used of various nerves and branches of vessels in the arms and legs
https://www.merriam-webster.com/dictionary/recurrent
If you observe a recurrent network within a single pair of neurons, you could also refer to this as a reciprocal connection, in that a pair of neurons are both post-synaptic and pre-synaptic to each other.
More generally, you could also talk about feedback as a general motif in neuronal circuits.
The function of recurrent connections likely depends on the specific network you are talking about, but they can be used for predictive coding, pattern generation, computation, and more. In organisms with 'simple' nervous systems like C. elegans, however, these connection patterns can be even more complex, because they have evolved to perform a lot of behavior with very few neurons.
Try searching Google scholar for recurrent neuronal circuits for some more information.


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Can someone identify this tree in Playa Del Carmen, Quintana Roo, Mexico?
I just noticed this tree in Playa del Carmen in Yucatan. It was swarming with bats, the bat seem to be eating either the fruit or the flowers of the tree. Any idea what it is?

Please provide approximate sizes of the leaves, fruit, and tree as a whole. Mentioning more specifics about the location (e.g., did you find the tree along the road, in town, in a wooded area, etc.) would be helpful. Finally, updating your post with clearer photos (of leaves, bark, and fruit) would all be ideal and likely would result in a more accurate ID. Thanks

You might also check out 101 YUCATAN TREES (Conrad, 2015) for a site with some decent photos and data for trees of the Yucatan.

This looks more like a fig tree...

The photos are blurred. We need a pic of the bark and of the fruit, sliced. Does it have pips or a nut? Perhaps a Palaquium variety, i.e.  Palaquium Gutta, which is for producing latex/rubber, because it's in a garden and its a useful commodity plant previously grown in south america. Perhaps slice and study the fruit for a better ID.
Latex plants attract bats.
You can check the bark for latex.
https://youtu.be/6DJHD91VKKY

your proposed species is native to Malaysia! (not Mexico). Actually, the entire Genus is native to Southeast Asia / Oceania (see here). What makes you think this is correct? Please update your answer with more convincing information. Thanks!

I'm quite aware of that! Corn is native to the US and quite a few million hectares are found in Eurasia. Cultivacion y laminado de caucho natural! https://youtu.be/6DJHD91VKKY besides i'm not certain, it's just a lead, he can check the bark. Otherwise its perhaps related to avocado. He has to check the fruit. We can't guess much from the blurry photos.

My guess is as good as the photos, which are not very accurate. the info fits though, quote: Palaquium gutta — The ripe fruit, but not the seeds, is eaten by fruit bats. ... its growing in a garden beside a wall, we commonly see many non native plants in gardens and cities.

Understandable. My concern is that many users and visitors coming through our site just look for whatever is written as answers and often don't think in terms of "this is a guess based on low quality starting info". As such, someone (including the OP) might just assume you're giving the "right answer". I think we all need to be very clear and explicit when we're guessing. I don't think you make that clear on the post, so please edit to clarify. I would suggest adding some additional context based on your comments.

Something like "based on your low quality photos, I'd guess it's ___ because ___. Although it's not native, ___ are some reasons I still think it's possible. You could check the bark or other characteristics to be certain. Perhaps you could investigate related species in your area. I'd recommend starting your investigation with species related to avacado because ___" something in that style let's us see inside your head and whatever expertise or research you bring to the table without judging your response to be definitive and allows a jumping off point for the OP. Please consider editing. Thx

The photos are blurry, the fruit isn't photod, neither is the bark, nor the petiole angles along the branches. It's perhaps a correct ID, and it taught me about plant latexes, and encourages proper identification of plants using bark, and fruit dissection. People identify non-native plants in gardens very regularly on Stack, I get 95 of my species ID's correct. so at least i tried. 95% is not bad. so i will leave the answer and Ill ask a colleague with zoology and botany degrees from Cambridge who works in the Amazon rainforest.

It's funny cos my dad was a forest ecology lecturer at oxford for about 46 years and i'm just randomly ID'ing stuff which is hard to ID and not even getting it, and then a forest ecologist is telling me off. That's the actual title of my dad's job "Forest Ecology tutor" but he is a prof at humanities and human ecology not forestry which was just a BSc. Wee-ird.

I'm not telling you off. I'm asking you to provide more detailed support and to be explicit + clear about how you got to your answer and how others should interpret and use your info. 2.There's no reliable method for judging ID accuracy here, so I'm not sure how you got 95%. 3. It doesn't matter who you/your acquaintances are or what any of you know -- your post should be detailed, explicit, and cited. See meta. 4. I'd advise not answering unclear ID posts unless they're edited. 5. Watch the language

not a fan of stentors thanks. chill out it's an adult website and i'm 42 not 2. the marking system is there for a reason. The OP isn't interested enough in this page to post more precise information therefore this ID is not likely.

If the ID photos are not updated with bark photos and fruit photos, it doesn't do justice to the people who volunteer to ID it, so if there is a problem with this page, it's the lack of flowers/fruit/bark photos essential for me to  update the post.

Right, that's why I advised not answering unclear posts. If the OP won't/can't update with clearer photos or more detail, then the best answer anyone can give is more likely not accurate (because IDing something is HARD if it's not clear what you're IDing!). Ask the OP to clarify, vote to close, and move on. If you think guessing or adding a formalized line of thinking would be useful to others, then by all means provide an answer. However, make it clear that your answer is approximating some species based on XYZ characteristics. You've taken this approach, but I'm asking you to expand/clarify


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Does human behaviour that is caused by inheritance depend on the environment and lifestyle in general?
Different breeds of common domesticated animals such as horses and dogs clearly show different behaviour, instincts, social relationships and similar, due to their biological inheritance. Still they can easily mate with other breeds of the same species. This also applies to wild animals, for example the wolfs living in the rainforest on the Canadian west coast prey on fish (and are maybe expected, with time, to go through a similar transformation as the predecessor to dolphins, that where actually wolf like animals, did when they resettled to the oceans) while inland wolfs prey on moose and elk etc, which requires completely different hunting technique, tactics, pack size and so on.
Are there any similar examples for humans? I reckon that living in the jungle or in the desert or on Greenland should reward different behaviours/traits that influence behaviour. Also going from a hunter-gatherer society to an agricultural society should reward different behaviours, social skills and similar aspect of human life.
Are humans like other animals in this respect (any examples?) or are we unique (?) in the animal kingdom when it comes to the influence of genetics on our behaviour?
One reason I ask is that I got second hand (without sources) information claiming that the natives of Mexico has the highest prevalence, of any population measured, of genes that are known to be connected with/causing ADHD. Mexico was also one the last places on the planet where humankind settled.
The argument went something like this: "during prehistoric time individuals with ADHD tendencies tended to be more adventurous than their peers and therefore traveled further". If this is true, people in Mexico's behaviour should be slightly different from people in current Kenya and Tanzania (by many scientists claimed to the birthplace of humankind), at least if you measure ADHD related traits.

I feel that 99% of the time that someone asks "are human unique concerning ?", the answer is nope. There's nothing exceptional about humans in this respect.
Rephrasing your question
Your question can be rephrased

Is heritability sometimes different from 0 or 1 for humans too?

If you do not understand well why this is a good rephrasing of your question, then you should definitely have a look at this post.
Is heritability sometimes different from 0 or 1 for humans too?
Yes, humans are not exceptional in this regard. In humans, other animals, plants, fungi, bacteria, archeabacteria and for any other living things, any behaviour (and any phenotypic trait in fact) can have a heritability that differs from both 0 and 1, or in other words, there can be for any trait both genetic and environmental variance underlying phenotypic variance in the population.
In fact, very few traits that have a non-zero genetic variance has no environmental variance. Have a look at the post List of heritability estimates in humans? for a list of traits on which we measured heritability.
ADHD
The difficulty with a trait like ADHD is that the methodology to measure it vary a lot from one country to another or even from one practitioner to another. But yes, for ADHD too, there is both genetic and environmental variance underlying the observe phenotypic variance (Thapar et al., 2000).

FYI, @Remi.b, Chrome is flagging your website for not being secure.  I would screenshot it to you except there is no capacity to post a screenshot in a comment.

FYI, my assumption was that humans are not unique in this respect. However, it is a very sensitive subject because a logical next step would be that certain ethnicities ("races") might be better on organizing their lifes or societies which would lead to the conclusion that different outcomes between ethnicities or countries are "fair" and well motivated.

Different ethnicities might differ for genetic reasons as much as they may differ for environmental reasons. The environment in which an individual is born will depends upon the climate, the social environment, etc... Environmental factors such as the social environment or the amount of wealth is greatly affected by the past events of the society in which the individual  was born. There is nothing too sensitive about that. It becomes sensitive when you try to put a judgment of what is "good" or "bad" and when you try to make an a priori judgment of why the outcome is as it is.

For example, if you consider that the situation in Great Britain is bad because you don't like their food, then you might either not realize that food taste is very personal and you might put too a weird emphasis on food when judging the value of people.

As another example, if you consider that the current political situation in Syria is bad (which, so far the vast majority of people would happily agree with) and that you assume this bas situation is caused by the fact that they are genetically more violent, then you ignore the history of the region and the various international interest that is causing the current situation. That's were subject become sensitive. Anyway, I am definitely off-topic here!

As @Remi.b said (I upvoted, by the way), humans are rarely completely unique. The first law of behavioral genetics is that all behavioral traits show non-zero genetic influence (This is one of the most replicated findings in the field). More precisely, heritability estimates of behavioral traits are larger than zero, $h^2>0$ (but smaller than one, therefore environmental differences also contribute to the variance of the phenotype).
Population Differences
You say the following:

Different breeds of common domesticated animals such as horses and dogs clearly show different behaviour, instincts, social relationships and similar, due to their biological inheritance. Still they can easily mate with other breeds of the same species.

Then you question whether humans are different in this way. As you noted, it is a socially sensitive topic, but influential geneticist David Reich has very recently written an opinion piece on this sensitive topic (which I suggest you read in full, given your question).
For example, here is a quote by Reich:

While most people will agree that finding a genetic explanation for an elevated rate of disease is important, they often draw the line there. Finding genetic influences on a propensity for disease is one thing, they argue, but looking for such influences on behavior and cognition is another.
But whether we like it or not, that line has already been crossed. [...]

Regarding population differences:

And since all traits influenced by genetics are expected to differ across populations (because the frequencies of genetic variations are rarely exactly the same across populations), the genetic influences on behavior and cognition will differ across populations, too.

Attention deficit hyperactivity disorder
I have not looked into the genetics of ADHD. It is possible that native Mexicans have a higher rate of ADHD-increasing alleles -- I simply don't know. However, I would suggest you don't completely accept this claim without good sources from primary literature (Also the evolutionary "story" for this claim didn't sound too convincing, in my opinion. However, that may just be because you've been given a weak version of the argument). As with anything, the variance in ADHD is partially due to genetic differences.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Why is Cysteine and Tyrosine used to calculate a sequence isoelectric point?
Why are the amino acids - cysteine and tyrosine used in isoelectric point calculations for a protein sequence, yet neither of them are positively charged molecules? and are not used in net charge calculations.

Both have ionisable side chains.

I still don't know why 7 amino acids are used for isoelectric point and only 5 for net charge?

Every amino acid has a different isoelectric point: a pH where they do not carry electric charge. This isoelectric point depends on the side chains:

By glycine the side chain $-H$ is neutral (while the amino and carbonic acid groups are not) so the IEP is 5.97.
By lysine the side chain $-(CH_2)_4\mbox{-}NH_2$ is alkaline $[R\mbox-NH_2 + H^+ \rightleftharpoons R\mbox-NH_3^+]$, so it will have a more alkaline IEP 9.74 than glycine.
By glutamic acid the side chain $-(CH_2)_2\mbox -COOH$ is acidic $[R\mbox -COOH \rightleftharpoons R\mbox -COO^- + H^+]$, so it will have a more acidic IEP 3.22 than glycine.

Every side chain has more or less contribution to the IEP of the amino acid. In your question

the side chain of cysteine $-CH_2\mbox-SH$ is a weak acid $[R\mbox-SH \rightleftharpoons R\mbox-S^- + H^+]$ so the IEP is 5.07
the side chain of tyrosine $-CH_2\mbox-Ph\mbox-{\scriptsize (p)}OH$ is an even weaker acid $[R\mbox-OH \rightleftharpoons R\mbox-O^- + H^+]$ so the IEP is 5.66

And every amino acid has more or less contribution to the IEP of a protein.
References:

Table of pKa and pI values
Amino Acids with Acidity Values
Introduction to Proteins; Amino Acids, the Building Blocks of Proteins
Electrospray Mass Spectrometry

Plus the phenyl group (or any group) can also exert effects on the ionizability of the amino acid (inductive and resonance effects). It is also incorrect to calculate pI of the entire protein from the sum of its parts.

@WYSIWYG Yes, I think they just want to roughly estimate the value of pI.

I only want a simple linear equation for pI. I still don't understand how if net charge/pI are more or less the same thing. Why you would use D,E,H,K,R for net charge and D,E,H,K,R and C,Y for isoelectric point? Sorry I'm not a biologist or a chemist.

@user2679447 http://en.wikipedia.org/wiki/Isoelectric_point The net charge depends on the pH, the pI of the protein/amino acid is the pH where the net charge is zero. So pI and net charge are completely different things.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Nature of Dengue Fever Genetic Material
Once the genetic material for Dengue Fever is inserted into the human DNA, would the Dengue Fever molecular material be in the form of its own isolated DNA fragment or will it be inserted directly into some existing piece of our DNA?

I'm looking at the life cycle for dengue virus, it looks like a positive-sense ssRNA virus. The viral genetic material doesn't integrate into the host genome. Someone correct me if I'm wrong!

@Kendall you are correct. ss(+)RNA viral genomes behave like mRNA in the host, and are directly translated by ribosomes. The viral proteins thus produced then direct production of more genomes and the assembly of virus particles to infect more cells and other hosts. Viruses that integrate into the host's genome are called retroviruses.

Ah, thank you for the clarification. If you wouldn't mind posting that as an answer I could accept it.

In a 2011 Nature review they provide a figure for the life cycle of the Dengue virus,

Source: Immunity to dengue virus: a tale of original antigenic sin and tropical cytokine storms
The Dengue virus is a positive-sense ssRNA virus. This means the ssRNA that enters the host may immediately be translated. The viral ssRNA does not integrate with the host genome!


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Insect identification request. Long anteni. Grasshopper legs

Found in solo cup used to catch drips from toilet valve. East coast of U.S.

Possible duplicate of Do you know what type of insect this is?

That is a camel cricket, Rhaphidophoridae. https://www.pestworld.org/pest-guide/occasional-invaders/camel-crickets/
Likely some species of Ceuthophilus


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Light Hyperoxia
Imagine you're in some lowland way below sea level were the oxygen partial pressure is higher than at sea level but still lower than the 0.5atm limit. Would their be any effect that isn't deadly or harming even if you stay there for weeks but very uncomfortable like the light hypoxia when you're at 3000m and can't do any effort without fainting ?

Well you can imagine anything. But earth's atmosphere has a pretty consistent composition. The largest variation would be much higher humidity at lower altitudes because of lower temperatures at high altitude.


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Regarding plant stress
I have to plan a bioinformatic study on a plant. Microarray data is available for various stress treatments (drought, cold, osmotic and flood stress) on root and shoot tissues. I am a bit confused as to which tissue is more important for the perception of stress and its direct effect. I want to start with one of them as of now, since the study will get too complicated with so many stress conditions and tissues. I am not from a botany field and look for some thoughts. Sorry if my question sounds silly.Thanks a lot.

All of them are too multifaceted for such a simple breakdown, imo. Drought stress, for example, can be detected at the root which generates ABA for signalling into the shoot, but can also be mediated by changes in air vapour pressure which provides a signal directly to the leaf.

I know this is not what you want to hear back, but I think you should go with all the samples/replicates at once. Only this way you will have the highest possible statistical power to claim the results that (hopefully) you'll have in the end.
When it comes to microarrays and RNASeq, also, it is important to remember that these are mostly whole-transcriptome techniques, therefore the way they are thought to be used is more like "sequence all > analyze all > fish for specifics" than the opposite.
I would use all of them, feed them to a proper pipeline (there are many, not my duty to suggest you one) and see what has a good score/p-value. If you had something in mind before doing the microarrays you probably would have assessed only a subset of the genes, and not the whole transcriptome. So go for both tissues and see what pops out!


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If virus is an inanimate(non-living) structure, why it poses tendency/intelligence to spread itself to others?
A virus has no aim, no agency but just a chemical propagation(DNAs, RNAs). Still, it accounts for millions of deaths and horrible nature.
Rabies, for example, is a very deadly disease with a fatality rate of 90%. One of the terrible symptoms of this disease is Hydrophobia(fear of water). I can surely understand the fact that the victim cannot drink or fear water because virus controls it to as water reduces the chances of transmission.
But why transmit in the first place. If a virus is still aimless like a rock on the ground with the couple of DNAs, how it evolved to replicate and reproduce.
If a virus being inanimate did it, why can't a rock or any other aimless non-living thing do it?

I would consider fungi or plants as pretty unintelligent and aimless as well (although they are living!), but still they are reproducing and growing and have amazing biochemical pathways.  It doesn't need an aim to reproduce, but the capability. And while viruses have the capability, rocks don't have it.

Why does a fire spread?  Or to get a little closer to viruses, why do prion diseases spread?

You're confusing semantics with reality. People referring to viruses as "inanimate" or "non-living" are simply playing silly word games. The terms that people use for viruses tell us about the history of the word "life" or "animate", but do not tell us anything about the virus; in fact, trying to apply these words to viruses is simply misleading, as this question shows.
Viruses have replication machinery, whether it be RNA or DNA, that allows inheritance with variation. These are the requirements for natural selection and therefore viruses evolve and, on a population basis, adapt to their environment (their environment mainly meaning the host they infect).
It should not be surprising that an agent that has co-evolved for 200 million years along with its host is well adapted to that host.
If your question is mechanistically how viruses are capable of doing this, the question is too broad (there are millions of different viruses with different approaches), and asking a more specific question would be helpful.

Related: Why isn't a virus “alive”?

Lets use a metaphor to say that a virus is like a cursed book. The book has milions of copies all around the world in random places. If a person finds the book, and opens it, he will immediately be cursed and will start to make copies of that book, over and over, until it dies. Then the copies of the book will be able to infect new people and this way there will always be copies of the cursed book around. The virus, just like  book, can't copy itself on its own. It needs a person with tools (pen and paper) who can read and write to make copies and distribute them.
In this metahpor the book is the virus RNA (or DNA), the person who read the book is just a random cell (human cell, bacteria, mice cell ...). In the metaphor the 'pen and paper', or the 'tools' to make copies of the virus are ribosomes and enzymes.

why can't a rock or any other aimless non-living thing do it

I'm sorry but this doesn't make sense. A rock does not have DNA. What do rocks have to do with viruses?

how it evolved to replicate and reproduce.

Tricky question. How did YOU evolve to reproduce? It's just a matter of trial and error. In the course of bilions of years nature produced countless viral DNA (RNA) strands, and 99,9999% of them couldn't replicate. The ones who could, did, and we are now able to see them.
Please clarify your answer, especially the rabies part that I didn0t quite understand.

Rocks do not have DNA, what are you talking about ?

I don't know, you mentioned rocks and you suggested rocks have something to do with viruses. Your question not only is very confusing and unspecific but you didn't even reply to our answers and comments.


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Potential obstacles to growing nanoelectronics within living cells?
Say there was a nanotechnology allowing to "grow" and wire up electronic components/sensors measured only a few nanometers in cross-section, though spanning in length across microns. Say this was possible inside living cells (for the purpose of monitoring or even controlling living tissues at individual cell level).
Would such a technology be doomed in the bud simply because cells will immediately deploy antibodies to fight the foreign objects off, and either succeed in it (rendering the growing of said components impossible) or die if they can't succeed in it? Or are there chances to get the cells ignore the electronic components and live with them happily?
What are any other potential obstacles to this sort of technology from biological perspective?

This is an opinion-based question because it is asking about a hypothetical situation. From the [help/dont-ask], avoid asking subjective questions where […] you are asking an open-ended, hypothetical question: “What if ______ happened?” We expect answers to be based on verifiable facts and references, along with subject-related expertise.

@MattDMo I am actually seeking facts and references, obviously not in relation to nanoelectronics in cells (unless such things exist) but in relation to implantation of foreign objects in cells in general (which, hopefully, is already not hypothetical). The reference to nanoelectronics is more of an indication of where the question is coming from rather than requirement for answers to reference it.

This question is still hypothetical, because to my knowledge no one has implanted materials of the type you're describing into animals (which you need in order to elicit an immune response. The devil is in the details here, and we simply don't have the information necessary to answer this question in anything other than a hypothetical manner... which is off-topic.

@MattDMo An answer along the lines "no one has done anything like that yet so the science does not know the answer as of today" would be a good answer then. When the time comes, it would be updated accordingly.

I think this is a really timely and interesting question. Here is a link to the online version of an article that appeared in Sci Am last month. It may be of interest to you and shows that nanotechnology is advancing pretty rapidly in this arena. Perhaps it can help you to narrow down your question and to rewrite it into an answerable format.


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quadrupedalism in human
Recently I saw a BBC documentary on a family from a remote village in turkey where one couple has 18 children and out of which 5 are walking on four legs. These children are 28-34 yr old & have been like this since the birth. Is that story true ? if yes, then what is the explanation behind this in terms of biological evolution ?

@Ruchid Dalwadi Hi welcome to Biology SE. Feel free to take a tour, and take your first badge ! :)  You will find out there how to ask in your SE.  And now about your question. I think you can give us a few refference such a neme of documentary. Last but not least you should do some research on your topic before you post it. Please prevent your question from beeing unanswer. :) Good luck with your biology knowladge seeking :)

this would be a better fit for the skeptic stack

@L.Diago I am grateful for the piece of advice to the new comer here :)

@John with all due respect I did not realize that this question does not fit here as I am asking for a biological explanation as well.

Its fine that you did not realize, I am saying you will have a better chance of getting an answer on the skeptic stack. IS the claim true is outside the biology stack wheelhouse.  It would be important to establish if the claim is true before asking the rest of the question. https://skeptics.stackexchange.com/

@John makes sense :)

peice of advice the first thing they will want is the source of your claim, so finding out which documentary will be helpful.

I'm voting to close this question as off-topic because 1) the source is missing and 2) the question is hardly a fit for Biology.SE and should rather be asked on Skeptics.SE

It sounds like this might have been the BBC2 documentary "The Family That Walks on All Fours", in which case the Wikipedia page about it (linked) may contain all the answers you need.
In short: yes it's real; this is the Ulas family in rural Turkey. This is thought to be the result of a an inherited recessive genetic mutation resulting in cerebellar ataxia that impairs balance, meaning that they cannot balance well enough to walk confidently on two legs. From the Wikipedia page on the documentary:

Not being able to manage the balance needed for bipedal walking, they
  perfected in its place their initial bear-crawl into an adult
  quadruped gait. The family's walking likely has nothing to do with
  genes involved in the human evolution of upright walk.

(a "bear crawl") is a four-legged walk which uses your hind feet, rather than your knees)
It does not tell us much about evolution, but it does tell us something about how plastic motor development is. However, several of the experts interviewed in the documentary became interested in the case because they wondered if it might in fact offer insights into the genetic basis of bipedalism, so it's not a ridiculous assumption.

Interested in knowing what motivated the downvoter - don't be shy, I'm not strongly emotionally invested in this one :)

Id say that this is the result of continuous inbreding, which can result in a deletion of the gene that codes for "learning how to walk".

There is no such gene.

This is pure guess work. Also, it make little sense; why would inbreeding lead to gene deletion anyway?! Finally, I don't think either that such gene exist (to double kmm's comment)


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Firefly mating displays
I live in the northeast US, and really enjoy firefly displays at dusk in the summer. However, when paying attention this summer, I noticed that the fireflies were not displaying every night, but somewhat irregularly, and only over a short period (both within an evening and across the season). I could not figure out what combination of environmental conditions were associated with their display behavior. What are the environmental conditions in which fireflies are most likely to engage in light displays in the temperate eastern US?

Welcome to Biology.SE, thank you for asking a specific question and for taking the tour :)


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Can undigested food proteins enter the bloodstream?
I know that food proteins in our digestive system are denaturated and broken down into amino acids or very small peptides that are then absorbed in the small intestine. If some proteins stay undigested they move to the large intestine and either gut flora eats them or they are excreted.
But lately, I've been hearing a lot of stuff like "if you eat a lot of eggs there will be egg proteins in your blood" or "drink liquid collagen and it will travel to your skin through the blood". It seems really stupid to me. I imagine if all sorts of food proteins entered our blood they would wreak havoc there catalyzing random reactions, triggering immune responses, etc. So it cannot be a very frequent event. But I've been wondering if some of the food proteins can on occasion end up in the blood of relatively healthy people. Does this ever happen? With food allergens maybe?

Possible duplicates/related: https://biology.stackexchange.com/questions/56131/can-proteins-peptides-pass-through-the-intestine https://biology.stackexchange.com/questions/36050/how-does-botulinum-toxin-enter-the-blood-stream-from-the-digestive-tract https://biology.stackexchange.com/questions/84089/why-are-prions-in-animal-diets-not-destroyed-by-the-digestive-system

Does this answer your question? Can proteins/peptides pass through the intestine?

Sort of.
Proteins can enter the body through the intestines by exploiting a few transport mechanisms, They are not truly crossing the cell membrane but are transported across the cell in vesicles. Though not into the bloodstream but into the lymph system.
M cells in particular will move antigens across the intestinal wall, a few more durable proteins (like prions) have been shown to piggyback on this system to cross in tiny quantities. Some viruses also exploit it. Collagen definitely does not enter this way but there are likely egg antigens that may.
Note this is very rare for non-antigens, the vast majority of food you eat will not contain anything that can exploit this although they may contain antigens that get passed to the immune system.
Source
Source 2

That's impossible, if it has to pass through your cells membrane , check this small protein of 3 amino acids (Garcia, A., Eljack, N. D., Sani, M. A., Separovic, F., Rasmussen, H. H., Kopec, W., ... & Clarke, R. J. (2015). Membrane accessibility of glutathione. Biochimica et Biophysica Acta (BBA)-Biomembranes, 1848(10), 2430-2436.)
Although going through cells intermembrane... I think that's possible in theory, but even if that's happens so few protein concentration would reach other places.


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By what mechanism do our nerves lengthen as people get taller?
How do nerves get longer as kids grow taller?  I searched for an answer but I can only find information on the formation of nerves in embryos.

They grow
Nerve axons can grow rather quickly as long as the body of the cell is intact, quickly as in the mm/day range. This is also the basis of how nerves can regenerate.


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Is every flower on a plant unique?
I've noticed on my dahlia plants that sometimes there's a flower which looks completely different then the rest . Either color or structural.  I dig these bulbs up each fall and keep inside to replant.  So my question is are these simply mutations, or caused by environmental factors or? I would assume the dna should be identical to the mother plant ? Thanks

Since the eggs in the flower are produced by meiosis they are all uniquely different.The products of fertilization are also unique combinations of DNA.

Dahlia cultivars are known to undergo somatic mutations, e.g. mutations that occur during growth that can lead to different flowers. See for example this old paper.
So it would be very possible that your bulbs yield somatic mutations that crop up as you regrow them each year. This could be the case even if your bulb has not undergone the mutation, because the mutation possibly is occurring in the meristem of the plant as it makes new shoots or inflorescences from the bulb.
Other possibilities would include epigenetic changes which do not actually modify DNA but can possibly lead to modifications of the expression of genes. These can occur due to changes in environment, but they are a bit more difficult to demonstrate as such.


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What is this large insect?
A large (body about 4 cm long) flying insect flew into my workshed when it was very dark, warm and humid outside, probably attracted by the lights. It fell onto the bench upside down and could not turn back onto its legs. Video here: https://www.youtube.com/watch?v=rQdFE4P-HHo

Can someone please identify the species? This is the very bottom of New Zealand.

For a full answer we would need to have further pictures of the back of the insect. However, NZ has few insects of that size range that are at all common, so I suspect that what you have here is a Huhu beetle (Prionoplus reticularis).
The Huhu beetle is a widespread, large, brown beetle that is often in the 40-50 mm (~2 inch) range, with a pattern of reticulated veins on the elytra. They have brown hairs on the head and thorax and long antennae, that are often 1/3 or up to as long as the body. The species are largely known as a "wild food", with the grubs (larvae) eaten raw or fried. They are also fairly heavy fliers and make quite a racket flapping around. Completely harmless to people.
Edited to add: Having watched the video; a couple of seconds from the end you can see the elytra with the patterns on, so I am confident that this is a Huhu beetle.
The larvae are commonly found in rotting wood, particularly conifers (pine, macrocarpa), so if you have those around, that's where they will be coming from.


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Are bees positively phototropic
One day I had found some bees have come around the light source like other positively photo tropic insects, I hadn't seen any bees coming over light before. I think bees are diurnal and they don't leave their nest at nights, I also read from an article that parasitic wasps may attack bees and these attacked bees would lose their mind and leave their nest at nights.
Is this possible or any other reason behind the night travel of bees and their positive photo tropism ?
http://en.wikipedia.org/wiki/Apocephalus_borealis

Honey bees rely on the position of the sun (and the ephemeris function) to navigate and communicate (i.e. the waggle dance). If they are out too late in the day to return to the hive (occasional), or if they are disturbed at night in the hive, they will fly towards a light.
Beekeepers and bee renters have learned that if you are going to disturb a hive at night, do so with minimal light so as not to lose bees. Also, they avoid lights in the vicinity of the hive in general.
There are a number of parasites and insecticides that cause bees to behave erratically. Colony Collapse Disorder is a major threat to the honeybee's survival.
Why are bees attracted to light? I don't know if anyone knows that.
Dinner and Dancing: Bee Navigation
The Cause Of Colony Collapse Disorder, Disappearing Bees Becoming More Clear

So if we create a large light source near the bee hive then bees would think its sun and they may start foraging, isn't ?

Mostly they fly into the light. Foraging requires more UV light; they need to identify flowers by color (though they perceive them differently) and pattern.

:Thank you for your valuable time. But I dont have enough reputation to up vote your answer. But virtually I am giving one. :)

I guess they think that they are in some sort of tunnel, so they want to fly out. Many insects, for example flies behave the same way.

"In some sort of tunnel" can you explain that further ?


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Do "Giraffe Weevil" males build Nests
I had came across an insect  near my backyard in India(Kerala). I haven't seen this one before and I searched web to find out what insect is this and found its image which saying its a "Giraffe Weevil" (Trachelophorus giraffa). The link below says that this insect is endemic to Madagascar.

http://en.wikipedia.org/wiki/Giraffe_weevil and
They are herbivore insects, with adults feeding on a tree that is commonly known as the "giraffe beetle tree"
(Dichaetanthera arborea)
This states that these insects need the "giraffe beetle tree"(Dichaetanthera arborea) which is also native to Madagascar.
So how come this insect could be found in India(Kerala), and further more all the above links state that the long neck of these dimorphic insects are evolved for fighting and nest making but they do tell that after mating the females will make the nest and lay one egg inside, So did the male insect make any nest in reality, if so then why the male have to perform both nest making and fighting.[Sorry for the errors,also there are more links to this]

Are these photographs of the specimen you found or are they taken from the web? If the latter, the likeliest explanation is that what you found looks very similar but is a different species.

Where have you read that the long neck is used for nest making (the second part of your question)? It is hard to evaluate how credible the statement is without this information.

This link says it http://en.wikipedia.org/wiki/Giraffe_weevil

As the comment by @terdon says, the most likely explanation is that your species identification is mistaken. The superfamily Curculionoidea, which contains the weevils (Curculionidae are the true weevils) is also extremely species rich. Without seeing a picture of what you found, there are many other similar species with long necks in the family Attelabidae, which is the family of Trachelophorus giraffa. For instance, the wikipedia page includes a picture Apoderus longicollis which is very similar to the Giraffe weevil from Madagaskar, and it is supposed to be found in India (see GBIF info):

Paracycnotrachelus is another genus found in Asia where some species have long necks. Another giraffe-necked species is also found in New-Zealand - see Lasiorynchus barbicornis - so the overall body shape is not that unique (note that much of the elongation in this species is of the snout though):

Even if we should never rule out the possibility of range changes/introductions, this must be based on close examinations of the specimen, and it is even more unlikely in this case since Trachelophorus giraffa seems to be a very specialized species.

I had seen the Wikipedia link and it also says that the female roll the leaves for making nest, so is this means males don't participate nest making. Also the photographs I posted are taken from web and I strongely identify the specie as either "Apoderus longicollis" or "Trachelophorus giraffa" and its brightly red colored as giraffa and the longicollis mentioned is light red in color .S I thought it was giraffa, From the day I found this insect I am thoroughly searching for another one but failed to find any.

Keep your eyes open! A proper identification of an individual is the way to go.

First of all, the beetle you found likely doesn't belong to Trachelophorus giraffa. There are lots of of species in the family Attelabidae, many of them having long necks in males and some were described or are known known from India.
I couldn't find any primary source on the nesting behavior of Trachelophorus giraffa, and I suspect that most of the web-pages mentioning the male participation in creating the cradle by rolling leaves stem from this popular book, while in at least another popular book it is explicitly written that females make the cradle.
As attested here, "all females of the species Attelabidae make their host-plant leaves into cradles where they oviposit", so I suspect that Trachelophorus giraffa is no exception to this rule. Here is a very detailed description of mating behavior of a species with similarly long neck: males take no part in building the nest and seem to utilize their necks only when competing for female.