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What are the rules for plasmid names?
What are best practices for naming newly created plasmids?
For example, a common format is pABC123. What is the exact specification? Must there be 3 letters?
What databases of plasmid names exist? How much care is taken to avoid name collisions?

So there are no rules per say (although I wish there were). But there are commonalities among plasmid names and they can help people identify them:
Include the empty backbone name in your plasmid name. This simple piece of information can often convey many important details. Once you know the backbone a plasmid is based on, you can usually derive: a) the bacterial antibiotic resistance, b) the promoter that drives the insert, and c) any other selection markers (for use in other cell types, e.g. eukaryotic cells).
Include information about the insert in your plasmid name. This is often a 3-6 letter representation of the gene (or DNA sequence).
Often researchers will add a lower case letter to the beginning of their insert abbreviation to specify what species it is. Example: ‘h’ is for Human (homo sapiens), ‘m’ is for mouse (mus musculus), ‘r’ is for rat (rattus rattus or rattus norvegicus), etc.
Add any tags or fusions that are on your insert. Typically you would list any tag or fusion protein in the order they appear in the plasmid and their relative position to the insert. Example, if you have a Flag tag on the N-terminal of your insert, you would list it first.
e.g.   pBACKBONE-Flag-hGene
If there was also an EGFP fused to the C-terminal of your insert you would list it after the insert.
pBACKBONE-Flag-hGene-EGFP
If your insert contains a mutation or modifcation, this should be included in the plasmid name.  Mutations are generally listed as the amino acid change and not a nucleotide change. The proper way to denote an amino acid mutation is to list the one letter abbreviation of the wild type amino acid immediately followed by its position (number) relative to the start Methionine (Met) followed by the one letter abbreviation of the mutated amino acid currently at that position.
Check for more information at Addgene.com they are the largest plasmid repository in the world.
By collisions I'm guessing you mean naming your plasmid something that is already "taken." This is a benefit of submitting to a repository, they will ensure this doesn't happen.if your planning on filing a patent, your parent attorney will do it.

One of the most common methods (described by AddGene) is p (for plasmid), followed by the name of the backbone, a dash, and inserts delimited by more dashes. From this we get things like: pBluescript-CMV-mACT1-GFP.
Another method which I prefer is to name all your plasmids in the format given in the question: pABC123. Here ABC is a 3 letter designation that the researcher should consistently use for every plasmid they create (often their initials), and the numbers are sequential (padded with zeros for better sorting by programs).
AddGene is one of the largest plasmid repositories out there. Unfortunately, collisions are a common problem - you should always search the name of a plasmid before assuming things based on the name. While the above two strategies help reduce the odds of collision, there are very few 3 letter combinations that haven't been taken.


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Why does the Vas Deferens detour over the pubic bone?
I was surprised to learn that the vas deferens detours over the pubic bone instead of taking the obviously more direct path.
https://human.biodigital.com/widget?be=u1P&uaid=1ly5V
Because I would assume that the vas deferens is more prone to damage facing the front. Also its damage would put procreation at stake.
Hence my question: Is there a biological reason for this path? Some advantage which outweighs or balances its disadvantages?

What do you consider the "obviously more direct path"? The vas deferens has to pass over the pelvis somehow to get back to the level of the prostatic urethra. Remember that the vas deferens travels with a number of other structures (vessels/nerves) in the "spermatic cord".

okay, probably I am being a bit naive here - I didn't study medicine or biology, after all. But just visualize your own reproductive system and think of direct path between testicles and prostate. That path would be a third or less of the actual - so this is what I wonder about. And the solid pelvic bone in the back increases the risk of damage in case of a hit from the front.

The path of the human vas deferens is a similar example. from Reddit AMA with Richard Dawkins So (at least) according to Dawkins the path which the vas deferens takes is simply an evolutionary "mistake".

You may want to look at where the abdominal muscles are, since they have go around them to get out of the body cavity.

The vas deferens following this seemingly odd path is just a result of the natural course of our evolution.  Millions of generations ago, our ancestors were quadrapedal (walked on all four limbs).  Similar to if you were to crawl on your hands and knees today.  In this position the pelvis is rotated forward by ~90 degrees from its position in humans currently.  The natural position of the testicles in this position would be to hang straight down due to gravity.  Which means the vas deferens would have a straight path up in front of the pubic bone.
Generation after generation, our taller and more upright ancestors were able to survive slightly better than their less upright siblings.  Meaning that many of the more quadrapedal siblings died while their more upright siblings survived and reproduced.  This process has continued for millions of generations, leading to our current homonid upright posture.
The path of the vas deferens was established long before our ancestors ever began this slow transition toward standing vertically.  So the vas deferens still follows the same path that it always has, but now our testicles have moved down because we stand vertically.  Which leaves the vas deferens with its seemingly odd route of going forward over the pubic bone and then down to the testicles.
Evolution is a continuous incremental process over the course of millions of generations.  There has been no point at which the vas deferens could be 'unplugged' and rerouted around the pubic bone.  So it now just loops in front of the pubic bone and then to its destination.
Richard Dawkins used the word "mistake" in his description because there is not necessarily an advantage to that particular route of the vas deferens(there may even be small disadvantages), but there was a LARGE advantage to our ancestors standing upright.  So as we evolved to stand more upright, the testicles moved down appropriately and the vas deferens just ended up where it is, simply because that's where it always has been.  Not really a mistake, just the way it worked out.
Hope this is helpful.

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Is burnt THC still psychoactive?
Asking from a more practical angle. If one smokes a joint - does the THC in the embers contribute to getting high - or is it only the THC released by the heat of the smoke in the not-burning section which contributes?
(same question for CBDs - I assume the answer will be equivalent)

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text:
What's a non-allelic gene?
Non-allelic or non-alletic
I stumbled across the term in my Human Genetics textbook. It didn't explain it there, and a quick google search only showed scientific papers that refer to 'recombinations with non-allelic genes' without explaining what they are.

http://www.newton.dep.anl.gov/askasci/mole00/mole00779.htm

Note that I have never read the term non-allelic genes in a peer-reviewed paper!

It is my understanding that a non-allelic gene is one that affects another's traits, but is not as a typical dominant / recessive manner. If I am correct, this is the same thing as  epistasis - meaning that one gene modifies how another is expressed.
There exists epistatic genes for horse coat color. One gene is the coat color itself (horses may have either brown or red color alleles at this loci), the second gene is for a protein that allows the coat color gene to be expressed.
For example, a horse has two brown alleles at the coat color locus. It also has a wild type gene in the second (modifier) position. This modifier allows the color brown to be expressed and the horse is brown.
B/B, wt/wt --> Brown
If the horse has the two brown alleles, but has a mutant allele at the modifier position, then coat color is not expressed and the horse is white.
B/B, mt/mt --> white
Because the modifier alleles are separate genes from the coat color alleles, the two are non-allelic - yet they both affect the same trait in some way.
I hope this helps.

+1 This is also my understanding of terdon's link. I would argue that the name non-allelic gene is very poorly chosen though. Theoretically speaking there might not have any single gene that does not affect the phenotypic expression of other genes. And of course a non-allelic gene can be a non-allelic gene only if it is polymorphic (and have multiple alleles)!

The context of the term "non-allelic" is non-allelic recombinations which means recombinations between genes that are not exactly alleles but have enough sequence homology to permit recombination.

Is sequence homology needed for recombination?

@CRags For homologous recombination, yes. Even for other kinds of recombination (for e.g. VDJ) there is a stretch of sequence that acts as a homologous block.

Just to expand that recombination is not always needed: there is NJEH (Non-Homologous End Joining), which for example, is how CRISPR works. As it's name suggests in NHEJ, no sequence similarity is required and 2 DNA stretches are simply ligated together at their respective blunt faces.

From "Gene Interactions: Allelic and Non-Allelic" (biologydiscussion.com)
'Non-allelic or inter-allelic interactions … occur where the development of single character is due to two or more genes affecting the expression of each other in various ways.'
'Two non-allelic gene pairs affect the same character. The dominant allele of each of the two factors produces separate phenotypes when they are alone. When both the dominant alleles are present together, they produce a distinct new phenotype. The absence of both the dominant alleles gives rise to yet another phenotype.'
'When a gene or gene pair masks or prevents the expression of other non-allelic gene, called epistasis. The gene which produces the effect called epistatic gene and the gene whose expression is suppressed called hypostatic gene.'
———
From "Genetic Terminology" (ncbi.nlm.nih.gov)
'Whereas Drosophila geneticists used to talk of two loci for a gene, and human geneticists used to talk of two genes at a locus, modern geneticists talk of “two alleles of a gene” or “two alleles at a locus”; this last, which is nowadays so common, is the terminology that will thus be used in this book. It then follows (rather awkwardly) that two alleles at the same locus are allelic to each other, whereas two alleles that are at different loci are non-allelic to each other.'
———
From slides "Interaction of genes" (slide_9) (slideshare.net)
'Non-Allelic gene interaction: In inter allelic genetic interactions, the independent (non homologous) genes located on the same or on different chromosomes interact with one another for the expression of single phenotypic trait of an organism.'


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Distinguishing between mitotic metaphase and metaphase II of meiosis
I'm sorry if this seems like a silly question, but I was brushing up on some cell cycle dynamics and realized that everyone was talking about the differences between metaphase I and II, and since metaphase II was so different from metaphase I (random orientation, tetrad, etc...) the distinguishing of the two didn't seem difficult.
However, I also always hear that metaphase II is similar to mitotic metaphase. In fact, I can't really figure out what the observable difference would be, though I'm certain this must be possible?
How exactly is metaphase II of meiosis different from metaphase of mitosis? I'm sorry if this seems like a silly question, but I haven't been able to figure it out.

I assume you want a differentiating element other than counting the number of chromosomes(i.e. assuming we do not know the haploid chromosome number of the cell)?

@SatwikPasani That is indeed correct.

I'm inclined to agree with @SatwikPasani.  I think you really can only know the difference by knowing what comes before and after (context clues).  If you are observing at the mRNA level, then there are some signaling differences, but the appearance down a scope would be quite similar.


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How is saltatory conduction faster than conduction of unmyelinated fibers?
It's always the same explanation that currents are able to "hop" along Ranvier nodes instead of passing continuously along the axon making saltatory conduction more efficient than continuous conduction.
However, if we take this down to the molecular level, I cannot understand how they are different. Conduction in unmyelinated nerve fibers are first triggered by an effective stimulus, changing the cell membrane potential and thus opening the voltage gated sodium channels, causing an explosive influx of sodium ions. The action potential is conducted along the fiber through stimulating sodium channels in nearby regions, causing rapid flow of sodium ions into the cell in membrane immediately near the segment of stimulation and this process repeats as the action potential passes unidirectionally along the axon.
Conduction in myelinated nerve fibers are usually described as hopping along the axon, but on the molecular basis, sodium channels are congregated at the site of Ranvier nodes, large numbers of sodium ions that made its way into the cell swim down the axon in the cytoplasma of the nerve fiber reaching the next ranvier node, changing the membrane potential in that specific site therefore triggering another influx of sodium ions.
So to put the question simply, the mechanism of continuous conduction is triggering voltage gated sodium channels continuously along the way, whereas the mechanism of saltatory conduction is triggering-swimming-triggering-swimming...how does this difference essentially make saltatory conduction faster?

Possible duplicate of Why is saltatory conduction faster than continuous conduction?


text:
Infection of urinary tract if the pH of urine is made alkaline
It is very well known that drugs like phenobarbiton,morphine are unionized, lipid soluble.So,in case if there is toxicity due to these drugs,the only way to save the patient is make the pH of urine alkaline and thus facilitating its excretion.But,the normal pH of the urine is acidic which protects the person from various urinary tract infections,if the pH is made alkaline is there a increased for the patient to have urinary tract infections?

There is a huge misconception here.  Morphine overdose is treated with Narcan (naloxone).  Phenobarbiton overdose is treated with artificial respiration (in extreme cases), blood pressure medication, and management of low heart rate.  The concept of lowering the pH of the urine to increase a drug excretion is (to my knowledge) never used in emergency settings.  Dialysis, which filters the blood, would be used to 'clean' the blood of toxins.  Think about it.  Time is life, and changing the composition of your fluids would take a lifetime compared to the implemented measures in emergency rooms.  You body has an extremely sensitive acid-base balance.  You do not want to try to increase or decrease the pH of your bodily fluids.


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Can a novel protein domain arise de novo in nature or did all protein domains evolve from a single ancestor?
I know there is extensive research into the taxonomy and evolution of protein domains and many connections are, and are continuing to be, found between numerous domains. However, as far as I can see, new domains always arise from preexisting ones. I have seen no paper, in any field, showing the development of a new protein domain from a random piece of DNA which just mutates a start codon and synthesizes a new protein with no apparent function. I know this is theoretically possible but has anyone seen any evidence it has happened in any form of life in any geological period of time? OR are there some other mechanisms that could generate novel domains from non-coding DNA that I have overlooked when searching the journals?
My thinking is that, if de novo protein domain generation doesn't occurr, does it mean that all protein domains are a kind of "progeny" of a single domain that arose at the onset of life as we know it (or maybe even was the first lifeform on Earth). It seems very strange to me that this hasn't been pointed out by now since it's a relatively simple deduction. Thus, I'm asking either for a reference paper showing evidence for the evolution of de novo protein domains from a random piece of DNA that somehow managed to turn into a gene or for a reference to a paper discussing the idea that all proteins originate from a common ancestor existing at the onset of life and even, possibly, a single domain as old as life itself?

You're right, it doesn't work this way. Which is why you've never seen a paper on it. "I'm asking either for a reference paper showing evidence for the evolution of de novo protein domain unknown by now from a random piece of DNA that somehow managed to turn into a gene" You won't get one; that's not how it happens.

Then how does it happens @anongoodnurse? Please, explain how we can get a brand new protein domain and even possible new family of domains if there is no previous domain it came from? As far as I know all domains come from previous domains, all genes evolved from previous genes and all proteins from previous proteins. But if that is true does it mean all domains, all proteins, all genes, the entire biodiversity evolved from a single ancestor gene, which coded a single ancestor protein and may be it had a single ancestor domain? Am I right on track or am I missing out something important here?

I've trimmed down your question a little bit, I hope it's still okay for you. I think it is interesting and will try and look for some literature.

Yes, there is no problem. I think it's better this way, too. :)  I hope I could know do novel domains rise from random pieces of DNA or all proteins and genes just like the cells they are in come from a single ancestor? Of course we could speculate about LUCA containing all the genes necessary for the entire biodiversity but even then the question remains: Did LUCA itself had its genes and proteins evolved from a single gene with a single protein and may be a single domain? I'm thrilled to know could we trace all biodiversity to just one molecule, even more-to just one domain?

Yes. Novel protein domains can arise de novo in nature. The evidence is quite solid as those new domains show all the expected mutation patterns and statistical properties (expected for something evolving from DNA that doesn't yet encode for a domain). E.g.: see the following meta-analysis, which also describes how those new domains behave relative to older ones, and how they integrate into proteins: Toll-Riera et Mar Alba 2013, BMC Evolutionary Biology, "Emergence of novel domains in proteins":  https://bmcevolbiol.biomedcentral.com/articles/10.1186/1471-2148-13-47
If you are additionally interested in new genes, the following mini-review: http://www.sciencedirect.com/science/article/pii/S0960982214001547#bib20 .
If you are additionally interested in in-vitro evolution, which is directly observable within the life-span of single humans, the following review: http://www.sciencedirect.com/science/article/pii/S0022175904001309

The link is dead for the first article. Could you write the titles/authors/etc for these articles?

Maybe the link isn't dead but rather my useless network is acting up. In any case, full citations would be appreciated.

note that presently NPG appears to have server problems (even nature.com is down), which also applies to the journal above.

@tsttst, if you could provide a list of the journals you targeted in your search and can provide me with a list of keywords I would give the price to you. It would be also useful if you can name the search engine you used. My background is in theoretical biology and the origins of Life, so, I'm not really good at genetics and modern fields connected to proteomics and may be have been using the wrong keywords, so, if you can tell me the 2 lists-of related journals and keywords I will be greatly thankful. I wish to know how to search better and if you can help me I will vote for your answer.

@YordanYordanov: I knew that the topics covered by links 2 and 3 would exist and concluded that they would be thematically close, if something on de novo evolution of domains existed. Since the latter seems to be a fascinating and important topic I concluded that it would be covered tangentially by reviews on topic of link 2 and 3. Thus I looked for first review in google scholar on topic 2 within a good journal ( main npg or cell press ) and would read it - hoping to satisfy my and your curiosity on topic 1. Indeed the first review would contain cognate citation towards specialist article.

Thank you very much @tsttst. :) I will give the reward to you for your efforts.

@YordanYordanov: thank you, and good luck and fun for your future research. No effort spent on my side as I also wanted to know the answer after seeing your question


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Why do doctors use a new thread for each stitch?
Why do doctors use a new thread of the same kind for each stitch instead of using a single thread for the entire stitch?

Using a single thread for a suture also known as continuous stitching has a major con that it has higher risk of failing if the suture is cut in just one place. So it is generally avoided eventhough it is very easy to do.
On the other hand interrupted stitching ( one thread for each stitch) is favoured because of lesser risk of failing, eventhough it is time consuming than continuous stitch.
Source:https://en.m.wikipedia.org/wiki/Surgical_suture

If they used a single thread, then a single break in that thread would cause the entire thread to fall out of place. Using multiple threads means that if a break were to occur, the rest of the stitches would still be able to hold their place.
One time I had 5 stitches in my hand while I was snowboarding. Sometime during the day I fell down and one of the stitches came out; there was a lot of blood, but it was probably nothing compared to how much blood there would've been if it was a continuous thread and the whole wound opened.


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Why is my blood group O -ve?
My parents have B +ve blood group in fact my brother also have B +ve blood group, then why my blood group is O -ve ?

Due to our being diploid, we have 2 genes for deciding blood type. the gene for blood type O is recessive and so is the Rh-. If your blood type is O- and your parents are B+ then your parent's genes are BO+/- for both of them. and you inherited O AND - from both of your parents.

Humans are diploid organism. So humans have two copies of every chromosome and gene.
When a person has B blood. We mean that the blood cells of that person expresses  the B antigen.
To produce the B antigen you will need at least one allele for the B antigen. Hence the B antigen phenotype can have a genotype of BB or BO.
Now if two people have the genotype of BO have children, a punnet square will show they they have a 25% of having a child with BB genotype, 50% of having a child with BO genotype and 25% of having a child with OO genotype.
Phenotypically, it means that there is 75% chance of having a child with B blood. And 25% chance of a child with O blood.
A similar system also occurs with rhesus +/- system. A person with +ve blood can have a genotype of ++ or +-. If two people with the genotype of +- have children together, there is a 25% chance that their child will have -- genotype and be rhesus -ve.
The two systems work together. So two people with genotype of BO blood type and +- rhesus antigen having children together, they can have a child with O blood and rhesus negative with a probability of 1/16 (6.25%)


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ID a marine creature found on a beach on the US east Coast
While walking on a marshy beach, I found this creature. It has no eyes, no feet, no fin, no gills. The only thing I know is that the skin lightly contracts. I found at least three of these. It is basically carried around by water.

Found this on a Maryland beach, roughly 150 miles east of Washington D.C.

Where was this found?

edited description to add this information.

It's positively a sea anemone. It retracts the tentacles when disturbed and become quite rigid. It's hard to identify it in this condition, leave it for a whlie in a jar with sea water and you'll see.

Based on your description, it could be a sponge (but I don't think sponges have a contractile skin), a tunicate or a sea cucumber.
I would favour the last option.

The following questions might help further identification: How many holes can you spot?
If there are 2, where are they placed with respect to one another?

I hope someone can propose something more precise.
Edit:
As noted in the comments, it could also be a sea anemone. In my experience, these have a quite soft body. In that case, it should have only one opening, and the opening should let tentacles out when the animal is left quiet in the proper environment.

Paranthus rapiformis has a similar form.


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Nucleoside triphosphates vs nucleotide diphosphates
A nucleoside can be defined as a nucleotide without its phosphate group. Thus, a nucleoside triphosphate (NTP) is a nucleoside bound to 3 phosphates.
This in turn must be equivalent to a nucleotide (whose name implies the inclusion of one phosphate already) plus an additional 2 phosphates. Thus, would it be appropriate to refer to an NTP as a nucleotide diphosphate?

I don't think this is technically incorrect, but why on earth would you want to give it a deliberate confusing name?

Did you check on Wikipedia or in Biochemistry at NCBI bookshelf before posting? Posters to this list are expected to make a reasonable attempt to find an answer from a standard source.  Or are you trying to make some sort of clever point? If so, it is not "appropriate" here.

Nucleoside is nucleotide without a phosphate group. That is something we say to understand and correlate nucleotide and nucleoside. But if followed Terminology by IUPAC a nucleotide should contain only one phosphate group, not more than that. Though NTP is a type of nucleotide, however, for the sake of technical terminology, nucleotides are given classifications as nucleosides with a suffix describing the number of phosphates present in a specific unit. For example, if a nucleotide has one phosphate, it is a nucleoside monophosphate (NMP). If the nucleotide has two phosphates, then it is called a nucleoside diphosphate (NDP), and for three, it is a nucleoside triphosphate (NTP). So you can say NTP as  nucleotide diphosphate, but considering the fact that nomenclature also indicate the chemical property of the compound, it would not be right.
Wikipedia


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What's the difference between constitutional samples and tumor samples?
I think the tumor samples have two copies of the chromosomes. But for constitutional samples, do they only have one copy of the chromosomes?

Every cell has two copies of each chromosomes - except for sperm and egg cells.

...and some cancerous cells.

Constitutional samples do, as you surmised, refer to germ cells (sperm or ovum). Hence they have 1 copy of DNA instead of 2.
Tumours, as they acquire more mutations, often have aneuploidy, or different numbers of chromosomes, and can also have increased incidence of Xn chromosomes where X > 2. This is polyploidy for humans and organisms with normal 2n chromosomes.


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Insect Identification: Possible Flanged Bombardier Beetle Encounter
Location: Southern India
Insect Length ~ 1 cm
I encountered an insect in my room, and upon attempting to catch it, the insect released sharp, pungent vapor bursts repeatedly. The smell was extremely strong and long-lasting, to the point where I had to vacate the room for 30 minutes.
Using Google Lens, I got a suggestion that it could be a bombardier beetle (Platyrhopalopsis melleii). However, the pictures I found online don’t match exactly with the insect I encountered. I would appreciate help with the following:
1.  Can someone help identify this insect?
2.  What chemical did it release, and what are its effects on humans?
3.  What is that metallic stuff on its back?

warning: graphic images

The gold colour is part of its patternation, many beetles have irridescent colours, including some that appear almost all gold (such as the golden tortoise beetle. If you mean the silver under the elytra (wing cases), that's the wings.

While I am unsure of the exact species I am fairly sure it is some sort of ground beetle. The metallic stuff on it’s back is it’s hind wings

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How harmful is aluminium?
I have been taught in school that aluminium is harmful for brain.
Thus sour meals should not be cooked in aluminium pots and it is unhealthy to add lemon juice to tea while there is teabag in the cup, as acid facilitates aluminium release.
The only safe limit for aluminium intake I know is FDA pediatric limit for parenteral sources (5 μg/kg bw/day). I know no research the limit is based on, but I have read an abstract of a paper claiming it was impossible to comply with the regulation in patients weighting less than 50 kg.
Nowadays aluminium ions are present in several vaccines, which are considered safe to be injected intramuscularly in infants despite despite being  nowhere near the FDA limit.
I'm quite confused how strict should I be in avoidance of aluminium intake (especially dietetary intake - which I expect to be far less effective than parenteral).
[EDIT]
It seems aluminium is also a component of some antacids which are used to treat heartburn.
Does it mean aluminium consumption is safe at general, or it is just considered to be less harmful than acid indigestion (there are some side effects  mentioned - but nothing about accumulation in the brain)?

@RonJohn I think iron is even more hamful then. ;)

Too true, but this wasn't a comparative question...  :)

Now I'm wondering if the discount was worthwhile on that depleted uranium skillet.

@jamesqf if God had wanted man to hit with aluminum bats, he wouldn't have invented trees!

well the thing to understand is that "toxicity"  is relative.Anything can be harmful if consumed in high quantities .

If cooked using aluminum pots ,the aluminium reacts with the aluminium creating aluminium salts ,which may be more harmful than the metal in elemental state, as it accumulates easily.

a bit of both and also, sorry for the typo .-. , been doing that all day

@pranavB23 it nicely fits the level of abstraction of other comments ;)

@pranavB23: Yes, for instance both water and oxygen are necessary for life, but too much of either will kill you.  E.g. https://www.webmd.com/fitness-exercise/features/water-intoxication#1

@jamesqf which reminds me about threat of dihydrogen monoxide ;)

Here is a link to the Public Health Statement for Aluminum produced by the Centers for Disease Control and Prevention (CDC) in the United States.  There is much more information on the web page but the following are some of the more pertinent points to your question.
Potential Health Effects
Workers

Workers who breathe large amounts of aluminum dusts can
  have lung problems, such as coughing or changes that show up in chest
  X-rays. The use of breathing masks and controls on the levels of dust
  in factories have largely eliminated this problem.
Some workers who breathe aluminum-containing dusts or aluminum fumes
  have decreased performance in some tests that measure functions of the
  nervous system.

Humans

Oral exposure to aluminum is usually not harmful. Some studies
  show that people exposed to high levels of aluminum may develop
  Alzheimer’s disease, but other studies have not found this to be true.
  We do not know for certain that aluminum causes Alzheimer’s disease.
Some people who have kidney disease store a lot of aluminum in their
  bodies. The kidney disease causes less aluminum to be removed from the
  body in the urine. Sometimes, these people developed bone or brain
  diseases that doctors think were caused by the excess aluminum.
Although aluminum-containing over the counter oral products are
  considered safe in healthy individuals at recommended doses, some
  adverse effects have been observed following long-term use in some
  individuals.

Some regulation and recommendations:

Drinking water

The EPA has recommended a Secondary Maximum Contaminant Level (SMCL)
  of 0.05–0.2 mg/L for aluminum in drinking water. The SMCL is not based
  on levels that will affect humans or animals. It is based on taste,
  smell, or color.

Consumer products

The FDA has determined that aluminum used as food additives and
  medicinals such as antacids are generally safe.
FDA set a limit for bottled water of 0.2 mg/L.

Workplace air

OSHA set a legal limit of 15 mg/m3 (total dust) and 5 mg/m3
  (respirable fraction) aluminum in dusts averaged over an 8 hour work
  day.

Yep, good catch.  I needed to remove the Inhalation at the beginning of the sentence.  I'll revise to avoid any further confusion.

Why is there one section titled "Workers" and another "Humans"?

@Phil each of these species obviously lives in a different environment, thus have a different aluminium exposure ;)

@Phil: Possibly because some of it is taken from information provided for industrial safety uses?  After all, the only people who are likely to be exposed to large amounts of aluminum dust are people who work in aluminum-related industries.  Note also that inhaling large amounts of any sort of dust is not a good idea, and is rather different from ingesting material in solution.

@jamesqf are the workers not human then?

@Phil: When have I suggested otherwise?

@jamesqf by defending the incredibly odd scenario where we have information under two headings: "Workers" and "Humans".  It's clear from the content "Workers" does not refer to bees (for instance), but human beings who happen to be working with the stuff.  Which makes "Humans" an odd heading for the next paragraph.  It implies the other paragraph isn't referring to humans (ie, the workers aren't human).  Perhaps "Workers" and "The general public" would be a better set of headings?  Just defending it as copy-paste means the author was sloppy and lazy.

@Phil: As I said, because the only people likely to have significant long-term exposure to aluminum dust are those who work in aluminum-related industries.  Whereas "humans" - the general public PLUS workers - is about equally likely to be exposed to dissolved aluminum-containing chemicals from cooking pots, antacids, and the like.

Just as a note: "some adverse effects [...] in some individuals" is extremely vague. It is unclear whether CDC refers to brain and bone disease observed in people with kidney disease, or to other adverse effects in otherwise healthy people.


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Why are vaccines a successful treatment of allergy?
As I understand the answer to Allergic rhinitis vaccine, the vaccine facilitates immune response against the antigen.
Given that allergy is an overreaction of the immune system against harmless antigens, how can facilitation of the immune response act as a cure (moderate the response or so)?

This is basic and also broad. I see you read this question: https://biology.stackexchange.com/q/30195/5198. Though it is not the same question, it does provide the answer. See also a possible duplicate: How Do White Blood Cells Learn? Or Do They?

@anongoodnurse Indeed, I had read the linked questions. Don't get me wrong, but I think one of us is misinterpreting written text again. Why do you think questions about facilitation of the immune response against a pathogen address moderation of the response against an allergen?

"...how can facilitation of the immune response act as a cure?" There is no mendion of moderation of the immune response in your question. That is a different (and also broad) question.

@anongoodnurse ok, now it is stated explicitly

Still basic (first question) and now too broad.

@anongoodnurse I definitely miss your point. I am not a native speaker, but IMHO there are two question marks, but only one question. Also I can not address the breadth issue.
Let's assume I am not clever enough, so unless you wish to devote a lot of time to explain it, I propose to drop the conversation. The question has been already interpreted as intended and answered.

The theory is that constant and gradual escalation of the administered dose of allergen eventually tolerizes the immune system to the allergen through the induction of peripheral Tregs or IL-10-secreting effectors.
While the purpose of a traditional vaccine against a pathogen is usually to rile up the immune system with and adjuvant or modulators, the idea of allergy immunotherapy is to sensitize the patient to the problematic allergen by implementing chronic exposutre. That mechanism is still poorly understand and is not thought to have immune memory, as the effects of the therapy tail off after discontinuation.


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Why is full cell/high antigen dose pertussis vaccine dangerous for adults?
I do remember that I have read (or heard) somewhere that as a human is older, the whole cell vaccine (and high antigen dose one) has more and more adverse effects.
As it is consistent with the target age group mentioned in the leaflets attached to the vaccines:

whole-cell DTP vaccine (Instytut Biotechnologii Surowic i Szczepionek BIOMED S.A.) is suitable "for children not older then 3 years",
high antigen doseInfanrix-DTPa (GlaxoSmithKline Biologicals S.A.) "shall not be used for children older than 7 years",
low antigen dose Boostrix (GlaxoSmithKline Biologicals S.A.) is "suitable for a person older than 4 years",

I suspect it is true. Unfortunately I lack a reliable source to both confirm that and read more about the effects. Can anyone provide a reference.
As there is a strain of pertussis "resistant" to acellular vaccine, IMHO it would make much more sense to use whole-cell vaccine for adults too.

It seems it is not about pertussis.
I have found information in the Infanrix-DTPa characteristic that it is not recommended for adults due to high dose of diphteria toxoid.
Both Infanrix-DTPa and whole-cell DTP vaccines contain over 30 international units (whatever it is) of diphteria toxoid while Boostrix contains "not less than 2 i.u.".

Yes, it is true that the whole cell vaccine can have more adverse side effects on older patients (and much younger patients also). This is because their immune systems can be weaker and they are more susceptible to side effects. Some of the vaccine adjuvants (preservatives) can also be dangerous for at-risk patients, and can have more serious long-term effects. According to the CDC, the ingredients include:
Each 0.5-mL dose of Daptacel® (Sanofi Pasteur) contains 15 Lf diphtheria toxoid, 5 Lf tetanus toxoid, and acellular pertussis antigens [10 µg detoxified pertussis toxin (PT), 5 µg filamentous hemagglutinin (FHA), 3 µg pertactin, and 5 µg fimbriae types 2 and 3 (FIM)]. Other ingredients per 0.5-mL dose include 1.5 mg aluminum phosphate (0.33 mg of aluminum) as the adjuvant, ≤5 µg residual formaldehyde, <50 nanogram (ng) residual glutaraldehyde and 3.3 mg [0.6% volume per volume (v/v)] 2-phenoxyethanol (not as a preservative).
With any vaccine, one must weigh out whether it would be riskier to get the actual disease or the side effects of the vaccine.
For further reading:

about the whole cell pertussis vaccine
another informative article
more about the ingredients

The problem is that whole-cell DTP vaccine is suitable "for children not older then 3 years" (Instytut Biotechnologii Surowic i Szczepionek BIOMED S.A.). Also Infanrix-DTPa (GlaxoSmithKline Biologicals S.A.) "shall not be used for children older than 7 years" while Boostrix (GlaxoSmithKline Biologicals S.A.) is "suitable for a person older than 4 years".
Thus it looks like the problem is with a mature immunesystem. I would bet it may be overreacting or so.

This is because their immune systems can be weaker What does this refer to?

I think we can safely say that the average person reading this response can just assume it is always safer to vaccinate.  In the unfortunate age where Jenny McCarthy's mommy instinct is given equal weight to actual experts, we should avoid ambiguity and plainly identify failure to vaccinate for what it is: irresponsible bordering on negligent / child abuse. Vaccines save lives. Diseases take them. It's almost like living with the benefits of vaccines has afforded people the luxury of forgetting why we need them.

@JustinMasters Any kind of propaganda (even one supporting vaccination) is a misconduct that should be avoided. It may easily backfire. It is fact that vaccination may have adverse side effects. In some cases (eg. TB in Canada) it is safer to not vaccinate. It is also probably the case with vaccines containing high doses of diphteria toxoid in adults. Failure to acknowledge it leads to be accused as a member of vaccine genocide lobby and no longer trusted as reliable source by people interested in facts.

When did we start talking about TB vaccines?  I can't remember ever having a doctor recommend that I be vaccinated against TB, but I can assure you that if I ever had to go anywhere where I had a high probability of being exposed to TB, I would take the vaccine prior to going. It's the only responsible thing to do.


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Reasons for a flower type to consume water faster than another?
This is an easy experiment where you put a white flower into a recipient filled with water and liquid watercolor, so that the flower gets dyed.
While doing this experiment for different types of flowers, and assuming equal ambient conditions, what would be the most important characteristics  (e.g. flower size, petal length, stem thickness, number of petals...) and the biological reasons for certain flower type to consume water (and get itself dyed) faster than another? (e.g., does a thicker stem mean the xylem is stronger?)
More specifically, I'm interested in comparing a rose like this and a carnation (like the one shown in comments) as an example to the answer.
(Note: I couldn't show a carnation sample image due to my reputation being lower than 10, but I'll update it as soon as I can).

light levels and temprature will have a large effect, so you should consider this.

@John Experiment was attempted to make under similar light and temperature values, although it wasn't exactly made in perfectly equal conditions (It was a school project). Yet I'd mostly like to know what should happen and why.

The major factor should be how much water each looses and thus needs to be replaced by the dyed water. photosynthesis levels and stomatal count will both effect this.  Stomata count is influenced by both genetics and the environment in which the plant is raised. Hopefully someone with more knowledge about these specific plants can help, but I would not expect the loss/uptake to be the same.

One problem with giving a definitive answer is that there are literally thousands of different varieties of roses, with different flower sizes and number of petals.  I'd guess (perhaps wrongly :-)) that water uptake is related to the area of the petals, so a single-flowered species rose would take up water much slower than something like a centifolia.

related: https://biology.stackexchange.com/questions/48023/do-flowers-transpire

Carnation flower that I'd like to use as an example is something like this.

people are touchy about the scientific qualifications of an answer, so i wont answer even as a fan of flower and gardening. fat stalks, woody stalks, aversion to vase water, waxy/long lasting flowers vs fast wilting ones, all contribute to your result. generally a fast wilting flower which absorbs vase water well by capillarity will go the fastest, if you find a list of flower wilting times from 1-7 days you'll be on the right track.

Don't forget to consider the 'engineering' of the plant, as brought about by evolutionary history. Some plants will build fewer openings in their leaves ('stomata'); others use a strategy that allows them to only open these at night (see 'C4 photosynthesis') or CAM (Crassulacean Acid Metabolism) photosynthesis.

rbrucep is totally right, the engineering of the plant, waxyness, stomata size and frequency, surface area, cils to stop air moving, water reserves within the plant, rigidity and pressure of cell walls, change the plant's responses.


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Specific Neurons that Require Glucose
I've been doing a bit of armchair biology lately, and have been interested in the metabolic flexibility of neurons. My understanding is that, besides glucose, many neurons can metabolize lactic acid or ketones. However, some reports point out that some neurons can only metabolize glucose, without ever indicating which, or in what regions of the brain. (It may be that the following exert is suggesting that each individual neuron is using a mix of fuel sources. I have not been able to find much via the Google.)
From the linked book:

When changing slowly from a carbohydrate diet to an almost completely
  fat diet, a person's body adapts to use far more acetoacetic acid than
  usual, and in this instance, ketosis normally does not occur. For
  instance, the Inuit (Eskimos), who sometimes live almost entirely on a
  fat diet, do not develop ketosis. Undoubtdly, several factors, none of
  which is clear, enhance the rate of acetoacetic acid metabolism by the
  cells. After a few weeks, even the brain cells, which normally derive
  almost all of their energy from glucose, can derive 50 to 75 percent
  of their energy from fats.

Which neurons and regions of the brain can only burn glucose?

Although PsychologyToday might look like a reasonable source, it's just a blog. Anyone can post there. There is no peer review of the content.

I've seen it somewhere else, too... I just can't find the link again... (grumbles something about wishing someone would organize the internet)

@NonSecwitter Can you reproduce the text here in text form from Guyton Hall?

@BryanKrause - I opened a meta psych question

OP this is why I wanted you to find a better source - see that the book says nothing about certain cells can only use glucose, it just says normally use glucose. That is, brain neurons (all of them I believe) use glucose when it is present. The bit in your other source about some neurons can only use glucose sounds like complete bullshit to me, I've never heard of such a thing and can't find any peer reviewed source making that claim.

The source you link does not report that certain neurons only use glucose, and I am unaware of any reputable source that makes this claim.
Neurons do tend to use glucose as an energy source when it is available, and the brain does not tolerate sudden drops in glucose. However, as your source notes, other energy sources can be utilized given enough time to adjust, such as during starvation/fasting as well as suckling.

Cahill, G. F., Herrera, M. G., Morgan, A., Soeldner, J. S., Steinke, J., Levy, P. L., ... & Kipnis, D. M. (1966). Hormone-fuel interrelationships during fasting. The Journal of clinical investigation, 45(11), 1751-1769.
Hawkins, R. A., Williamson, D. H., & Krebs, H. A. (1971). Ketone-body utilization by adult and suckling rat brain in vivo. Biochemical Journal, 122(1), 13-18.
Nehlig, A., & de Vasconcelos, A. P. (1993). Glucose and ketone body utilization by the brain of neonatal rats. Progress in neurobiology, 40(2), 163-220.
Owen, O. E., Morgan, A. P., Kemp, H. G., Sullivan, J. M., Herrera, M. G., & Cahill, G. J. (1967). Brain metabolism during fasting. The Journal of clinical investigation, 46(10), 1589-1595.
Pollay, M., & Alan Stevens, F. (1980). Starvation‐induced changes in transport of ketone bodies across the blood‐brain barrier. Journal of neuroscience research, 5(2), 163-172.


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Does drinking water from stainless steel increase hemoglobin?
I'm pretty sure iron molecules will be present in water.
Cooks who use iron or stainless steel pots increase the amount of iron they consume

Welcome to Biology.SE! What research have you done before asking it here?

I'm voting to close this question as off-topic because the answer is found in the article cited.

The article which you cite (which seems accurate and informative) already contains your answer, with a citation for further reading: "Cooks who use iron or stainless steel pots increase the amount of iron they consume. [22]" Iron-deficiency anemia was less common when people used cast-iron cookware. Steel releases much less iron. But food itself  remains by far the major source.

I don't have time to write an answer, but this study examined the effect of cooking in stainless steel and found that it did not alleviate iron deficiency. I imagine that simply drinking water from a stainless steel container would be even less effective. Also I think this is an interesting question.


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Phasing haplotypes
I'm new to this area (but not to programming & algorithmics) and I want to help a friend to solve a problem (I don't need source code, I just want to understand the problem itself).
He needs a cycle to phase haplotypes ("I need find haplotype pattern(s) from SNP string"). He also said "The method is simple, I need to compare homozygot combinations (AA, BB) in sequence with haplotype chains. And ignore heterozygot pairs (AB) at their right positions."
An an input he has a SNP string and a bunch of haplotypes strings (array).
Any help is greatly appreciated.
Thank you!

Rather than re-explaining the basics of haplotype phasing, I will refer you to useful documentation.
One of the first works on haplotype phasing has been perfromed by Andrew Clark. You can find here a nice slide presentation detailing the problem.
Useful discussion is going on here on Biostars.
I suggest you to use of the several approaches that have already been developed: my favorites are Beagle and fastPHASE.

Thank you. I managed to do it in PHP (really great on working with strings)


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Biological meaning of read length
I have some FASTQ files in two datasets which are sequences from 16Srna region. The first dataset is amplicons form V4 region and the second is V3-V4 region.
However all the reads are 250 nucleotides long, whereas one region is strictly included in the other. So what is the biological meaning of the length?
I'm expecting reads to have the same length as the sequenced/amplified region. I don't know the size of the regions but one is obviously longer than the other.
Thank you
(I thought it was better to ask here rather than on bioinformatics.stackexchange.com)

This is absolutely on topic here, I just wanted to let you know that it would also be on topic on [bioinformatics.se] as decided in this meta thread. Which of the two sites you choose is completely up to you.

Could [edit] your question and clarify what seems strange to you? What length of reads were you expecting? What you describe is standard but something seems to be confusing you. What is that?

I edited my question after @terdon comment.

The read length has absolutely nothing to do with what you are sequencing. It is a characteristic of the sequencing technology you use. NGS sequencing techniques typically produce this sort of short read you're seeing. The read length does not change because you are sequencing a longer molecule. You would still get ~250nt reads even if you were sequencing an entire genome. Your reads are something like this (image source):

So the vast majority of your 250nt are overlapping and cover slightly different parts of your target sequence. This is one of the reasons why NGS analysis is not trivial. The first step in any NGS analysis is to assemble your reads into a bam file that covers your target region. If you need help on doing that, come on over to http://bioinformatics.stackexchange.com.

Thanks you for you answer. But there is something I don't understand: with this technique of "cutting the molecule" that has to be sequencing, where do you put your barcodes? (when there are multiple samples from different sources)

@MrSnake on the end of the read but that really should be a separate question.

My understanding is that if the reads come straight from the sequencing machine, they will all be the same length. That corresponds to the number of sequencing cycles that the machine was set to perform. This has no biological meaning.
I don't know what the machine will read once it reads more than the length of the fragment subjected to sequencing.
If the fragments are shorter than what the sequencer reads, there will be some library preparation adapters to remove from the sequences in order to recover the actual fragments. Then you should be able to see the real fragment lengths.
If the fragments are longer than what the sequencer reads, see @terdon's answer.


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Strange planarian/leech like creatures found with California blackworms
I've been trying to ID these things myself but to no avail.  They came with a shipment of California blackworms from Florida.  I've heard so many ID's and apparently it's not uncommon to get these kinds of flatworm like hitchhikers with blackworms, but apparently different suppliers have different hitchhikers, so what one layman claims they are doesn't necessarily apply to another supplier.
I've heard these guys are planarians, leeches, or some sort of parasite specific to blackworms. I can probably eliminate most of these guys, but I just noticed they gave "birth" or something.  I thought they reproduced via fragmentation, but I saw one with what looked like legs, and realized it was actually dozens of smaller babies wiggling underneath.
I'm worried, because I don't want them to kill my blackworms, or accidentally kill my fish.
The creatures are about a half an inch stretched out? the creature is inside of a standard 3ml pipette in the later pictures. They tend to wiggle back and forth (see the video). They scrunch up into a small ball when I disturb them.

It's hard to tell because they are transparent, but the below gif is definitely the same type of creature.   Basically half the time I see them, they stick their heads out of the water and wiggle back and forth like that (but not sway, like the blackworms).   My phone isn't good enough to capture this behavior well.

https://i.sstatic.net/I9v24.jpg

Welcome to Biology.SE! You need to upload individual images (e.g. files ending in .jpg). I expect the problem you are having is that you are trying to upload your entire page of videos and images, which this system wont do. Each image in imgur has a separate url that must be individually uploaded. If you want to include information from videos you need to capture stills from that and then upload them. HTH

@tyersome All the images are too large, and in linking it claims that the images are not the right format.  I also have no idea how stills then uploading works?

(+1) Glad you got the images figured out! Can you provide some additional details about what we are seeing in the final gif? It looks to me like an entirely different type of organism ...

@tyersome It's hard to tell because they are transparent, but it is definitely the same type of creature.   Basically half the time I see them, they stick their heads out of the water and wiggle back and forth like that (but not sway, like the blackworms).   My phone isn't good enough to capture this behavior well.

Wild — I hope someone comes through with an answer for you. If you don't get an answer here you might want to try iNaturalist, which specializes in identifications. If you do get an answer there please post an answer here to your own question so others can find it in the future. Good luck!

@tyersome Thanks for that link!  I found bigger versions and more of them, hopefully I'll be able to get better pictures.


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What is the length of gene when calculating TPM (transcripts per million)
What is the length of gene when calculating TPM (transcripts per million)?
Assume I have a dataset matrix with k rows(each row is a gene) and n columns (each column is a sample), is there any way I could transfer the data set into TPM? Many thanks!

Trusted Platform Module? Total Productive Maintenance? Technology Park Malaysia? Come on, give us a clue!

@David I am sorry, TPM is transcripts per million

http://www.rna-seqblog.com/rpkm-fpkm-and-tpm-clearly-explained/

Nice walkthrough, thanks!
When I was using it for implementing it as a function, still I spotted a small error in the calculations. When normalizing for the gene counts, GeneB-rep3 should be 14 (not 35, which you get if you divide by the 2k).
F
(sorry, could not add as comment due to the newbie status ;) )


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What is this bizarre looking animal we found in the forest? Bug identification
Please can someone identify this?
I can't find anything on the Internet like it. 2 cm long. North Bohemian mountains (Czech Republic).

That is the caterpillar of a lobster moth (Stauropus fagi), family Notodotidae. It is mimicking a scorpion to help protect it from predation. An amazing insect.

Comments are not for extended discussion; this conversation has been moved to chat.


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What measures are commonly used for the complexity of an organism?
I'm aware of measures like number of distinct cell types being used as a measurement of complexity in biology, for example in the G-value paradox. But this doesn't really help for unicellular organisms. Is it possible to define a unit of complexity to make comparisons between different organisms?

This is a very interesting question. Not sure if there is any way to answer without specifying a definition for complexity.
It is clear that everything is made of only the same few elements, so complexity must involve more than that. Do the number and position of identical molecules matter? If so, size matters and we would label a large jelly-fish as more complex than a cat and the air in a large hot-air ballon as more complex than any single living organism (assuming it is bigger).
I think it is clear that this is not what is meant by biological complexity. Molecules acting identically should not count multiple times; the number of different molecules matters more than the mere number of molecules. But are immune cells really more complex simply because of a relatively minor difference that allows them to generate a wide variety of genetic variants?
What about the variable coat color of a calico cat. Does the complex and non-repeatable (even with cloning) pattern mean it is complex, or does the fact that a simple genetic process underlies it mean it is simple.
The difference in complexity of different representation of the same thing is a classic problem in information theory (see Kolmogorov complexity). The ratio of the circumference of a circle to its diameter requires an infinite number of decimal digits to describe, but it is just a single geometric concept and it can be represented with one or two characters, as pi or π. This applies to the problem of using phenotypes to measure complexity -- the language and definitions we use to describe or to differentiate phenotypes determines what is complex and what is simple.
Moving beyond a simple static snapshot case, biological complexity involves time-dependent evolution. The "game of life" demonstrates how simple rules + initial conditions yield apparent complex behaviors, and the beauty of fractals arises the same way. Many apparently complex organisms grow from small seeds plus time-evolved exposure to simple things like water and light and CO2. Are trees only as complex as the seed they grow from?
Finally, what about higher order complexity? One human brain is very similar in general makeup to another, but the concepts and memories stored seem complex and very different. Comparing the complexity of stored information between two people is the whole complexity problem over again.
It seems to me that complexity can only be cleanly measured within a specific context, and then only relatively. One can measure the relative genomic complexity of two organism as the edit distance between the alphabetic sequences representing their genomes. The relative regulatory complexity can be measured as mentioned above by @user1682. Each of these says something about an organisms complexity. But what if organism A has higher genomic complexity and organism B has higher regulatory complexity? It might be possible to derive something like a principle component "basis set" from several of these kinds of measurements using a training set and a list of organisms with predefined complexity values. Applying this "standard" scoring metric to another organism would allow ranking it on a "standard" scale, but it would be difficult to generate and obtain consensus on the initial "expert" ranked organism scale. Such a standard might have some value, but is not really theoretically satisfying in that it describe an organisms complexity in the same way that the average of a small sample describes the distribution of a large population.

I think your answer raises a few deficencies in the question, so I think I'll have to address them in another question. Thanks.


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Calculating the canopy size (crown) of a newly planted tree at a future date
Assuming that one knows the maximum area of the canopy and the age of the tree when it achieves this. And given an initial canopy size from the nursery. How would I calculate the canopy size at a future date.
Whilst certain aspects of the growth are obviously variable... how would I model the growth over the year(s)? I'm looking for a simple formula that I could give to a user in a planning department to develop adaptive lighting solutions for trees in streets.

Maybe trees branch randomly so there might be no such formula.

If you can tell the weather years in advance this might be possible. Other than that just interpolate linearly and that'll be close enough maybe?


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What is TILLING?
How does TILLING (Targeting Induced Local Lesions in Genomes) work? What is needed to perform a TILLING experiment, and what kind of information can we get out of it?

You can easily get the answer to this question in wikipedia article on TILLING


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What happens if we use Pvu2 to insert a gene in the rop of pBR322
My book shows that pBR322 has a Pvu II site in the rop, I know that rop codes for proteins required for replication of the plasmid, so what happens if we use the Pvu II Restriction Enzyme and insert a foreign gene there.
Will the replication stop?
If yes, the what is the significance of having a site at such an essential position.

I think that inserting Pvu 2 might reduce the rate of duplication of the plasmid.

Have a look where the PvuI is sited - what is that region used for, and why might this be important for your cloning.

I couldn't get what you mean to say...

Sorry, misread PvuII as PvuI. The comment applies still - what would happen to the plasmid if you insert a DNA segment into the PvuII site? Would that region look the same and do the same function?  As to why there's a site there - because that's the cut sequence for that restriction enzyme and it just so happens to lie there.

Yes, insertion of foreign gene at this site would disrupt the process of replication as rop protein is essential for the replication of the plasmid.
The significance of having a site at such a position is that it would help the researchers to control and manipulate the plasmid. It would be helpful to study gene function as well as its regulation.


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Flower Classification: Hypogynous, Perigynous, and Epigynous
I am struggling to understand the classification of flowers as hypogynous, perigynous, and epigynous.

According to my textbook (Biology NCERT Grade 11), diagram (b) is classified as perigynous. However, it seems to me that the ovary is positioned below the other floral parts (since the point of attachment of the ovary to the thalamus is lower than the attachment point of the other floral parts), which would typically categorize it as epigynous.
I am referring to the definition provided in my textbook:

Based on the position of the calyx, corolla, and androecium with respect to the ovary on the thalamus, flowers are described as hypogynous, perigynous, and epigynous. In hypogynous flowers, the gynoecium occupies the highest position, while the other parts are situated below it. The ovary in such flowers is said to be superior, e.g., mustard, china rose, and brinjal. If the gynoecium is situated in the center and the other parts of the flower are located on the rim of the thalamus almost at the same level, the flower is called perigynous. The ovary here is said to be half-inferior, e.g., plum, rose, peach. In epigynous flowers, the margin of the thalamus grows upward, enclosing the ovary completely and fusing with it, while the other parts of the flower arise above the ovary. Thus, the ovary is said to be inferior, as in guava, cucumber, and the ray florets of sunflower.

Could someone clarify the criteria for classifying flowers into these categories and explain how the diagram I’ve provided fits into this classification?
Additionally, I would appreciate if someone could elaborate on the concept of a "half-inferior" ovary in perigynous flowers. Why is it referred to as "half-inferior" and why not "half-superior"?

It's all related to the position of the female parts of the flower (gynoecium) with respect to the other flower parts.
In A you can see that the ovary sits clearly above the insertion points of the petals, sepals etc. In B and C you can see that these parts are mid-way up the gynoecium, while in D, the ovary is enclosed and below the insertion points of the other parts.
If it helps, the roots of the words offer clues:

Gyno: as in epiGYNous or GYNaecologist, means female.
Epi: as in EPIcentre (earthquake), means over or upon.
Peri: as in PERImeter, means around or about.
Hypo: as in HYPOdermic needle, means under.

So, in the word epigynous, the other parts of the flower are over (epi) the female parts (gyno); likewise in the perigynous, the other parts are about (peri) at the same level as the female part.
I'm not sure on the origins of why inferior is used rather than superior; conventions in botany were established quite some time ago. However, there is one possibility: you can only be so superior, but you can have many levels of inferior. Once the ovary is above the petals etc. insertion point it is superior, above all others, and it can't get any more superior. On the other hand, if it is inferior, then it can be partly inferior until it become superior.

Sir, thank you very much for taking the time to write this detailed answer.

Sir, you mentioned, "Likewise in the perigynous, the other parts are about (peri) at the same level as the female part." Based on this explanation, diagram C appears to fall under the category of perigynous, whereas diagram B does not. Would it be correct to say that the book is mistaken in categorizing the flower shown in diagram B as perigynous? Shouldn't it instead be placed under epigynous?

@MadaraUchiha The gynoecium includes all the bits in white (ovary, style and stigma), so B still fits the description. I'll edit my answer to make that more clear. It certainly isn't epigynous as it isn't enclosed.

The terms also relate to where the other tissues connect to the ovary, not simply the vertical position on the diagram. Example b is perigynous because even though the calyx, corolla, and androecium converge at a point above the ovary, they form a  combined tissue (hypanthium) that meets up with the ovary on it's lower portion.

@Darlingtonia, could you please mention the sources where I can find the complete definition of this classification?

Could you please clarify one more thing: Is the hypanthium formed by the fusion of floral whorls and distinct from the thalamus, or is it an extension of the thalamus to which the floral whorls are attached?

Here's a collection of sources. The first definition there (by Marilena Idžojtić) is interesting in distinguishing classification of the ovary and classification of the overall flower. Under that scheme, your example b is a perigynous flower with a superior ovary.

The hypanthium is normally taught as a fusion of the floral whorls. Ideally, developmental studies would show the precise origin of these tissues and if/where they are distinct from the receptacle. I wouldn't be surprised if this varied across flowering plants. Some definitions consider the hypanthium as part of the receptacle, but it's not clear to me whether this is in conflict with also considering them a fusion of the floral whorls.


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How do you consider an organism to be a new species?
How do you consider an organism to be a new species? Can a new parthenogenetic organism be considered as a new species?

The answers here https://biology.stackexchange.com/q/34594/107 cover species concepts.

There are various hypotheses and concepts proposed to define a species, but no definitive answer. Mostly a combination of these concepts are used because each hypothesis has exceptions. Classification is constantly being debated, reevaluated, and changed as we learn more. Some of the most notable definitions are:
The is the biological species concept in which Ernst Mayr defines a species as actually or potentially interbreeding populations that are reproductive isolated from other groups and produce viable, fertile offspring. But this doesn't by definition exclude hybridization between species, but often hybridization does not produce viable or fertile offspring. (This definition doesn't work with parthenogenesis. Also, hybridization is accepted as a mechanism that can lead to speciation, most notably seen in plants, where the hybrid offspring can interbreed with other hybrids, but are not able to reproduce with their parental species.)
There is also the morphological species concept which uses morphology and body features to classify organisms, which is more useful when there is little population information available, such as for fossils. But this can result in one sexually dimorphic species being classified as two. (The eclectus parrot was initially classified as two species because the males are green, while females are red.)
In the phylogenetic species concept Willi Hennig defines a species as the smallest group of individuals sharing one common ancestor and a set of fixed heritable differences to make up one phylogenetic branch. Genomics is often used to define this. There is debate that this method creates "taxonomic inflation" and creates more species than necessary because different populations may be able to interbreed, are not reproductively isolated, but are genetically differentiated enough due to local adaptation.
The ecological species concept defines species by their environmental niche--organisms that look, act, and share similar life history patterns. This definition includes parthenogenic species as a separate species from its non-parthenogenic relatives.
(It becomes much more complicated when trying to classify prokaryotes and viruses because mutation occurs at a much higher rate and many of the above definitions cannot be effective applied.)
Ultimately, yes, there are various accepted species that reproduce only by parthenogenesis (like the mentioned New Mexico whiptail lizard), and parthenogenesis can be a defining factor which separates them from a sexually reproducing counterpart species that is similar in morphology, niche, and evolutionary history.
Information comes from courses and textbooks from my Ecology & Evolutionary Biology major within the last year.

A quick look in the Wikipedia article for parthenogenesis gives an example of New Mexico whiptail (Cnemidophorus neomexicanus).
It is a hybrid between the little striped whiptail (C. inornatus) and the western whiptail (C. tigris). It reproduces through parthenogenesis - there are only females from these species and they lay unfertilized eggs.
The answer to your question is obviously: yes, a new parthenogenetic organism can be considered as a new species.
However the taxonomy undergoes continuous changes and what has been a subspecies might be later classified as a species or vice versa. There are no clear and unambiguous criteria deciding when a new discovered organism is a species on its own.
Generally speaking if the individuals of a population can reproduce and have offspring resembling their parents, but can't reproduce with individuals of other populations resulting in reproductive able offspring, then they are considered to be a species. Although there are many exceptions and no strict rules.


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Evolution of dinosaurs
What did dinosaurs evolve from? Was it the reptiles that evolved from amphibians? I have been researching this but am very confused with who their direct predecessor was. Amphibians evolved from fish...reptiles from  amphibians...dinosaurs from reptiles (?)...and birds from dinosaurs. That is my understanding, but it could be wrong. How are dinosaurs related to reptiles? And if they did evolve from reptiles, which kind of reptiles (such as lizards, crocodiles, or turtles for example)?

Related: If dinosaurs could have feathers, would they still be reptiles?

Source of information
See the post The best free and most up to date phylogenetic tree on the internet? for info about how to find such information.
Generally speaking, you might be interested in an intro to phylogenetics such as the one provided in this answer for example.
Where are dinosaurs in the tree of life?
Dinosaurs fall within the Reptiliomorpha clade. Please note that Reptiliomorpha does not quite correspond to what we today call reptiles. Please see the post If dinosaurs could have feathers, would they still be reptiles?
Reptiliomorpha is the sister clade to Amphibia (from here) which contain all living amphibians.

If you look within the Amniota, you will find all of the following

Here, you see that turtles and mammals are an off-shoot of Diapsida. So dinosaurs are not mammals and there are not closely related to turtles. Now if you click on Diapsida you will find ...

the Archosauromorpha which contains all crocodiles, birds and dinosaurs. You can keep going to find Therapoda which contains many dinosaurs and birds. You can keep going like this for yourself and discover the entire tree of life!

Reacting to your sentences

What did dinosaurs evolve from?

When asking this question, please do not forget that no species evolved from an extant species. If this is unclear to you, you should have a look at this post.

Was it the reptiles that evolved from amphibians?

Well... the term reptile is a mess because it does not represent a monophyletic group (see this post). If you do not understand the term monophyletic, then you should have a look at this answer.

Amphibians evolved from fish...

Well... sure. However, fish is also not monophyletic so it is misleading. Also, I am afraid when you say "Amphibians evolved from fish" that you are thinking of modern extant fish which would be wrong.

reptiles from amphibians...

Nope, this is wrong. Reptiles and amphibians are sister(-ish) clades.

dinosaurs from reptiles (?)...

This is more or less true although again, do not think of modern reptiles and also, reptiles is a mess because it is not a monophyletic group. But Dinosaurs are Reptilia

and birds from dinosaurs.

Yes, this is pretty much true.
Note generally though that it is misleading to say "birds evolved from dinosaurs", "humans evolved from apes" and "mammals evolved from vertebrates". It is more correct to say "birds are dinosaurs", "humans are apes" and "mammals are vertebrates". I would be even better to use the latin names to avoid confusion with misuse of these words in the popular culture.

Nice answer!...

When you say no species has evolved from an extant species, why is that? Wouldn't the Galapagos finches have evolved from an extant species of finch in South America? Meaning that they did indeed evolve from an extant species? (I did read the linked post, but I am still a bit confused)

@Hawkeye The sentence you are referring to is followed by "If this is unclear to you, you should have a look at this post".  This post would also give you a good explanation.

@Remi.b If I am understanding the linked posts correctly: No species has evolved from an extant species because the species has also been evolving and is now different, no matter how slight. Am I thinking of that correctly?

@Hawkeye Yep pretty much! Good job!

Thanks for the informative answer! Just a few questions to make sure I properly understand it. At some point in time, Reptilia divided into Anapsida and Romeriida. Turtles are included under Anapsida while dinosaurs fall under Romeriida. So they are related, but one is not the ancestor to another. Is this correct? Dinosaurs and turtles are more related than dinosaurs and members of Amphibia but less related than dinosaurs and birds. Your anwser cleared a lot of things up, but I just want to make sure I grasp the concept

You got it! It feels good when the OP fully gets it! Good job @Vanessa! Note that tolweb.org (the reference I used) is a little bit updated. OneZoom.org is a bit better (see the tetrapods here). There are a few changes what you just expressed remains true.


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What does fitness really mean?
Fitness is certainly the most important concept in the theory of evolution. My question does not have to do with practical measures of fitness but with the theoretical definition of it.
I am a bit lost with the concept of fitness. Below I give some possible definitions of fitness and I am hoping to get critics for these definitions. The broad question is What is the definition of fitness?
In the following, to make things easier I will consider only one bi-allelic locus. For simplicity, I will assume a panmictic population of infinite size evenly distributed into age classes.
1) Let the variable $M$ be the mean time of a generation in the species of interest. Measure the allele frequency $p(t)$ and measure the frequency $p(t+M)$. By comparing the two you get the ratio of fitness of the two different genotypes. Obviously it does not work if we have sexual reproduction or diploid selection.
2) Genotype the individuals and wait until they die by counting the number of offspring they had and take the mean per genotype ($W_{AA}$, $W_{Aa}$, $W_{aa}$). This method would not work if they have different lifespan. One individual might make two babies in 8 years and the other would make two babies in 2 years but they would have he same fitness.
3) Do the same that at 2) but don't wait until they die, wait 1 month, Or 2 years?, or $M$?, or $2\cdot M$?, or...? What is the right decision? The more you wait, the closest you will be to the long term effect of natural selection. The less you wait, the more probable you will suffer of genetic drift.
4) Fitness is just a measure of natural selection that is not perfectly accurate because it is measured at short-term. In some circumstances, our measure on this short term is representative (Wright-Fisher equation) enough of what will happen on the long term.

What's wrong with "ability to survive and reproduce?"

Over what time amount of time should one measure this ability? One generation? His measure would suffer from drift! And not everybody has the same generation time. Over 10 years? It does not give the same result if you make this measure over 5 years. It seems rather arbitrary the time one should consider, isn't it?

fitness has no definition if the selection criteria are not specified. Having specified it, the fitness is a measure of reproductive potential.

@WYSIWYG Could you develop your comment?

@Remi.b.. I meant that something is said to be fit for some condition. Therefore fitness is conditional. There is nothing like absolutely fit. Unless you know what the selection pressure is you cannot measure fitness.

"As I said I don't want to talk practical issues but theoretical ones, therefore we will assume to work on a panmictic population of inifinite size evenly distributed into class age." infinite versus finite population is not a practical concern, but a very important theoretical distinction in particular if you have stochastic events.

I don't understand your four points & I feel they should be fleshed out for clarification if you're still interested in the question (I see you asked it three years ago). You might have already come across this, but in The Extended Phenotype, Dawkins' wrote a passage about the various meanings of the term "fitness."

I must have 50 reputation to comment.

Fair enough.  Seems you should be a moderator (if you want).  You're carrying the site.

I appreciate it.

I don't see how #1 wouldn't work, given sexual reproduction.

The concept of fitness is very general. An adequate definition of fitness is hard to specify in the same way that a definition of "species" is hard to give. To be useful, scientific or technical definition of such broad concepets will often need to be so narrow that more than one is needed. A uselessly broad definition of fitness might be:
"Fitness is modeled as a utility function, where higher fitness is indicated by a higher score"
Here every important detail about whatever's fitness is being tested, how that fitness is measured, and the environment in which that fitness is determined are simply wadded up together and transformed into a different question that is no easier to answer.
The hypothetical problems you raise with various definitions are not (in essence) problems with the definitions, but problems with the definitions not being applicable to the domain in which such problems matter. You have to define your criteria for success, and then these constraints can be translated into a "fitness" function that allows the desired predictions.
Some issues that might matter are:

Are predictions about populations, or individuals.
Are predictions about dynamic fitness (snapshot at some time) or long-run steady state fitness.
Are predictions about quantitative values (like heights) or discrete values (like sex).
How do you want to present error in your predictions - p value, sensitivity/specificity, confidence interval, etc.

I'm sure this is not the kind of answer you were looking for, but I think part of your question revolves around a confusion that there is "one" technical definition for fitness. Part of the process of learning is comparing different presentations of the same concept, and realizing where they are different. A full walk over all the different ways one could evaluate and apply fitness would be a book, not a short answer. Perhaps some other people can provide good links to more detailed information.
I just found a blog posting, by Dr. John S. Wilkins, which says some of the same things. His perspective comes with a good pedigree; his PhD work was on trying to define "species" and he has authored a couple of books on the subject.

This answer will also give some hints about the various definitions of fitness

As I see it, your question is also encompassing an inquiry for a theory of fitness.
In recent years the inclusive fitness theory has seen its share of interest, which can be applied to social entities.
Freely citing from wikipedia here:

An organism is judged by the number of offspring it has, how they support them, and how their offspring could support others

As for the mathematics and informatics this paper

JY Wakanoa et al. "A mathematical description of the inclusive fitness
  theory", Theoretical Population Biology, Vol84. March 2013. pg 46–55

explains:

Recent developments in the inclusive fitness theory have revealed that
  the direction of evolution can be analytically predicted in a wider
  class of models than previously thought, such as those models dealing
  with network structure. ...

It takes a Markov chain approach.


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I'm not sure, are there 46 or 92 DNA strands in each somatic cell. Whatever, how many, then these strands join together to make a 6 or 7 ft long DNA?
When a cell is not divided it has DNA in chromatin form. Usually it is written in books that DNA is 6 ft long. In each cell there are 46 chromosomes, so there are 46 or 92 DNA strands. When a cell is not divided, do all these strands join together to make a 6 ft long DNA strand?

no its total length, each chromosome is a separate strand

This is a science website. Please, keep it clean, keep it metric! 6.5 feet ≈ 200 cm.
The exact length is subject to quite a bit of variation from estimates to estimates, at least according to hypertext.com (non-peer reviewed). All estimates are in between 1.5 meters and 3 meters. Hypertext.com cite "Cell." The World Book Encyclopedia. Chicago: Field Enterprises, 1996

On the average, a single human chromosome consists of DNA molecule that is about 2 inches [(~5 cm)] long.

They deduce from it a total length of 230 cm which mean that they computed 5 * 23 * 2 = 230 cm.
This total length is hence computed from the diploid genome but counting only a single chromatid per chromosome. For a haploid genome, the length would be closer to 115 cm and for a diploid genome when counting the sister chromatids, the length would be about 460 cm.

I've have this doubt for the longest time about a chromosome being a monad or diad and when. DNA is always in the form of loose chromatin fibres at all times except during metaphase- when it is condensed onto chromosomes. If you were to condense these chromatic fibres into chromosomes, it would form monads with one sister chromatid only. While during metaphase they form dad's with 2 sister chromatids, twice the dose and thus twice the length of total DNA


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Do reproductive organs function before puberty?
Testis means one of the two male reproductive glands that produce spermatozoa and secrete androgens.
Ovary means one of usually two organs that produce oocytes and secrete oestrogen and progesterone.
Do these organs function before puberty?

No, they are not functional before puberty.
For males:

Most males begin puberty between the ages of 9 and 14, but commonly puberty will begin around 12 years old. When the human body reaches a certain weight (which differs among individuals), the hypothalamus releases gonadotropin-releasing hormone. This hormone signals the pituitary gland to release the two hormones that begin the onset of puberty: leutinizing hormone and follicle-stimulating hormone.7 In males, these hormones stimulate activity in the testes, which start to produce the male sex hormone testosterone and begin spermatogenesis. Spermatogenesis is the process of sperm production.

source (warning: contains NSFW drawings and images)


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Number of hair cycles in humans
I've seen several websites claim the amount of hair cycles a follicle will go through is predetermined at around 25-30 complete cycles. Is there any genetic evidence to validate this claim? How can this even be determined apart from observationally seeing people lose hair as they age?
Here's a link referring to what I'm talking about:

The number of hair growth cycles is limited: our hair will experience about 25 to 30 cycles like this during our lifetime.

note that is an individual follicle, we do grow new ones.

The link in this question is dead. :(


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In centrioles, what type of fibers connect the triplet microtubules?
In a centriole, each "arm" (a triplet microtubule) is attached from its A-tubule to the C-tubule of the adjacent arm. What is the type of fiber that connects each arm ("connecting fibrils" in the image below)?

Winey M, O'Toole E. 2014. Centriole structure. Phil Trans R Soc B 369:20130457

Cross-sectional images of centrioles and basal bodies show a linker between the A- and C-tubules in many different organisms... Surprisingly, candidate molecules serving as constituents of these linkers have not yet been identified.

That's as of 2014. I don't have the time right now, but I'll try at some point to find if there are more recent developments.


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Double Digestion with Restriction Enzymes Using Different Buffers
I am currently working on preparing a 9 kb sequence of DNA for restriction digestion into the pBAD30 expression vector. There are very few restriction enzymes that do not have a restriction site located on my insert, and since I am using 2 restriction enzymes in my digestion, I had little choice in choosing my restriction enzymes. The only two restriction enzymes that will work for me are Xmal and KpnI. XmaI uses CutSmart buffer while KpnI uses NEB buffer. The efficiency of XmaI in CutSmart buffer is 100% while the efficiency of KpnI in CutSmart buffer is 50%. Would it be easier to perform a double digestion using CutSmart buffer and 2x KpnI than to perform two consecutive digestions?

Hi Hunter. What conclusion have you come up with yourself? You've received a close vote on your question because another user likely assumes you're looking for others to do your work for you (i.e., figure out which approach is best). I think you'll get a positive response if you can demonstrate a little more explicitly that you've thought about this on your own and that you've spent some time researching to support one way or the other. It will likely sharpen your question and create a more interesting dialogue and answer. Thanks!

I am definately not asking others to work for me. I am simply asking a scientific question that I was unable to find the answer to. I should not have to fear asking a logical scientific question. Closing this question is only holding back the scientific community and preventing others, like me, from learning more about science.

Hunter please don't get mad. I'm not even the one that voted to close. I'm just letting you know that some have interpreted your question as asking for an answer to a question you haven't fully indicated you tried answering on your own. If you were to indicate explicitly what you have already done to try to answer the question (e.g., where have you looked, what have you read, etc.), then this concern is avoided. Closing questions might be holding back some individuals, but it's encouraging most to take that extra step toward being effective scientists: self-guided learning.

(You've got to learn where else to look for answers b/c you can't always rely on Q&A websites to exist or to give you accurate (or even any) answer at all.)

@theforestecologist I apologize for sounding angry. I will do better in specifying my efforts to solve the problem in the future. Thank you for the advice.

In my opinion question seems to be in correct format (may be I am seeing edited version). @HunterRees question is more of practical than theory.He is facing problem as he is stuck at one of the steps of his experiment.In search of solution, he has explained what he has found (like combination of buffers he mentioned).However, before performing the experiment he is seeking some more advice from the experts on this.

In my experience, a double digestion in CutSmart buffer will work perfectly well. The reaction may proceed slower, but incubate it a little longer and run a gel after the digestion - you'll see whether it has worked. The other answerers unfortunately did not mention that the best way is to check the restriction products yourself on a gel. Cut out the fragment from the gel you need (and purify) if you want to avoid undigested plasmid. See if the plasmid fragment sizes correspond to the correct cutting sites. Basic lab practice and it takes very little time!
Beware of star activity - ask a technician to sequence your fragments or plasmids to be sure it's all going well (this is good lab practice), in case you see unexpected bands on your gel that may indicate unwanted restriction activity. This is not so common, though :)

I would have thought checking a restriction digest on a gel goes without saying. Also, is your experience actually using KpnI in CutSmart? NEB explicitly warns that extended digestion with this enzyme may result in star activity, though I don't know how serious of a problem it actually is.

Even with star activity, the enzyme is partially doing its job correctly and the plasmid is partially digested correctly. Running the product on the gel and purifying the correct fragment is the best way to do it for three reasons: (i) you know exactly what your product is, (ii) you don't need to purchase, wait and/or troubleshoot new enzymes, and (iii) you're fostering that sweet sweet scientist thinking, rather than being a protocol zombie - my technician's words, not mine :-) There is one quite minor downside: you can't do this with very little quantities of plasmid (does not apply here).

Fair enough. I still prefer to use the optimal buffer, which is especially easy for me since I do sequential digests. To each their own.

If you haven’t already ordered your enzyme, you could get high fidelity KpnI, which has been engineered for use in CutSmart.
You could also consider doing a sequential digest rather than a double digest (ie digest with one enzyme in its optimal buffer then change the buffer for digestion with the second enzyme). It is more work but benefits from easier troubleshooting in case one of your enzymes is not cutting (which can occur frequently if you have a freezer full of 10 year old enzymes).

NEB double digest planner is suggesting to use 2.1 buffer for your combination of restriction enzymes (XmaI 50% and KpnI 75% activity). I would be more worried about the star activity of KpnI in CutSmart buffer than the lower activity. The latter can be overcomed by prolonging reaction time or using more enzyme.


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What species is this turtle in Houston?
This turtle was displaced by hurricane Harvey in Houston, Texas, USA (Buffalo  Bayou and Dunlavy). It appears to be a snapper. Can someone identify the exact species?


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Can streptavidin be conjugated with EDC-activated carboxylates?
Recently I conducted an experiment to conjugate amine-modified oligonucleotides with hydrogel particles having carboxyl groups. However, the fluorescence (from hybridized FAM-DNA) only appears on a small area of the particle and its shape is this ill-defined, like in the image below.

My advisor said that "DNA is negative charge and carboxyl group also have negative charge so there is no possibility of conjugation, conjugation of streptavidin to particle, attaching biotinylated DNA and proceed with hybridization".
However, conjugation using NHS / EDC requires both an amine group and a carboxyl group. Does streptavidin have the requisite chemical groups to do such a conjugation? Streptavidin is Sigma Aldrich's 85878 (Streptavidin of Streptomyces avidinii, affinity purified, 10 mM potassium phosphate, lyophilized product of ≧ 13 U / mg protein).
PS: Please tell me if there is a secret to make it conjugate evenly on the surface.
PPS: We use 5 μM anime modified oligonucleotide and 100 nM FAM-DNA.

I really don't get why this question had a downvote.

The EDC-activated carboxylate is actually positively charged, though I cannot speak to the density of carboxylates in your hydrogel or the extent of activation with your protocol. Subsequent NHS activation generates a negatively charged adduct. If charge repulsion is an issue during coupling, you can try experimenting with salt concentration or adjusting pH around streptavidin’s isoelectric point (but keep in mind that the reactions themselves also have a pH optimum).
Streptavidin has plenty of primary amines (lysine and N-terminus) to react with EDC- or EDC/NHS-activated carboxylates, and is routinely conjugated to carboxylate functionalized resins. As streptavidin also has carboxylate groups, it may be desirable activate the resin first and then conjugate streptavidin to avoid unwanted side-reactions.
You can read about the EDC/NHS reaction mechanism here (ThermoFisher).


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What is the identity of this spider from India?

I came across this strange guy today at my classroom in Tamil Nadu, India. It is a spider which is not very much bigger than an ant but with an artistic body. He has 8 legs, but the two on the front are raised above his head, just like a crab does. Can anyone identify this little guy?


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Why marker and control are loaded in the beginning or ending lane of the gel?
I have seen gel images in several literature. Almost in all, markers and controls are loaded in the  extreme lanes (before 1st sample or after last sample) of the gel. I am just curious, is there any reason or logic to do so? Is there any problem if I load it in the middle lanes, in between my samples

Control or marker?

No important reason. It is for esthetics, and also for ease of description in figure legends. One could argue that it might be confusing to have the markers or the control in the middle, but since the relative locations of these wells would be recorded, it does not matter where you put them. In publication, it would be easier to say, for example, "The control is in the far right lane, and the ladder is in the far left lane" Rather than saying, for example "Third from the left".