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Do we see protocells forming in nature today?
I understand that the current theory of chemical evolution (aka origin-of-life, abiogenesis) involves lipid-based protocells that enclosed RNA and perhaps some other compounds as a first steps to life.
I'm wondering if we see them forming today in nature, and if not, why not?
Are there successful experiments creating them in the lab?  If so, what are the required conditions?

we don't think so, some parts are easy. liposomes form all the time, and can be created in lab quite easily. They quite readily encapsulate any material present when they form, including DNA. So once you have the right stuff (likely RNA) it is very easy to enclose it in a lipid bilayer.
RNA has been formed from scratch in a lab it is even easier than we thought it would be. It may form in nature today but is unlikely , the current atmosphere is very oxygen rich and bacteria are not just willing to eat RNA but also basically all the chemical building blocks as well so it is difficult to build up a concentration of the precursors in nature today.
Worse evidence of it forming today would be ridiculously difficult to demonstrate because there is a constant contamination of biologically produced RNA from decaying organisms. There is basically no place on earth today with liquid water that does not have life in it.
Here and here is a review of our current models for the origin of life, Be warned the first link is a file.There are many steps involved to get a cell but it all starts with the first molecule capable of making copies of itself.
Forming self catalysis strands in a lab would be the best evidence but has one major problems, Money. Earth had an ocean sized laboratory and millions of years to stumble one of the strands with one of the right codes through random chance (remember a self-replicating code only has to happen once) which likely could only be duplicated by doing millions or even billions of identical laboratory experiments.
Finally while the Urey-miller experiment was historically important it is by no means the best nor most modern experiment you can find much more information about the variety of experiments at this question.

The file link doesn't work for me - seems it's a local link.

My bad, there that should fix it, if not here is a different link https://www.scribd.com/document/166508345/entropy-12-01733-v2

sorry - still having problems.. could you put up as a google doc or dropbox?

did you try the scribd.com link? I don't personally have the document.

In present environment  the conditions are not favourable for the new type molecules /coacervates or microspheres formation because the present atmosphere is oxidizing in nature, presence of oxygen inhibits primary molecules formation.
The early conditions were of reducing nature it has enormous lightning, high temperature, decaying radioactive compounds. Moreover, there were no organisms to feed on newly created molecules in water bodies
.
The first organisms formed on earth were Chemoheterotrophs i.e they feed on others for food and they cannot make their own food from sunlight.
The first major toxic was Oxygen in gaseous form, earlier it is present in combined form or as metallic oxides in the water bodies as H2O.
Now in atmosphere O2(in gaseous form) and tiny microorganism present oxidizes the the basic elements like C, NH3 to other forms like CO2.
However, experiments by Miller and Oparin in-vitro conditions shows the formations of primary cells having amino acids, purines, pyrimidines - The basic requirements.
Miller and Urey proved the Chemical Evolution theory in their experiments showing the formation of many amino acids, sugars, nitrogen bases.  Oparin stated that mixing large protein with a polysaccharide leads to formation of coacervates; same experiment was also done by Sydney Fox.

Welcome on SE.Biology. In order to improve your answer, please add some references and links

Thanks for the answer - but I don't understand. Wouldn't the protocells be forming underwater?  You're talking about oxygen in the water?  Why would other organism eliminate all trace? - eg, even for bacteria that eat other bacteria, some of the original survive - they don't eat them all.

some of the original survive - they don't eat them all. It's not the bacteria. The abiotic factors themselves inhibit development of protocells.

@PrittBalagopal - I was referring to the statement "Moreover, there were no organisms to feed on newly created molecules in water bodies".  Which I assume means "even if they could form, they would get eaten..".  But I would still expect that we could control the factors and build them in the laboratory which would have neither problem.

But I would still expect that we could control the factors and build them in the laboratory which would have neither problem. Of course, if you have the perfect environment, you can have anything. But life doesn't evolve in perfect environments. Besides the title of the question is "Do we see protocells forming in nature today?"

@Yehosef The first organisms formed on earth were Chemoheterotrophs i.e they feed on others for food and they cannot make their own food from sunlight.
The first major toxic was Oxygen in gaseous form, earlier it is present in combined form or as metallic oxides in the water bodies as H2O.
Now in atmosphere O2(in gaseous form) and tiny microorganism present oxidizes the the basic elements like C, NH3 to other forms like CO2.
However, experiments by Miller and Oparin in-vitro conditions shows the formations of primary cells having amino acids, purines, pyrimidines - The basic requirements.

@PrittBalagopal - The question was about in nature today - but I added the question about success in the lab in the details.  "Of course, if you have the perfect environment, you can have anything."  Do you have references where they have done these experiments and found these results?  I would expect that if it could happen in natural under non-ideal conditions, it would be able to achieve in ideal conditions.

@AbdulKhan - thanks for the explanation - do you have references of where they formed "primary cells" in-vitro?  I had never heard of such an accomplishment.

@Yehosef Miller and Urey proved the Chemical Evolution theory in their experiments showing the formation of many amino acids, sugars, nitrogen bases.  Oparin stated that mixing large protein with a polysaccharide leads to formation of coacervates; same experiment was also done by Sydney Fox.  For references you may have to search the google.

The Miller/Urey experiments are a long way from "proving the Chemical Evolution theory" - they basically showed how amino acids formed which a step but far away from proving the theory.  The closest I've found is this article: https://www.nature.com/articles/ncomms9352 - but it requires a delicate balance of external conditions to stimulate "reproduction".  I'm not sure what natural selection is going in their experiment.

There are some examples of lab-made protocells although they cannot reproduce and they die because of dilution of their components after a while.
In nature we haven't seen any, most probably because 1) nobody is looking for it and 2) even if they form they have to compete with all the other life-form, that are already optimized for that particular environment, leaving no chance of long-term survival.

Basically the closest we've come to a living organism from scratch is an autocatylitic RNA set. Look it up.
But we haven't actually made any self contained life yet, although this video is VERY interesting.
Life can't form anymore. We have oxygen, which like Abdul said, smashes delicate primordial molecules. Also, we have an ozone layer, which stops the UV rays from hitting the earth, which as demonstrated in variants of the miller Urey experiment, were probably instrumental in the formation of life.

don't tell them to look it up, provide a source


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Is there a resource that has quantitative data about cell proteins?
I am a MSc student working in mathematical biology. In my thesis I am modelling diffusion of a protein that can bind to cell surface receptors. In order to simulate this I need some rough figures about the binding rates, degradation rates, diffusion rates etc. of components involved in this system. I have managed to find some information about these things, but they have all come from reading papers - biology papers where I only barely have enough knowledge to grasp the key concepts and (lets face facts) barely have the patience to read.
Is there a better way to find this quantitative data? Ideally I would love to come across a database that had this kind of data in it, but I'm not holding my breath.
What techniques do people in my position use to find this kind of information?(short of trawling through incredibly dense biology papers)

I'll list the papers that I obtained these parameters from. BioNumbers is a very useful resource and some of these papers that I cite have been obtained from the reference mentioned in BioNumbers. So BioNumbers should the first place to look for things like this. If you are not satisfied then start googling around :)
You should, however, keep in mind that simulation using exact parameters may not be very helpful. You can try varying the parameters in some given range and see the effects. Some parameters actually vary a lot.

Protein translation rate: 11 amino acids per second. Assume some steady state concentration of mRNA. This parameter is highly variable as there can be multiple ribosomes per mRNA [1]. Also see Schwanhäusser et al. (Supplementary excel sheet) [2]
Protein degradation rate: Take an average or one of the values reported by Schwanhäusser et al. (2011) [2]
Association/dissociation rates: See table shown by Zhou (2003). It lists different known interactions.[3]
Protein diffusivity: This differs for cytoplasm and water. You can assume diffusivity in ECF to be same as that in water. See Arrio-Dupont et al. (2000) [4]. They report it for specific proteins. You can extrapolate for other proteins using the Stoke-Einstein relation which says that diffusivity decreases inversely with the radius of the particle.

[1] Siwiak, Marlena, and Piotr Zielenkiewicz. "Transimulation-protein biosynthesis web service." PloS one 8.9 (2013): e73943.
[2] Schwanhäusser, Björn, et al. "Global quantification of mammalian gene expression control." Nature 473.7347 (2011): 337-342.
[3] Zhou, Huan‐Xiang. "Association and dissociation kinetics of colicin E3 and immunity protein 3: convergence of theory and experiment." Protein science 12.10 (2003): 2379-2382.
[4] Arrio-Dupont, Martine, et al. "Translational diffusion of globular proteins in the cytoplasm of cultured muscle cells." Biophysical journal 78.2 (2000): 901-907.

Thanks for the references and +1 for bionumbers! That is exactly the kind of thing I was looking for

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Thermodynamics of one directional passive membrane transporters
I have read in my biochemistry textbook, that some membrane transporters transport only in one direction, moreover, they don't require ATP energy. I wonder, why these proteins do not act as  Smoluchowski's Trapdoor and break second law of thermodynamics.
It seems that concentration of substance on the "A" side somehow affects protein's ability to pump molecules, even though on that side  protein doesn't bind with former (on the A side protein has conformation with low affinity to the molecule, thus complex disassociates). So I don't understand how this form of Maxwell's demon is countered, or how concentration on the A side affects protein's function.

Can you quote from your textbook where it says "transport only in one direction"?

the transport is only in one direction but only as long as a gradient exists, it is no different than a ball rolling downhill and not back uphill. the gate just stops the gradient working in the opposite direction. think of one way seals

Thank you for your attention. Bryan Krause, my textbook is not in English, so I translated it. @John you confirmed that these kind of proteins exist, thank you. I will soon post my question's improved version and I hope for your help there as well.

I am afraid that this is a biology site, and I, for one, have never heard of Smoluchowski's Trapdoor. You have provided no links to this, and the obscurity and complexity of the thermodynamic ideas are evident from a paper in the journal  Entropy from which your diagram appears to be taken: “Skordos and Zurek [1], in their deliberations on Smoluchowski’s trapdoor, fall into the same syllogistic error as does Feynman [2,3] in his discussions of a ratchet and pawl within the micro- domain.” If Feynman got it wrong, do you expect us to get it right?

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Solubility of lithium carbonate in blood
When a person with Bipolar Disorder ingests a pill of $\ce{Li_2CO_3}$ and it enters the stomach the pill cap is dissolved in the hydrochloric acid; however, when it gets absorbed in the blood how does it dissociate?  Does it dissociation is there an enzyme, is that enzyme Carbamoyl phosphate, or is it the blood that separate them. Thank you.  I have also been reading biochemistry books, and would be willing to cite the information that lead me to guess.
Reference:
Data for Biochemical Research
Third Edition
Rex M.C. Dawson, Dophne C Elliot
The book notes that the enzyme does 100 percent hydrolysis of $\ce{Li_2}$ salt in 2 min. at 100 degrees Celsius, 50 percent in 2 hours at 30 degrees Celsius.
This confused me because lithium carbonate is a salt. So I was confused.  Thanks again.

Do you have any resorses or how did you make it up?

@L.Diago Yes let me add them

Are you asking about some quote in a book? Because the uncertainty in the question about salts is a bit confusing (i.e., if you know what a salt is, and how it works in water, it's unclear what your question is). It might be better to reproduce the actual quote here.

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What chemicals will kill P1 Phage but not E. coli?
I'm working with E. coli and P1 Phage. I'm wondering if there is some chemical agent that will kill or disable P1 but leave E. coli untouched? It is not enough to just prevent infection. It must destroy the Phage.

No such chemical exists. Otherwise we would use it whenever we have a phage breakout in labs across the world.

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Can qPCR primer with several mismatch works?
I am designing primers for qPCR from conserved regions of a few different fish species.This is because gene sequence for my fish species are yet unavailable in NCBI database.
Is it OK (can the primer anneal to the target sequence) if the primers have several mismatch at the interior and towards it 5’ end? At the 3’ end, I can only design primer with maximum 5 conserved bases.
Thank you.

qPCR will not work reliably with so poorly matched primers, so either create multiple primer sets with higher specificity or create multiple primersets amplifying subsets of the target... this will create multiple better fitting fragments, that will act as optimised primers in later rounds of the qPCR experiment... keep in mind that the latter option will produce quite a lot of background noise.

QPCR is extremely sensitive, so I would not do this. Instead I would get those primers you mention in your question and instead sequence using them instead of doing qpcr with them. Then I would make new primers specific for the region you want to do qpcr on based on the sequence.The advantage of this is that you would now know the sequence and so you would have better primers for qpcr.


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How to calculate RPM?
I´m just starting my postdoctoral fellow and my new project involve sRNA Deep Seq. I´m having problems with the data normalization.
I´ve been reading papers about it and the variety of normalization method is huge!
The simplest one that I found is by TPM or RPM (transcript per millon or reads per millon), in which each raw read count is multipled by 1 millon and then divided by the total read count of the whole library.
The question is: which library?
I have 3 treatments. In one of them, the number of raw seq were 10 millons. After filtered of adaptor, length < 15nt, # <3 count, we generate 8 millons of mappable reads. Then, once we mapped against Arabidopsis genome, 3 libraries were generated. The mapped mRNA, tRNA, rRNA, RFAm, Repbase library (5.7 millon; 72%); the custom virus we sent library (20; 0%) and the miRNA (sRNA) library (2.3 millon; 28%). On the 3 treatments the numbers were diferent and always the miRNA library was smaller than the mRNA library.
In order to a direct compare between data set, we have to normalized the counts.
If I want to do it with RPM, which library do I have to use? The total mappable reads (including mRNA, tRNA, etc) or only the miRNA library?
I have noticed that the result is very different with one or the other, because the percentage of the libraries are not the same between treatments.
Any hint you can provide me will help me a lot.


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Genomic instability of cancer cells in h&e image
Is there are any books or papers on the topic of visual differences(analyzing H&E microscopy) of high grade cancer cells vs low grade cancer cells vs non-cancer cells?
In particular, I am trying to measure how much of genome was altered by analyzing images.

That seems like a substantial undertaking.  How familiar are you with histopathology generally?  The identification and grading of tumors is a large topic in histopathology, about which a good deal has been written (to my knowledge, none on your question specifically, but I am by no means an expert in pathology). Are you looking at a particular type of neoplasm?

@Hans you are absolutely right, this is a very challenging problem. I am CS major and have some datasets and interesting algorithms that I am going to apply, but first I wanted to get at least a little bit of understanding of the field. I read some articles about histopathology and this was useful and insightful, but I decided to ask this here in case anyone can give me some pointers to more relevant books on this topic. I am looking at a prostate cancer, but I believe general principles are the same -- I read that some mutated cells change shape\function\invade tissues and blood vessels\etc

Maybe I am misinterpreting your question. Tumor grading would be done histologically. To determine alterations to the genome itself, I would think that the only thing you could do visually is karyotyping. You could get a sense of translocations, loss of chromosomes, indels, etc. Otherwise you would likely need to do sequencing.

Histologic diagnosis of tumors is made using the so-called  WHO blue books.
Different tumors show different patterns of cellular and tissual aberrations.
On h&e  karyorrexis and  pyknosis  are examples histological markers of nuclear aberration.
A recent  paper reviews the salient visual and subvisual morphological changes of cancer nuclei and their possible cause or etiology and significance.


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Difference between water and tea
My friend heard that tea is worse for drinking than water because "cells have a special membrane and tea has special supplements and membrane doesn't let tea pass and this is why skin is dry even when you hydrate with tea a lot", something about "lipid bilayer".
Is there is some nice scientific article on water andd tea difference to human organism?

Your question is very awkward.
Let's define Tea as boiling leaves in water. At the end, you remove the leaves and drink the flavoured water.
At this point, the "tea" is still very much water - as in tea is water with dissolved chemicals from the leaves. Note, the word chemicals is not to be interpreted in a negative way because everything (including water) is a chemical.
So, the difference between tea and water are the chemicals that dissolve. What are these chemicals? The answer to that depends very much on the tea. Another difference is the temperature - tea is typically hot.
You can look at this article about chemicals in green tea and their associated health benefits. You can do further searches for other tea types and for each of those chemicals.
In short, no you do not get dehydrated because of tea vs. water. Dry skin can be caused by a lot of different reasons. Oh and no, caffeine doesn't cause any significant amount of dehydration as far as I know.

Depends on the tea, but most tea (unless herbal) contains caffeine, which is a diuretic. This means it dehydrates, and why one might experience drier skin. However, this is not a direct relationship and the actual reason why one's skin might be dry is a lot more complex. However, for a basic answer, caffeine is your culprit.

Please add citations to relevant scientific literature supporting your claim. The old wives tale about caffeine dehydrating you is completely false. Yes, it may increase your urine flow, but not enough to counteract the actual fluid intake from the tea (or whatever beverage) itself. Plenty of construction workers in the US rely solely on tea or soda beverages for their hydration during the day, and they have no symptoms of long-term dehydration. These actions are unhealthy because of the massive sugar intake, but they don't dehydrate.

@MattDMo Caffeine can be diuretic - but only in high concentrations (much higher than found in a cup of coffee).

@Chris yes, I know. My point was that the amount of water you are consuming outweighs any minor diuretic effect of the caffeine.

@MattDMo For normal beverages, there is no effect.


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Demultiplexing symmetric PacBio reads
I have PacBio CCS.h5 and the corresponding fasta and fastq files and I would like to demultiplex them. Does anyone know of how this can be done in the absence of bas.h5 files.
Thanks for your help!
Mandy

It is more likely that you will get an answer over at biostars.org. Not that it is wrong here, but this place is dedicated to bioinformatics.

I'm voting to close this question as off-topic because it's about a specific problem in a specialized software environment.

@Chris Stronks, Which software are you referring to? I am not sure how familiar you are with PacBio and demultiplexing but in my opinion, the question fits within the topic of sequence-analysis.

Do you mean demuxing the FASTQ into the FASTA and QUAL streams? The FASTA format only contains one data stream, so I don't see what you want to demux out of it.

authors: Илья Рубинштейн


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What is the relationship between protein-protein interaction networks and metabolic networks?
I am trying to find out how these networks can be linked together. I know that Protein-protein interaction networks and metabolic networks both fall under the Intra-cellular type of biological networks that describe the cellular functioning. But what is the relationship between them?
Thank you very much.

Metabolic processes are carried out by enzymes and regulated by hormones. Both enzymes and many hormones are proteins. You may have to specify your question further.

Did you find answer helpful?

Proteins interact with each other often for regulation purposes and for localization of several enzymatic reactions for increased efficiency. For example, some proteins inhibit their binding partners. Or DNA replication complex is made of bunch of proteins, many of which do different jobs, but they are in physical complex (e.g. helicase with DNA polymerase).
Metabolic networks are sets of chemical reactions, they might even happen in different compartments inside the cell. While you can try to investigate protein interaction network by cross-linking proteins and then analyzing complexes you extract, metabolic networks are constructed by deciphering sequences of chemical reactions (e.g. metabolic cycles) and finding appropriate enzymes for each reaction.
Metabolic process (e.g. DNA replication) can be run by interacting proteins, but also might include proteins that don't directly interact with each other. For example, DNA polymerase complex does not produce nucleotides, but they are necessary for it's function.

In short, proteins in Protein-protein interaction networks perform a function by directly interacting with one another.  They may for instance bind to one another forming permanent or momentary complexes (e.g. insulin binding to insulin receptor or the pieces of F0-F1 ATPase combining), or they may chemically modify one another (e.g. protein kinases adding a phosphate to the residue of another protein).

Proteins in a Metabolic network might never be in physical contact one another. They effect one another by producing chemical compounds which are utilized by other enzymes, forming a network of chemical transformations.
Of course an enzyme in a metabolic network might also have its activity modulated through interacting with other proteins in a protein-protein network.  The two terms are of course not mutually exclusive, but describe different sorts of relationships between proteins.

I think you should try to connect the figure more clearly to your answer.

The basic struture of the metabolic networks  (MN) is like this:
molecule1 -> molecule2, where the edges are enzymes.
And the basic structure of the PPIN is like this:
Protein1 - Protein2, where the edges are van der Waals forces between proteins.
There are some diferences, PPIN isnt directional and  MN is directional in the way of the spontaneous reaction. PPIN has two modes of interaction date interactions (1-1) and party interactions (many-many).
One easy way to combine both is to invert the MN so the enzymes are now the nodes and the metabolites are now the edges, like this: enzyme1 -> enzyme2, and then add the proteins in the PPIN, like this: enzyme1(protein1) -> enzyme(protein2). But in this way you need to demostrate that some properties of the network are conserved.


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How does the Pectoralis Major work when doing a bench press?
Disclaimer, I'm not a biology undergrad and I only know the basics about muscle movement.
I know that doing a bench press works the chest, and specifically the Pectoralis Major because, well, I feel muscle soreness. However, it is not obvious to me what the Pectoralis Major has to do with extending the arm.
Thinking about muscle contraction, I see clearly how, for example, the Bicep flexes the elbow when it contracts. In a similar way, when the Pectoralis Major contracts you get horizontal shoulder adduction.
But what about the bench press? The majority of the movement consists of raising the arms upwards from a tucked position, and the is little shoulder adduction.
Thanks!

The pectoralis muscle attaches to the top to the inner half of the clavicle, just underneath the biceps on the inner part of your arm and the breastbone (a.k.a the sternum) which is found in the middle of your ribs. See below:
So taking that in account the pectoralis muscle helps bring your arm closer to your body (adducts your arm), pulling it forward in front of you (flexes the humerus) to push up like you would when you bench press. This action can be seen below.

Oh okay, pretty stupid on my part. There is a lot of adduction in a bench press. The only difference is that the triceps also extend the arm. Thanks!

Not a stupid question :) It also assists in forward flexion which is part of a bench press.


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Why people fear GMOs? Can't we map a plant composition?
My main question is can we map what a fruit is made of? For instance apples are made of 0.0002% of protein X, 0.00001 of protein Y, 0.001% of amino acid Z... etc...
If we can, then my next question would be why do people fear eating GMOs?
I understand the argument that if you introduce a new compound to your body you don't know its effect on you, but if for instance you insert a new gene into the plant where it is resistant to drought- can we not simply analyze its product and if its composition haven't changed than everything is alright?
Thank you very much!

I think this is mostly a matter of not understanding how the technology works. And also thanks to the fear mongering of some activist groups.

I guess only time can prove if those fears are true. There is too much which we don't still understand to say with certainity that inserting a segment of gene will not have any deteorating effect

Note that 'fear' of GMOs often have two different angles - human health effects and environmental/biodiversity concerns - which are conflated in this question.

thank you guys, my question was however about the health aspects of eating plants where the edible part haven't been changed and is 100% identical to the original source.

Why do some people fear vaccines, nuclear power, radiation from cell phones, or any of a thousand other scare-mongered things?  Usually it's the result of some very cynical people preying on mass ignorance for their own political and/or financial advantage.

People are not always rational when it comes to what they eat, especially when the compounds that make up the food have long, arcane-sounding names.
It is indeed possible to analyse the amino acid composition of a food substance. However, this has no bearing whatsoever on the safety of the food product.
For example, the following are two truncated protein sequences. One of them is a fragment constituent of cobra venom, the other is a fragment of harmless DNA polymerase. Without looking up or otherwise referring to the PDB IDs, it is not obvious which is which, even to an experienced molecular biologist.

3HRZ:A|PDBID|CHAIN|SEQUENCE
  ALYTLITPAVLRTDTEEQILVEAHGDSTPKQLDIFVHDFPRKQKTLFQTRVDMNPAGGMLVTPTIEIPAKEVSTDSRQNQ
1KLN:A|PDBID|CHAIN|SEQUENCE
  VISYDNYVTILDEETLKAWIAKLEKAPVFAFATETDSLDNISANLVGLSFAIEPGVAAYIPVAHDYLDAPDQISRERALE

Furthermore, even if scientists can prove beyond reasonable doubt that the two products are chemically identical, people will still irrationally purchase them. A clear example is the different prices commanded by "natural" versus "artificial" flavourings, as seen in this Scientific American article.

Consumers pay a lot for natural flavorings. But these are in fact no better in quality, nor are they safer, than their cost-effective artificial counterparts.

Thank you very much for the reply.
First of all I must note that I'm a complete layman (who skimmed over Wikipedia about SCOP and protein structures) so I'm probably missing something obvious and my question is stupid...
Those two PDB IDs that you presented seems different, so it is more of a case that is hard to diagnose their function rather than say that they are a 1 to 1 copy. Have I understood you correctly?
As for the article, well, some might say that it is not that health concious consumers are wrong about how bad artificial flavours are, it is that

it is that they are wrong about the meaning of 'natural flavours' (which raise the association of fruit juices/extracts).
Also, I obviously know very little, but are those flavours the same? Even according to this article ----"So is there truly a difference between natural and artificial flavorings? Yes. Artificial flavorings are simpler in composition and potentially safer because only safety-tested components are utilized." "There is little substantive difference in the chemical compositions of natural and artificial flavorings."---- maybe it's my

maybe it's my english but it seems like he's saying that a minute difference is still there (even if the author see this as an indictment toward the natural substances).
The thing is, you are right about peoples irrationality, but in this case the argument that such GMO food (lets say the transgeneic variety) introduces a new set of variables to the human organism which we can't trust unless rigorously tested for many many years (a generation or two if we want to see long term effects)- seems quite rational.
If someone were to

If someone were to sequence every single molecule in that new apple/tomato and show that the new product is a 100% clone of its counterpart then maybe it won't affect everyone, but at least the pro GMO will be on an unshakable ground... (Actually I just googled natural 'colorants' and it seems that some green sites are against them due to the same scientific reason like in your article- so, the trickling of knowledge is present).
If it's possible is there a reason why it is not being done? (or is it simply a calculation of cost/expected results in public opinion?)

Dang it, what happened to my paragraph division?  sorry if my response is too long.

I agree with March Ho in general: people are not rational about food.
That said there are two fairly different kinds of GMO, with different implications on the fears to have about them.
1) GMO embedding genes from the same species
These are not supposed to be any different from plants obtained using classical breeding techniques. The process in brief is for example: you see a wheat individual with short stems, an other with big grains. You want both. In classical selection you have to breed the two, select the descendants, breed again, select etc... until all descendants have both characters. Using GMO you can simply pick the gene you want and put it in the strain of your liking. It is much, much faster and the changes in the genome are much less than what you get by breeding two strains.
2) GMO embedding genes from other species
This can be more problematic as the gene you brought in could be from an organism nobody did ever eat, such as the Bt toxin in MON 810, hence the questions about toxicity. It doesn't mean it's toxic and the controls are very stringent about that but I can understand better why such GMO should be carefully checked.
3) The false problem of GMOs and environment
A Last problem is the indirect effect of the GMO, for example, if it's designed to be herbicide tolerant it might allow more herbicide to be poured on the plants and hence cause more herbicide residuals to be in the food, or in the environment, people then not liking GMO for environmental related reasons. But that should be addressed by checks on herbicides in food or in the environment, not by banning GMOs!
That said, GMOs have been around now for 20 years and people against GMO have a very hard time showing any kind of negative effects (see links posted previously), and some studies "proving" the toxicity have been shown to be statistically weak, not to say fraudulent.
Conclusion
There is no good reason to reject type 1) GMOs based on food safety and very little reasons to reject type 2) GMOs. I would personally push hard for a general adoption of GMOs bearing genes from the same species or other edible plants. It would already make a lot of things easier!

Thank you for the expounding,
I must ask though about type 1, do we know about the concert and interplay of all the genes? Can we predict all the cascading effects in all the plants that we change?
Do we know that all those genetic alterations that occur when you use classical breeding are not actually necessary in order for the edible end product to convey some yet unknwn characteristics (certain protein and etc)?
thx.

Answers to questions in your comment in order: No; No, but this is the case for normally bred organisms too; the organism modified already conveys those characteristics and there's no a priori reason to expect any change in that.

Yes, but if we don't actually know everything about the chain reactions that happen when we artificially introduce a new gene, then how can we tell that no characteristic indeed will be affected?
Like the famous Rumsfeld quote about unknown unknowns, the only way we can be sure that our product is "as nature intended" is if the artificial result will be 100% identical to the classically bred (which we can't compare unless we actually make both).
no?

Do you consider a plant that has a genome recomposed from two different species+ duplicated to be "as nature intended". That's the wheat you eat everyday. Obtained by very artificial selection several thousand years ago. Was there a risk to taste that incredible mix. Probably but I'm fairly happy they tried. All new varieties are extensively tested but I see no reason why type 1 GMO should be prohibited and not just extensively tested.

Perhaps I should have not used the term "as nature intended" since it might bring some association with other ideas...
However, when you say "two species" you are not exactly being accurate and you give a wrong impression as well. If they can cross polinate then they belong to the same family which in genomic terms is (or might be) quite important.
Furthermore, like you said, they started doing it thousand of years ago. The first aspect to this is that there are plenty examples where human behaviour changed our physical evolution (in relatively short time), if we'll all start

start eating somewhat poisonous transgenic GMO right now then our future descendants would indeed have no adverse effects from it.
The second aspect is that even if those experiments were somewhat detrimental to their health, the process was slow (so effects could be noticed among generations), regionally dispersed (so the bad results would be contained and only harm one village) and the changes were gradual (easier to see what went wrong)- they experimented on themselves but those conditions were a far cry from todays globalized, fast paced, risk aware, scien

, scientific western world.
We have volved alongside  this system.
And finally, if you also agree that some risk is involved then why do  you seperate between type 1 and type 2 when introducing to the market?
Don't get me wrong, by no means I object to the idea of GMO, even cross-species (hence my original question about GMOs where the fruit itself is 100% identical to non GMO), like you, all I want is a (very,very,very,2 human generations long) rigorous testings.

"However, when you say "two species" you are not exactly being accurate". On the contrary, I'm very accurate, but plants have porous boundaries between what are considered species, specially if you help them a bit. Triticum aestivum (common wheat) is an hexaploid of Aegilops tauschii and Triticum turgidum himself an hybrid of Triticum urartu and Aegilops speltoides


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Parasites with both plant and animal hosts?
Are there animals (or plants) that are parasitic on both animals and plants?
Especially such that they rely on their plant host being eaten by their animal host?

haven't heard of a plant/animal like that... there are micro-organisms that wait to be ingested by animals to continue their life cycle though

My guess is that fungi would be the best candidate, without knowing about a particular answer/example to your question. I know that there are groups of parasitic fungi that have switched between animal and plant hosts (i.e. in relation to speciation events, not host switching/complex life cycles within the same species of fungi).

Plant to animal switching is known in e.g. rust fungi (from Pucciniomycetes), where you can also find complex life cycles with intermediate hosts (a Heteroecious life cycle).


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Which mushroom species is this?
Which type of mushroom is this? Hope the image has enough quality to allow answering the question.
Following community rules...

Images: please find below
Location: West-Northern Germany
Size - about 7 cm height, 5 width
Prior research: very hard to undestand which species is this, therefore asking here. Maybe this could be a Gymnopus peronatus - but here the stem is darker.
Specific characteristic: hollow stem

Please see here: https://biology.stackexchange.com/tags/species-identification/info including the specific info on mushrooms as well as all the other more generic requirements.

If you had a good book, you could identify that very fast. the particular features are, irregular stem, irregular widely spaced gills, no viscous pellicle on top, tan on top, grey gills, here is a identifier which might help: http://www.mycokey.org/agaric1.shtml?language=uk&localLanguage=uk&searchMode=full&atlasmode=false&r=132029.27384465246 there are other identifiers too. it looks quite unsuitable for a home ID for culinary, i've seen those already though, very common, i think they are related to the bright yellow ones with the grey gills.

google searching by image is giving me Russula integra.

You are probably right that it is a Gymnopus, It's difficult to know which one. There's also Gymnopus Fusipes. For a difficult ID, it's best to have a cross section, a description of the scent, compare the color under the youngest specimens, as the gills often change from very light to very dark with age.

Could you please provide some sort of support for the ID method claims you make? (I understand that they're likely based on your own experience. However, to be most helpful, providing reputable support that other users can explore really would increase the broader utility of your answer). Thanks!

Genus Amillaria species may be mellea

@atxgis citing reputable sources is also strongly advised, especially when referring to species IDs (since so much misinformation exists online!). Thanks

It has characteristics of a Chantrelle ; I would start there to identify it. Chantrelles are usually more orange or yellow but I have mushrooms in my yard that look very similar to the picture and after checking several references I believe it is a Chantrelle .

Definitely not a chantrelle, that should have decurrent ridges.

I never downmark but that's the worst ID i ever read, especially because it's dangerous. A chantrelle has round gill folds, and a trumpet gill base, it's smaller, doesnt go translucent or grey. There is a false chanterelle that is dangerous which has more in common with that mushroom. http://www.gallowaywildfoods.com/wp-content/uploads/2016/09/trumpet-v-sinuous-e1474988442548-900x1024.jpg common chanterelle: http://tcpermaculture.com/site/wp-content/uploads/2013/12/C_cibarius02.jpg

I was concentrating too much on the branching of the gills.However , been eating wild mushrooms for 40 years and I am still here.


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From where does the oxygen in glucose come in photosynthesis?
Is it carbon dioxide or water? I'm talking about the oxygen present in glucose and not the oxygen that is released after photolysis of water.

RuBisCO attaches one molecule of CO2 onto Ribulose-1,5-bisphosphate (RuBP). RuBP gets split to two molecules of 3-Phosphoglyceric acid (3-PGA). Via reduction to Glyceraldehyde-3-phosphate (GAP) the link to glycolysis is established. By doing the Glycolysis reactions backwards, you reach Glucose.
This is the reaction of RuBisCO (from humboldt.edu):

EDITED to correct: One molecule of RuBP, one molecule of CO2 and one molecule of water are converted to two molecules of 3-PGA. This compound then is either used to refill the Calvin cycle by production of new RuBP, or is inserted into glycolysis, where it can be converted to Glucose. So, as David correctly points out, the oxygen comes from water as well as from CO2.

Thank you @David, my bad, I missed that. I hope the edited answer is better.

Fine. I'll remove my original comment.


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Anatomy of joints of human hand
Q) A girl slipped and is falling. She puts out her arms to prevent falling. Which joints are most affected by her fall?

Fibrous and Synovial joints.
Cartilagenous and Synovial joints.
Fibrous and Cartilaginous joints.

The answer is 1.
Attempt:
Since it is the arms that will be affected, Synovial joints will be affected. But I don't remember there being any fibrous or cartilaginous in hands.
Are there any fibrous or cartilaginous joints in hand?

What does "cartilaginous joints" mean? That seems really imprecise.

The intermediate radio-ulnar joint is fibrous in arms.

[Source: Slideshare.net]
You can see the the interosseus membrane between radius and ulna which is composed of white collagen fibres.
Furthermore, there is a cartilaginous joint between epiphysis and diaphysis of humerus which is made up of hyaline cartilage. But it is lost during development and is absent in adults.


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Solubility of thromboxane A2 agonist U-46619 in H2O
First of all, I'm not sure I can dissolve U-46619 in water so that's also part of the question.
If it is soluble in water, how much can I dissolve before saturation?
If not, what's the right solvent to dissolve this agonist?


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Why does damage to myelin sheath in multiple sclerosis lead to a decrease in information reaching the brain from sensory receptors?
In multiple sclerosis(MS), myelin sheath is attacked and damaged. When this happens, there is a decrease in the amount of information reaching the brain from sensory receptors. How and why does a decrease in the amount of information occur?
I know that myelin sheath speeds up the conduction of nerves by which the action potentials can jump from node to node by saltatory conduction by their local circuits; but how when this stops happening action potentials and information can be lost (I believe that it must have not decreased in information but the whole amount of information will reach the brain but slowly because of lower speed of conduction)?
I got more mixed up when I saw on a website that:

The myelin sheath prevents these impulses from escaping from the nerve
at the wrong point.

Can please someone tell me how this happens? And how in the absence of myelin sheath or it being damaged, how the nerve impulse can escape from the nerve?
Reference:
https://www.emedicinehealth.com/myelin_and_the_central_nervous_system/article_em.htm

Related: Why is saltatory conduction in myelinated axons faster than continuous conduction in unmyelinated axons?

As you write in your question, myelin is an insulating sheath that speeds neuronal transmission.
However, the mechanism for transmission in myelinated axons is very different from unmyelinated fibers. In an unmyelinated axon, voltage-gated channels are present along the entire length of the axons; in a myelinated axon, these channels are concentrated and only present at nodes of Ranvier.
The way that myelination speeds up transmission is by not allowing ions to leak out along the distance between nodes of Ranvier. More accurately, myelination reduces the capacitance (see cable theory) of the membrane. However, electrical transmission in neurons is still ultimately driven by ions moving across membranes, so the nodes of Ranvier are the locations where that movement can happen at gaps in the myelin sheath. This is called saltatory conduction.
The fastest possible conduction velocity would be for nodes of Ranvier to be as far apart as possible without the signal from one node failing to reach the next one. Nodes of Ranvier are roughly spaced according to this distance, with a bit of safety margin built in. However, if the integrity of the myelin sheath is damaged, the distance that an action potential can propagate in that damaged stretch of axon may be shorter than the actual distance between nodes of Ranvier. In that case, there is not sufficient depolarization at the next node to trigger voltage-gated channels to open. This causes a "failure" in transmission.

I will try to explain in layman's terms
Myelin sheath is the protective covering which basically works like the rubber insulation of a typical electrical wire.
Now here's how the impulse in neuron network works - I tried to explain in points

In the normal condition, the outer side of neuron has Sodium ion i.e. positive charge and the inside of neuron has negative charge. This phase is called the resting phase and the neuron is said to be polarized

On stimulation, this polarization breaks and the axon membrane (myelin sheath) becomes more permeable to sodium ions. This is called depolarized state

This depolarized spot becomes stimulation for the immediate next spot and it follows so on.

Meanwhile, the previous spot regains its polarity because sodium ions are "pumped" out using energy from ATP

This simply means that damage to myelin sheath will sure cause disturbances in polarization and depolarization, which means improper impulse or may be delay in transmission time.
Hope I could help


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Numbers in the names of tumor markers
In tumor markers such as CA 125, CA 19-9 and many other, CA stands for Carcinoma antigen, but what about the number?

There are dozens of cell marker genes. The number refers to antigen protein from one of those specific genes. The number itself can be a result of any of a variety of things, from the order in which the protein was discovered to the corresponding antibody being the 125th antibody produced against the cell line or organism. These are often used as biomarkers of various cancers. CA-125, for example, is sometimes found at high levels on the surface of blood cells in women with ovarian cancer.

So there is no systematic way for numbering ?

No, not as far as I can tell. CA-125 was named so because the antibody to it was the 125th antibody produced against the ovarian cell line the group was using. I'm not sure how CA 19-9 was named though.


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What is the difference between "gene delivery" and "gene therapy"?
What is the specific difference between gene delivery and gene therapy?
As far as I understand, gene delivery is the first step of gene therapy, but where does gene delivery end and gene therapy begin?
Does gene therapy necessarily imply that the host DNA is itself changed, or is it just that there is "extra" DNA floating around with the host DNA that also gets replicated?

Citing wikipedia:

Gene delivery is the process of introducing foreign DNA into host cells.
Gene therapy is the therapeutic delivery of nucleic acid polymers into a patient's cells as a drug to treat disease.

In other words, 'gene therapy' refers to the use of 'gene delivery' for therapeutic goals.

So you're saying that literally the only difference is the purpose? It seemed to me (indeed, from the Wikipedia article) that Gene Therapy goes far beyond just delivery into the cell and includes the processes involved in getting the DNA into the nucleus and accepted by the host cell.

In my opinion the terms are interchangeable. The only difference I see is that "Gene Therapy" could be limited to therapeutic proteins, while "Gene Delivery" could be any gene, such as luciferase or GFP. Nuclear entry and transcription are still necessary by both, because even simple reporter genes won't do anything if they can't get into the nucleus or make mRNA. If you want to avoid nuclear uptake, look into mRNA delivery. Nuclear uptake is hard.

Gene therapy is not just delivery of genetic material into the cell. There are processes such as homologous recombination and reverse mutation that are also a part of Gene therapy that helps in correcting the genetic makeup so as to cure disorders.
Gene delivery is delivery of gene into the cell where as Gene therapy has an objective of correcting the genetic make up by inserting or correcting the defective gene. I hope that helps.

I dont understand. How and why could you deliver a gene to a cell not for the specific purposes of correcting a genetic makeup?


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How only one follicle develops into graffian follicle?
I've studied that one out of many follicle develops into mature or graffian follicle. The fact which confuses me is that, since all follicles are in same ovary, close to each other with equal supply of nutrients. What causes the other follicles to give up the race? Why our body cannot develop mature follicle from a single one?

Why our body cannot develop mature follicle from a single one?-What do you mean?  What causes the other follicles to give up the race?-They don not 'give up'. Though not all but eventually many of the follicles of each ovary with the primary oocytes arrested in diplotene in them make it to Metaphae-II.

It doesn't mean only one follicle maturates within a lifetime of a woman. For every ovulation only one follicle maturates from the batch of primary oocytes stored within the ovary. Before a female is born, all the primary follicles are arrested in the diplotene stage of prophase I. Still, we do not know exactly the mechanisms that let only one follicle to release a mature egg cell, but studies have shown why it possibly happens.

Granulosa cells surrounding the oocyte have receptors for FSH (follicle-stimulating hormone), FSH activates the production of aromatase, which transforms testosterone produced under the influence of LH (luteinizing hormone) in cells of theca interna into estrogens. Estrogens activate expression of LH receptors on the surface of granulosa cells and further stimulate the production of LH. The more LH activates thecal cells, the more estrogens are produced in granulosa cells and that at the same time increases production of LH receptors on granulosa cells.
FSH also stimulates granulosa cells to proliferate, providing the whole follicle with a large number of FSH receptors and increased production of aromatase and at the same time stimulates the follicle to finish meiosis I. Eventually one of the growing follicles will have enough FSH and LH receptors on the granulosa cells to become able to respond to large surge of LH, which results in ovulation. The rest of the follicles that started to develop degenerate due to insufficient number of FSH and LH receptors. The fact that FSH and LH concentrations drop rapidly after ovulation also halts the development of remaining follicles.
The follicles that did not receive enough FSH, won't grow to the point, where granulosa cells start expressing LH receptors and they won't pass through the 1st meiotic block, therefore they still may be activated in the next month. Those that did pass the 1st meiotic block but couldn't be ovulated, will degenerate.
It is still unclear whether there are some additional mechanisms that help the atrophy of underdeveloped oocytes.
Sources:

Larsen's Human Embryology
https://kjcscientific.wordpress.com/project-excalibur/


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What is working definition for female infertility?
I've studied infertility and found that its quite complex to define. However, I came to know about a useful working definition of infertility; which was " Failure to achieve pregnancy".
Few days later I've hit upon a idea that proves that definition wrong. As I studied the turner syndrome, in which condition was XO but individual was infertile female. Further I studied that if they are subsequently treated with Gonadotrophin hormones, they have menstrual periods as well. There I found that if a fertilized egg is implanted in their uterus, pregnancy would be achieved. Now how would we call that female infertile?

Infertility is defined as the inability to conceive after one year or longer of intercourse without the use of contraception or therapeutic donor artificial insemination.

That definition does not include a state of permanence.  That is, with treatment, fertility can indeed be achieved in many cases.

You may want to consider the term sterility as a definition, which has a permanence to it. But even then, if you consider tubal ligation (female sterilization) or a vasectomy (male sterilization), then you'll quickly conclude that sterilization can be reversed.  At that rate, you may want to state "irreversible sterility" where a genetic basis cannot be overcome with treatment/intervention.  Even then definitions may vary.

As you've discovered, even some genetic-based infertility can be overcome with IVF.  In terms of your genetic interests, the condition of XX male syndrome, resulting from loss of the SRY gene during crossover, causes the inability to produce any sperm (azoospermia).  There is no existing treatment for that or even a reasonable theoretical one.
This could get more complicated/interesting as new medical therapies mature.  If one were to clone a human for example, is that a type of reproduction? Likewise, there is gene therapy, which could overcome some types of genetic-based sterility.
Sources:

http://medical-dictionary.thefreedictionary.com/Infertility
http://medical-dictionary.thefreedictionary.com/sterility
http://www.acog.org/~/media/For%20Patients/faq011.pdf


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Can someone tell me what kind of reptile is this?

It was found in El Paso Texas. It was very scared and weak when I found it. But I bought it a small aquarium and some food to make sure it’s ok before I let it go. It’s tail is broken off. It have blue and yellow dots on top of it and I think it’s a male. Can someone tell me about this lizard?

Yeah, I agree that it looks like a Fence Lizard.  The "scared and weak" is almost certainly related to the missing tail - indications that it had a close encounter with a predator like a house cat or maybe a bird.

My guess is that you have in your a hand a lizard of the Genus Sceloporus , and perhaps Sceloporus occidentalis longipes.
Commonly called the Great Basin fence lizard is a subspecies of the western fence lizard . It is genrally found in the western part of North America

Here is  a link to a guide of small spiny lizards .


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What is the name of this tree with compound leaves?
Can anyone tell me what is the name of this tree?
It was found in Northern US.
(click on image to enlarge it)

Is it a tree or a shrub? (I can't tell if that's a pot or a trunk.) Whatever, that's one of the prettiest leaves I've ever seen. I hope someone can identify it.

You have the tree in a pot 1) so is it a native tree you found and replanted? 2) Or did you buy it at a nursery or had it given to you? 3) Did it stay outside through the winter? 4) If not, has it been subjected to below freezing temperatures - at least briefly? 5) What part of the northern US as in location (which won't matter if this isn't a native tree or survived the winter)?

It is Cussonia spicata,  It is one of the favorite foods of wild elephants.
The attractive leafs grow from the end of thick branches to form rounded heads.

Source
Wikipedia

Wonderful that you identified it! I figured it couldn't be any native tree that in NA as its leaves are so unusual, otherwise I'm sure I'd remember seeing it online. I love the leaves but considering it's a tropical tree, not likely to find it in garden shops either. Curious how you knew it - have you been to Africa and saw it there?

The image you put doesn't have the same type of leaf as in the question. You should argue why you think it corresponds nonetheless. Are the leaves of this plant variable in shape? (I know this is the case in Hedera helix, another Araliaceae).

This Cussonia leaf looks more like the one on the photo: http://www.zimbabweflora.co.zw/speciesdata/image-display.php?species_id=142930&image_id=6


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In endochondral bone formation, why does only hyaline cartilage get ossified to form bone?
There are three types of cartilage: hyaline, fibrous and elastic cartilage.
Fibrous cartilage does not have perichondrium...so it does not take part in ossification because perichondrium needs to develop into periosteum.
Hyaline cartilage has more matrix in comparison to elastic cartilage. Hence, during ossification the quicker spreading of calcification of the matrix will lead to the death of the chondrocytes which will develop into osteoprogenitor cells. Is my theory correct?

'... calcification of the matrix will lead to the death of the chondrocytes which will develop into osteoprogenitor cells.' How can dead cells develop into living ones?

yes this is correct, i think hyline cartilage gets transformed to bone more quickly due to the fact that is has the matrix which is closest to bone in terms of density, also the cells are located more closely, therefore it is easier to convert this tissue to bone.

Welcome to Biology.SE! This sounds reasonable, but without supporting references only an expert in this area can evaluate your answer. Consequently, answers are much more likely to receive a favorable response if they include supporting references (primary literature is best). ——— You may also wish to take the [tour] and then consult the help pages on the standards for additional advice on [Answer] effectively. Thanks!


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DNA replication during Mitosis
I am a bit confused.
During Meiosis, DNA is replicated to form a cell with half the DNA and likely to have variations.
But since the replication process of meiosis and mitosis are the same, why do DNA in different cells of an individual organism not have variations? Or do they have variations that are just not expressed?

Welcome to Bio.SE! In order to ask a good question, you are expected to show some research effort. Did you try googling "differences between mitosis and meiosis"? It could lead you to the answer!

Individual cells do have variations, those are just not inherited as during mitosis you don't produce gametes.

So can DNA in hand skin cell and leg skin cell be same

Think of Meiosis as a means of producing half the genetic material you (and your partner) need which, once combined, produces offspring that inherits genetic material from the both of you. Think of Mitosis as a means of producing a full, exact (as exact as possible anyway) copy of chromosomes during cell division =)
Meiosis - results in a cell with half the genetic material (haploid), which is later fused with a similar haploid cell from the opposite sex (gametes) to produce a single cell with a full set of chromosomes (diploid cell). I.e. a sperm and an egg (each haploid) which fuse to produce a zygote (diploid). Important to note that during Meiosis, there is cross over between chromosomes, so that you end up with genetically diverse gametes (i.e. each haploid cell is different to one another - part of the reason your kids don't all look exactly the same).
Mitosis - results in a cell with a full genetic copy of the cell it was replicated from. That zygote will replicate using mitosis again and again until the organism dies. During Mitosis the cell tries to preserve as much of it's integrity as possible, so there isn't cross over. But the process isn't perfect in humans - each division results in shorter telomeres, and a cells also accumulate mistakes that result in "bad code" being passed on - UV damage for example.
With regards to expression, there is the concept of epigenetics - you may inherit certain genes, which (through various mechanisms) will be "locked" and not expressed in yourself, but may be expressed in your children. You might notice that kids have characteristics of their grandparents which aren't present in their parents.

In meiosis crossing over takes place which leads to variations
 in chromosomes while in mitosis no crossing over takes place


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Does the genetic sequence of SARS-CoV-2 end with 33 A's?
Looking at the DNA (or RNA?) sequence of the Covid-19 virus here: https://www.ncbi.nlm.nih.gov/nuccore/MN908947.3
I notice it ends in 33 a's. Does the virus really look like that, or is it some artifact of the sequencing process, or some sort of padding to round out numbers?
Here's the last few lines:
29761 acagtgaaca atgctaggga gagctgccta tatggaagag ccctaatgtg taaaattaat
29821 tttagtagtg ctatccccat gtgattttaa tagcttctta ggagaatgac aaaaaaaaaa
29881 aaaaaaaaaa aaaaaaaaaa aaa

Related: https://bioinformatics.stackexchange.com/questions/11227/why-does-the-wuhan-coronavirus-genome-end-in-aaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaa

@jpa is that not a duplicate?

@MCMastery That's the issue with having overlaps between Stack Exchange websites and not allowing“crossover questions” between sites.

This is a poly(A) tail, which is a feature found in the majority of eukaryotic RNAs (especially mRNA) and is also not uncommon in RNA viruses (which essentially mimic endogenous mRNA for their own replication). As with mRNA, this poly(A) tail in coronaviruses is bound by poly(A) binding protein in the cytoplasm [1], which is involved in translation initiation. In coronaviruses, this poly(A) tail is also necessary for replication independent of its role in translation [2].
[1] Lin Y-J, Liao C-L, Lai MM. 1994. Identification of the cis-acting signal for minus-strand RNA synthesis of a murine coronavirus: implications for the role of minus-strand RNA in RNA replication and transcription. J Virol 68(12):8131-8140.
[2] Spagnolo JF, Hogue BG. 2000. Host protein interactions with the 3′ end of bovine coronavirus RNA and the requirement of the poly (A) tail for coronavirus defective genome replication. J Virol 74(11):5053-5065.


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Any idea what this fish is?
Bought this Fish at the pet shop today. Forgot it's name.
That pink fish

It might be easier to go back to the pet shop...

I believe that is a Pink Dottyback.

[Source:Blue Zoo Aquatics]

Seems like your identification is correct. I suggest you add an image from google here instead of telling to double check it.

Also +1 since I had no idea who downvoted the answer.

@user33990 I have added the image for you, but please provide some description of the species that why you think it's correct.

Welcome to Biology.SE! Please add some more details in your answer.

Are you sure? The top fin seems much longer, the shape of the tail is very different, the color of the eye is different. I'm fish biologist, but I have doubts.


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In human embryology, what starts ovum cell division?
Maybe I am not using the correct search keywords in Google, but I cannot seem to find anything beyond basic information taught in schools about fertilisation of the egg by the sperm.
After the sperm has fertilised the ovum, I know that the zygote starts with one cell, then divides into two cells, then four cells and so on, but what initialises cell division, and how does the cell divide?

Actually an ovum doesn't ever start cell division because once it is fertilized by a sperm the combination of the two cells is call a zygote.  In humans, the zygote proceeds with the many steps following fertilization leading to the first division; this takes on the order of 24 to 30 hours.  At that point the set of cells may be termed an embryo or various other technical terms.  The succeeding cell divisions occur by the normal cell division mechanism, which is called mitosis.  In the context of the development of the human embryo, an early stage cell division is often called cleavage.
More details are available from the links in the above.  For greater technical depth on the initial stages of the division of the zygote, you might want to see this article.

Thanks for pointing me in the direction I need to go in order to answer my question. Although I am not yet 100% sure on all this, I am not sure I can completely accept your answer as of yet. It's the mitosis part that's causing me an issue. I may be wrong, but I am under the impression from reading that mitosis (or even cleavage) is not the complete mechanism/process of cell division. I need to get this all straight in my head before I upvote or accept this answer.


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What are important temperature breakpoints for plant distributions?
I am working on a climate classification system. Some previous works like Koppen and Trewartha use temperature breakpoints of 18℃ monthly minimum of daily average to delimit tropical climates, and 0℃ monthly minimum of daily average to distinguish subtropical from continental (Koppen only).
The first question, is there any scientific basis for these specific temperature breakpoints?
As an example of what I am looking for, I want to point out something in plant distributions in the area of the world I'm most familiar with; the South of the US. In Atlanta, where January averages are 6.3℃ and lows are 1.3℃, most of the natural trees you see around are either conifers or deciduous hardwoods (Oaks, hickories, yellow poplar (Liriodendron tulipifera) and sweetgum (Liquidambar styraciflua). However, towards the coast in New Orleans 11.9℃/7.1℃ or Savannah 9.8℃/3.7℃, there are a lot more evergreen non-coniferous trees. If you look at the (very similiar) distributions from Wikipedia of evergreens such as southern magnolia, live oak, or swamp laurel oak, you can see that there is a cline where the coolest month-averaged daily temperature goes below around 6-8℃ where these evergreen plant no longer grow.
So the general second question is, are there temperature breakpoints that are significant in controlling what sorts of plants can actually grow in an area?

Can't help with citations.  For temperate climates there are several critical temps that I know of:
First one is 0 or possibly -2.  The freezing point of water.  Most plant cells have enough dissolved material in their sap/protoplasm that there is 1-2 degrees of freezing point reduction.
Next one down seems to be somewhere around -10 C.  There is a big reduction in plant species counts around this temp.
Not sure where the next one is.  Jack Pine can tolerate temps down to -60C  Apparently their protoplasm has enough sugars and alcohols that it becomes a glass -- no expansion.

Climate imposes other limits.

I bought 500 mountain hemlocks one year.  Everything I read said zone 3.  Maybe for the tops.  Where they grow, there is typically several feet of snow in winter.  Roots never got below freezing.
In our region of central Alberta Crimson King Norway maple is hardy -- most of the time.  If it gets cold early, say November, it kills the buds.  It's not just how cold it gets, but when and how fast it gets cold.
Near Edmonton we can grow a variety of birches.  Calgary 300 km south is a growing zone warmer than us, but birches don't do well there.  The chinooks are warm enough that they break bud, then the buds die when it gets cold again.  Other plants avoid this by having a chilling requirement matched to our winters.
Our winters are very long.  Some of the problem isn't cold as much as desiccation.  In some cases a warmer winter will be more fatal -- warmer air can draw off more moisture from buds and twigs.
I think there are temps above freezing that are important:  When trying to grow eggplant, any day that got below +10C seem to make the eggplants sulk and do nothing for about 3 days while they were recovering.
Another critical temp is in the high 80's/low 90's. (Farenheit)  Many plants shut down photosynthesis to conserve water.  Greenhouse operators go to great lengths to keep their houses below 90 F


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What kind of spider is this?(Rajasthan, India)

Hi there, I found this insect in India/Rajasthan. Is this a spider or scorpion? It was nearly 50 mm in length.


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What are these shrimp-like insects in my cat's water bowl that appear overnight
Our family has 2 cats and a dog.  We keep food and water bowls outside for them.  We clean and refill the water bowls every day.  Almost every morning, the water bowl is teeming with small aquatic insects of some kind, which look and act like little shrimp.  I would guess them to be 5 to 8 mm in length, on average.
What are these, and where are they coming from?  They appear to be aquatic, since they survive and swim in the water for hours -- but how do they get there?
We live in central Florida, USA.

They are not fleas are they?

No, much larger than fleas.  I would guess them to be 5 to 8 mm in length.  I'll add that to the question.

After more research, my leading theory is that these are springtails.  Springtails are water-loving.  They come in linear and globular forms, and these seem to match pictures I've seen of the linear form.  The globular form look more like a spider.  If anyone can confirm this identification, that would be great!

I live in south west Florida and found them in my dogs water bowl this morning! I’ve had saltwater aquariums for years and I am very familiar with these. They are definitely amphipods. I am in shock though as I can’t imagine where they came from. We are not close to the beach and I haven’t had my aquarium set up since I lost it in hurricane Irma in September. So weird. They must be around in the back yard around my banana trees or something.

They are probably some species of amphipod.
According to that link, two species common to Florida are Talitroides topitotum and Talitroides allaudi, though there are dozens of species in the US alone. In some areas, amphipods may be known commonly as "scuds."
These guys like to live in fairly wet places, depending on species - on the beach, in decomposing mulch/leaf litter/grass. They seem to be finicky with moisture: they tend to seek drier areas when it rains, often bringing them onto sidewalks or indoors, then they get dry and look for moisture. I'm guessing this is how they end up in your cat bowl: you certainly are not the first one to observe this.
https://www.whatsthatbug.com/2004/11/10/lawn-shrimp-3/

I'm not sure at all about the precise species...the species most commonly encountered by people on the sidewalks and such don't seem like they would survive long truly immersed in water since they avoid rain, but I wasn't able to find anything definitive on that - maybe their behavior is to avoid very wet but they can still survive immersed for awhile.


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What is the species name of this moth?
This insect was found in India. It looks like a hawk moth to me, but I still can't get the exact name for this species.

I believe that it is the vine hawk moth (Choerocampa rosetta).

https://www.whatsthatbug.com/2010/11/20/vine-hawk-moth/

Welcome to Biology.SE! It would be highly appreciated if you add some more details and some images for comparison. Link-only answers are generally not welcomed since links can get invalid if they break or the link address changes.

I would be happy to. Is there a way to copy/paste pictures into the answer or can I only do it through "upload"?

You can paste a link to the image. Just above the answer-editing box, there is an image button. When you click on it, you will get options to both upload an image as well as paste a link for it. If the site refuses the image format, you will need to upload it.


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Are my plasmids single-stranded?

Hi, in this agarose gel photo (70 volts, 3.5uL Gel Red in 30ml of TBE, 1% Agarose, 1 hour run), I've checked the digestion of a large plasmid (15Kbp, one cut site). The theory says that the digested plasmid (linearized) should migrate slower than the supercoiled form of the uncut one (bigger band of the Undigested Plasmid). In my case the digested plasmid is faster than the undigested one.
I've found that my digested plasmid could be single-stranded (http://bitesizebio.com/13524/how-to-identify-supercoils-nicks-and-circles-in-plasmid-preps/). Do you think that could be the case?

You assume that the undigested plasmid is supercoiled, but more probably it is in the relaxed circular form due to single strand nicks. This form migrates slower than linear DNA.

I think that the simplest explanation of what you are seeing is that the uncut plasmid is in the form of dimers formed by recombination between monomeric circles. These would be resolved into monomer-sized linear molecules in the digestion.
I haven't seen this idea of single-stranded circles before, but if it did happen then I don't think this form would be predominant, and of course such ssDNA circles would be unaffected by digestion.

In my opinion the undigested plasmid is ok, maybe during the digestion or after the plasmid became single-stranded.

Why would the plasmid spontaneously convert from dsDNA to ssDNA, in your opinion?

I don't think that the plasmid spontaneously convert to ssDNA, but maybe  I do something wrong, maybe something like pipetting too vigoursly? I don't know. My tutor says the band in the gel must be higher. I've done the cut 3-4 different times, also with a different enzyme but always the same result.


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No. of meiotic divisions to produce specific no. of seeds
If I want to produce 100 seeds. Then the no. of meiotic divisions is 125 which can be calculated by the formula x + x / 4.
x = no. of seeds produced.
How is this formula derived?

Assuming that you have studied megasporogenesis and microsporogenesis. To produce a seed, you require the production of pollen(n) and egg(n) and their fusion.
Let's start with pollen grain(n):

4 pollen grains are produced after 1 meiotic division in the pollen sacs.

$$4~\text{pollen grains} = 1~\text{meiotic division}$$

To produce 1 pollen grain.

$$ 1~\text{pollen grain} = 1/4~\text{meiotic division} $$

For production of $x$ pollen grains.

$$ x~\text{pollen grains}=x/4~ \text{meiotic divisions}\quad(1) $$
Now coming to egg(n):

Only 1 egg is produced after 1 meiotic division in the megasporangium.

$$ 1~\text{egg}= 1~\text{meiotic division}$$

For production of $x$ no. of eggs.

$$ x~\text{eggs}=x~\text{meiotic divisions}\quad(2)  $$
For production of $x$ no of seeds(2n):

$x$ pollen grains and eggs are required. No. of meiotic divisions to produce $x$ pollen grains and eggs.

$$x~\text{seeds}=x + x/4~\text{meiotic divisions} \quad\text{From}~(1)~\text{and}~(2) $$

For producing $x$ number of seeds (or say zygote) $x$ number of egg cells must fuse with $x$ number of male gametes.
In angiosperms, 1 meiotic division of Megaspore mother cell leads to formation of one egg cell.
So $x$ egg cells are formed from $x$ number of meiotic division.

But 1 meiotic division of Sperm mother cell (2n) leads to formation off 4 haploid cells (male gametes).
So by Unitary method,
4 functional male gametes are formed from 1 Meiotic division
$x$ functional male gametes are formed from 1/4 x $x$ Meiotic divisions

So total number of meiosis needed to produce $x$ seeds = $x$ + $x$/4.

Prerequisite: Knowledge about Sexual reproduction in Angiosperms (ncert)

@Mesentery It's alright.


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In the future, it is plausible that we can change the physical appearance of a living animal by editing DNA?
http://www.independent.co.uk/news/science/revealed-scientists-edit-dna-to-correct-adult-genes-and-cure-diseases-9273555.html
This article explains that scientists managed to change the DNA of adult laboratory mice with an inherited liver disease, thereby curing them of the disease.
The change in the liver is not be a change in physical size and shape, instead it was a change in the liver metabolism.
If we used this same method to edit our hair follicles, could we alter our hair color? The new hairs would have altered DNA, and come out a different color depending on what the cells have been altered to.
And then, is it possible to change the physical size and shape of a living animal by editing DNA? For example, if an animal has porous and small bones, is it plausible that we could edit its DNA so that its bones start to become more dense and thick? The physical appearance of the living animal would be changed, since the bones are larger than before.
Along these lines, could we then edit DNA of an adult human to change bone structure so that we have sharper noses? Larger eyes?

Yes it is perhaps possible. I do not really understand what the fundamental point of your question is. Anything can happen in future. Please ask a precise question as this tends to be opinion-based.

@WYSIWYG I am asking if it is a scientific possibility to change how a living animal looks. This is not an opinion based question.

This article explains that scientists managed to change the DNA of adult laboratory mice with an inherited liver disease, thereby curing them of the disease.

Yes, Read about CRISPR-CAS9 method of gene editing. This is not the only method which can achieve this. There are many others like TALEN or Zinc Finger.

If we used this same method to edit our hair follicles, could we alter our hair color?

Yes, similar studies like this has already shown this potential but using different method as mentioned in article you linked.

The new hairs would have altered DNA, and come out a different color depending on what the cells have been altered to.

For this you need to express such constructs in cell specific manner. Drosophila geneticists are doing such things for long long time.

And then, is it possible to change the physical size and shape of a living animal by editing DNA? For example, if an animal has porous and small bones, is it plausible that we could edit its DNA so that its bones start to become more dense and thick? The physical appearance of the living animal would be changed, since the bones are larger than before.

Plausible but remember such characteristics are controlled by many factors which will be hard to control. Plus there will be age/environmental/epigenetic factors which you can't control with such techniques.

Along these lines, could we then edit DNA of an adult human to change bone structure so that we have sharper noses? Larger eyes?

Most of these techniques required change in germ cells. Hence it will be difficult to implement such techniques in adults. However 'ideally' you can use techniques like RNAi which can be triggered by specific inducers at any stage of life (like temperature sensitive UAS-Gal4 system used in fly genetics).


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Thinking quickly causes elevated mood
I read this article: http://www.sciencedaily.com/releases/2006/09/060926171045.htm
It says, "When people are made to think quickly, they report feeling happier as a result. They also say they are more energetic, more creative, more powerful, and more self-assured. In short, they reported a whole set of experiences associated with being "manic."
"The results of our experiment suggest the intriguing possibility that even during moments when people feel stuck having depressed thoughts, interventions that accelerate the speed of such thoughts may serve to boost feelings of positive affect and energy."
Is there any biological basis for these claims or could the results be self-reporting biasness?

The original paper can be read here: Manic Thinking: Independent Effects of Thought Speed and Thought Content
on Mood


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How is e-value calculated in BLAST 2 sequences (BLAST+)?
In the BLAST+ packages, you can align two sequences instead of searching a database:
tblastn -query seq1.fa -subject seq1.fa
The web BLAST documentation states that e-values are calculated from the nr database:

Because BLAST 2 Sequences uses the size of the current nucleotide or protein nr database to calculate Expect values, you may need to significantly increase the Expect threshold in order to see shorter alignments.

However, the command-line documentation explicitly states that you cannot provide both a database and a subject sequence:
-db <String>
BLAST database name
 * Incompatible with:  subject, subject_loc
-subject <File_In>
Subject sequence(s) to search
 * Incompatible with:  db, gilist, seqidlist, negative_gilist,
   db_soft_mask, db_hard_mask

How is the e-value calculated when using BLAST-2-Sequences on the command line? (I am fairly certain I do not have the nr database downloaded.)
Thanks!

You do not need the nr database for BLAST to calculate an E-value.
It will be calculated based on the alignment of n sequences.
The exact procedure is mathematically complex but if you want to read the original paper it is here:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC53667/pdf/pnas01031-0226.pdf
a simplified version you will find here:
http://homepages.ulb.ac.be/~dgonze/TEACHING/stat_scores.pdf

BLAST does need a database to calculate the E-value. A database should first be made out of the n sequences and then, as you said, BLAST will calculate E-value from that.

Well yes in the sense that you need sequences to look after but the database can be as numerous as one other sequence

You should first understand what the meaning of E-value is. E-value is the likelihood of a random match having a certain score in given database. So, you are right that a database is required to calculate E-value. The online algorithm calculates it from not necessarily the nr database but any selected target database which could be RefSeq or organism specific databases (nr is the default).
When you are just aligning two sequences, E-value does not make any sense and there is no need to look at E-value at all. If you are aligning a sequence with a list of many sequences then you have to first make a database of your selected sequences using makeblastdb.
Now, when you do the alignment, E-value will be calculated from this database.


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How to remove duplicate results from BLAST?
If I run BLAST using a protein sequence (e.g. human p53), I get many matches to the same protein, presumably from different research projects. As you can see from the screenshot, all are similarly named and close to exact matches. Is there any way I can filter the results to get unique genes only?

imagine, you can. then how do you want to pick those that are "unique"? What makes one accession number better than another for same protein? my point is that those are all a bit different, but all as real as the other

Choose reference protein as a database. Then you can avoid the same sequence from different projects.
http://www.ncbi.nlm.nih.gov/refseq/about/

BLAST against a non-redundant database (for e.g. nr and UniProt). nr contains all non-redundant sequences collected from different primary databases but nonetheless there is some redundancy. You can also specify (or filter out) the species if you are not interested in all species.
Finally, you can also choose the best hit (post-BLAST, using simple scripts).

My point is that those results are already from the nr database, and are nevertheless all the same protein from the same species but with different accession numbers.


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Rabies transmission via barking
According to CDC, non-bite exposure includes scratches, abrasion, and contamination of the mucous membrane from a rabid animal's saliva.
So, is it possible to catch rabies if a rapid animal barks near you? I mean, it can have some tiny droplets of saliva on it, right? Or the contamination of the mucous membrane should come from licks as stated by WHO?

Between 1956 and 1977, 4 human cases of rabies virus infection were
  attributed to aerosolized rabies virus;

Possible but very rare.
https://academic.oup.com/jid/article/195/8/1144/816583


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Is this black locust?
This grows in Modiin, Israel. The leaves look like black locust (Pseudoacacia robinia) to me, but the branches are very knobby. Can anyone identify it?

Doesn't look like locust to me, but that's just a guess.  If it's a locust, the stems will probably have thorns on them.  Also, if mature enought it will have clusters of cream colored (or pink in one variety), fragrant, pea-shaped flowers in another month or so.

Although the photos are less than ideal, and I can't see any flowers or fruit, I can clearly see that the leaves are "evenly pinnate" and rounded distally (not pointed). The wood structure also looks bumpy.  Given Israel as the neighborhood, it is likely to be a carob tree (Ceratonia siliqua) which is native to the Mediterranean region.  This tree is sometimes mistakenly called a "locust" tree.  See Links below.
https://en.wikipedia.org/wiki/Ceratonia_siliqua
http://tree-species.blogspot.com/2008/04/carob-tree-ceratonia-siliqua.html


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Palm Tree Identification
I need help identifying this particular palm tree. Unfortunately, I don’t have many details to give, and I’m by no means one to say I’m even an amateur at plant identification. We are unsure of its origin and can only confirm it’s age by how long we’ve resided here in Hockessin, Delaware. The plant is over the age of 14, and it stands a little over 12 feet high. The foliage is composed of single green shoots coming from the head of the plant which descend gracefully and reorganize into what one without knowledge would say is bark. We are looking to purchase another tree of this species or a close relative; there was a recent loss of an identical tree which sat opposed to this one.

Probably not a palm, looks like something in the Agavaceae so for example, a yucca or joshua tree (though not that specifically).  Try searching your local nursery websites for "yuccas" or something similar.  Or show the picture to your local nursery/landscape person or horticulture expert (maybe county extension agent).

I'm not sure about the species, but the staking seems a little intense. Was the other tree staked the same way?

I notice the soil is sandy and there is Opuntia growing nearby.  Yucca and Opuntia like it dry typically, and warm.  I see you are outside Philadelphia PA USA, where there are very cold winters.  This must be a species of Yucca that can take the cold.

Appears to me to be a Yucca tree, from the family Asparagaceae, whereas palms are typically a member of Arecaceae.

After searching various sites about cold-hardy yuccas, and looking at images, I think you have Yucca rostrata or possibly a hybrid of it.  According to Wikipedia it can be grown in zone 5.  Your location is zone 7, but perhaps if the microhabitat is just right it can survive your winters (perhaps the sandy soil evident in the picture helps it survive, since sand drains well).  I suggest you look at the description of the plant and images online and compare it to your specimen to see how well it fits.