text:
Approaches towards a theory of innovation in evolution
Evolutionary biologist Andreas Wagner writes in his book "The Origins of Evolutionary Innovations: A Theory of Transformative Change in Living Systems" (Oxford University Press, 2011):

We are familiar with many examples of innovations (qualitatively new
  phenotypes that can provide a critical benefit) but have no systematic
  understanding of the principles that allow organisms to innovate.

About the term innovation itself he writes:

It may be difficult to define rigorously what an evolutionary
  innovation is [538,616]. However, these and countless other examples
  show that it is usually easy to recognize: a new feature that endows
  its bearer with qualitatively new, often game changing abilities.
  These may not only mean the difference between life and death in a
  given environment (just think of biosynthetic abilities), they may
  also create broad platforms for future innovations, as did innovations
  of photosynthesis and of complex nervous systems.

and at another point:

Nature’s many innovations—some uncannily perfect—call for natural
  principles that accelerate life’s ability to innovate.
Can random mutations over a mere 3.8 billion years really be
  responsible for wings, eyeballs, knees, camouflage, lactose digestion,
  photosynthesis, and the rest of nature’s creative marvels? And if the
  answer is no, what is the mechanism that explains evolution’s speed
  and efficiency?

He then tries to develop such a framework for this crucial ingredient without which our understanding of the evolutionary process seems incomplete.
My question
Have Professor Wagner's hypotheses about innovation in evolution (what he calls a "theory of innovation") been corroborated empirically and are there other approaches towards a "theory of innovation" (according to his definition)?
NB
Definitions about what Prof. Wagner means by "innovation" and "theory of innovation" can be found in the above mentioned book, see e.g. here.
A brief overview of Wagner's "theory of innovation" can be found in the answers to my follow-up question: Key points of Wagner's theory of innovation

Does he present in his book an argument that random mutation is insufficient? The phrase "uncannily perfect" is horribly subjective and the word "mere" to describe 3.8 billion years is jarring and counterintuitive.

I upvoted because even if I question the premise of the book that doesn't mean the OP has asked a poor question. A negative score seems punitive  if unaccompanied by an explanation.

I downvoted because I feel the question is not well formulated and, without even a brief explanation of the theory, is unclear as a stand alone piece (requires reading a lot of external material before it can be understood). I requested clarification giving you the opportunity to improve the question before voting, and you declined said opportunity, so I downvoted. I think that is fair enough.

"..it appears that his theory of innovation is that mutation is potentially non-random in its effect - is this how you interpret it?" this was one of my requests for clarity. That was my interpretation based on what I have read of his work, and what I know from my PhD in evolutionary genetics. I felt that your question required an unreasonable amount of highly specific knowledge, so I requested a clarification, twice. As far as I am concerned that was a legitimate reason to downvote.

Can random mutations over a mere 3.8 billion years really be responsible for wings [...]? This is an argument from incredulity, a logical fallacy. Just because you can't imagine something happening, doesn't mean it can't happen.

@vonjd You should read some of Wagner's papers. A part of his research work is about possible mechanisms of evolutionary adaptation.  I haven't read this book but have read some of his articles. His articles on this topic are based on mathematical models and inference of bioinformatics data. The question does not deserve 6 downvotes but is a bit unclear to me.

@vonjd This is not same as the case of differential equation. Wagner's specific research is not that basic. Your question should be clear in itself. If you use a definition that is possibly not a textbook definition then quote it (along with citation). One does not need to be an expert on Wagner's research to answer this. You just need to provide the context. Wagner does not postulate any special theory.  He just uses the word innovation to mean evolutionary adaptations at a molecular scale. Did you check out his articles?

@vonjd please address WYSIWYG's concerns in his last comment. On Stack Overflow (and other Stack Exchange sites) there is the concept of an MCVE, a Minimal, Complete, and Verifiable Example. Questions need to be self-contained - don't post your code on pastebin, put it in the question. Don't link to your input file elsewhere (unless it's very large or in binary), put it in the question. You have asked a rather vague question about a random book, and seem to expect all of us to be fully up-to-date on Wagner's ideas. Providing a summary is common sense.

@vonjd additionally, your Google Books link is broken. Please fix it, and in the meantime, please summarize the contents of the link, as is expected on many other SE sites. The link should merely be a reference, in case it is moved or otherwise breaks.

The flaw in his argument, from what I can see in your quotes, is to equate evolution to natural selection. Natural selection was never proposed to explain all evolution, nor how advantageous traits arise, but was proposed to explain how advantageous traits spread. Ultimately, why adaptation is so prevalent?
The modern theory of evolution is so much more than a theory of evolution by natural selection. It can explain perfectly well how all variation has come in to being. Its mechanisms of mutation, migration, drift, and selection can both erode and generate new genetic variation. New genetic variation, and the phenotypic changes that brings, occurs by mutation. Various types of mutation can occur.
Mutations are random in their effect. Now it is possible that mutation rates are not random; if you imagine two theoretical species which have both gone through genetic bottlenecks, such that they both have little genetic variation, then the species with a higher mutation rate might have a better chance of staving off extinction because mutation will increase genetic variation, and genetic variation limits the rate of adaptation. Therefore, if there is a genetically coded trait which increases mutation rates then it may spread. Conversely, mutation is generally detrimental (see Fisher's Geometric Model) so, in general, there will also be selection for lower rates of mutation. From what I can gather on Wagner's theory on innovation is that mutation may be some kind of premeditated, directed mechanism with the organism trying to make a certain trait evolve. This is generally considered to be highly unlikely within the evolutionary biology community and, as far as I am aware, there is no evidence of it occurring.

Related posts I've made on biology SE:

Are humans evolving since their first appearance?
Why do some bad traits evolve, and good ones don't?
How is evolution possible in contemporary humans?
If evolution is not about increased complexity, why does so much complexity evolve?
Genetic Diversity and Adaptation
Evolution- Variations, adaptations and selective advantages
Evolution in 37 years, is it possible?

Having read some more on his theory, I think I am more clear on what he means. He uses the term innovation as other evolutionary biologists would use adaptation. I've no idea why he does this, there's no need to be using divergent terminology. Ultimately he is proposing adaptation by natural selection.

"Very occasionally, one or more mutations may also bring forth evolutionary innovations—new phenotypes that are qualitatively different and superior to the existing phenotypes."

"Evolutionary innovations can be difficult to define rigorously [1,2], but they are often easy to recognize as qualitatively new and adaptive traits of organisms. In addition, they also frequently provide new platforms upon which further evolutionary change can unfold."

The problem with this comes because he uses his own preconception that time simply has not been sufficient to allow all of the genetic variation to arise, to insinuate that random mutation is insufficient.

"Random change by itself is not sufficient, because it does not necessarily bring forth beneficial phenotypes."

The writing is suggestive (strong emphasis on suggestive, he never states this as far I can tell but the writing lends itself to misconception) that he will invoke some kind of directed mutation argument. However, his actual idea seems to be that genes interact and therefore this will increase the rate at which mutations cause phenotypic change. Because there is temporal and spatial variation not just in genetic variation, but also in selection, neutral mutations may accumulate in genes which later have an effect on fitness (either by interacting with new mutations elsewhere in the genetic network, or by shifts in the adaptive landscape).

"Wagner has emphasized how epistasis – interactions among genes that shape the adaptive consequences of mutations – allows neutral variation to modulate the effects of other mutations, producing a vast range of possible mutant phenotypes that may lead to an adaptive innovation."

This is nothing particularly new or controversial (see epistasis, gene networks, and read on evolution from standing vs. novel genetic variation). Basically, Wagner appears to suggest that Darwin's theory relies on novel mutation arriving after selection changes, which it does not, and Wagner's theory is simply a way for standing genetic variation to persist through gene networks. I don't think the concept of standing genetic variation is novel here, but the possibility that standing genetic variation may come under selection because of further mutation elsewhere in the gene network does appear to be novelty of his work.

MattDMo makes an excellent point on Wagner's assertion that all mutations occurring at random over just 3.8b years is implausible:

This is an argument from incredulity, a logical fallacy. Just because you can't imagine something happening, doesn't mean it can't happen.

"The flaw in his argument is to equate evolution to natural selection." No, he doesn't but I agree that the quote above seems to lead in this direction, it is a little bit too catchy. I think many of the mechanisms you refer to are in his book too. The thing he tries to achieve is to create a consistent framework for these phenomena in his theory of innovation.

Hi @vonjd - I was just in the middle of editing when you commented, just so happens that includes that sentence :) could you give an explanation in your question of what his theory of innovation is?

No problem. When you click on the link I gave you will find a good overview in the sections "innovations everywhere", "Towards a theory of innovation", "What must a theory of innovation accomplish?" and "What kind of information does a theory of innovation need?" but perhaps there are other approaches out there? This is the second part of my question.


text:
Typical cellular respiration lab with a respirometer -- why is potassium hydroxide (KOH) necessary?
For context, if you are unsure what this question is in reference to, feel free to take a look at this video by Bozeman science and go forward to about the 2:00 mark. In a typical cellular respiration lab, in particular the one outlined by the College Board, a respirometer and some peas are used to measure the rate of respiration. What confuses me is why KOH (potassium hydroxide) is necessary so that the interior volume of the respirometer won't change. Why wouldn't the solid formed by 2KOH combining with CO2 (K2CO3) cause a change in volume, since it occupies space in the respirometer just like the gasses? Sorry if this seems like a silly question, I have very poor background knowledge of chemistry.
For an animation, feel free to view this link from Pearson.
Thanks!

The solid precipitate does not contribute as much to the pressure inside the vial as the gas does. Intuitively, the gaseous molecule contributes to the pressure by collisions that exert force on the vessel (which would push the water out). By contrast, the solid precipitate only contributes to the pressure insofar as it decreases the volume of the vessel, which is negligible in comparison to the loss of kinetic energy per gas molecule.
Basically, just because they both occupy space, doesn't mean they occupy the same amount of space (or rather, they don't contribute equally to the pressure in the vial). Gases tend to occupy more space than liquid or solid phase molecules of identical size, due to their kinetic energy of motion and the force of their collisions on their surroundings. The KOH reacts with the CO2 to remove it from the pool of high energy gas molecules, converting them to low energy molecules in the solid. With the lower number of molecules contributing to the pressure (ideal gas law), the pressure is lowered and the force of the water becomes greater than the force of the gas, and the water enters the respirometer.

Cool. Is there anything I can add to improve the answer, like including a more quantitative explanation using the ideal gas law?

No, I think I understand it. Thanks again! And sorry for forgetting to award you the bounty yesterday.

source: Stack Exchange

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

sort: votes


text:
Comments on Experimental result regarding Anti-Bacterial soap
After using soaps, we rinse our hands with water.
Do bacteria from the water attach themselves to our hands again?
If we wipe our hands to cloth after washing our hands, do bacteria from the cloth also attach to our hands?
Or, do antibacterial substances remain on our skin and, in a sense, 'protect' us from bacteria in a given amount of time?

These are at least two different questions. Some antibacterials used in sanitizers remain on our skin for a time; others (like alcohol) just evaporate. In general, though, they don't protect us from bacteria we will encounter, but rather are formulated to destroy pathogens already on our hands so that we don't then transfer those pathogens to others or to the useal entry points on ourselves (e.g. eyes.)

Additionally: Bacteria belong to the surface of a healthy skin. This is perfectly normal, so you usually need only normal soap.

Chris's comment above can't be emphasized enough. Regular soap is enough to remove dirt and other contamination from our skin, which is where pathogens often are. Anti-bacterial compounds are not needed, as the contaminants are physically removed from the skin with appropriate washing techniques. The artificially-created hype about having to "sanitize" and "disinfect" everything is nonsense - bacteria and viruses are on and around us all the time. Overuse of substances like triclosan just lead to the build-up of antibiotic-resistant bacteria in the environment.

After using soap, the pathogens that were previously present in hands are removed by the soap and water. But yes, bacteria from the water do attach themselves to our hands again, for that we should wash our hands with clean water, which may not be sterile but at least free from pathogens. Also if we wipe our hands to cloth after washing, the bacteria that may be present in the cloth adhere itself to human hands. The attachment of bacteria depends on the concentration of microbes, increase in microbial count increases the probability and risk of contamination. Unfortunately antibacterial soaps that use triclosan may kill more microorganisms while washing hands, but then they can't "protect us" from bacteria for some longer periods of time. Also it has been found that antibacterial soaps have the potential to create antibiotic-resistant bacteria, and some may even cause allergies.

Do bacteria from the water attach themselves to our hands again?
Yes if the water does contain bacteria. Also, the chance that your hands will get contaminated is directly dependent on the concentration of bacteria in the water.
If we wipe our hands to cloth after washing our hands, do bacteria from the cloth also attach to our hands?
Same as with the water, if the clothes do contain bacteria when you touch them your hands get contaminated!
Or, do antibacterial substances remain on our skin and, in a sense, 'protect' us from bacteria in a given amount of time?
Unless you are talking about some specific fancy soap, the answer is NO, washing your hands with common soap will wipe out most (not all) of the bacteria from your hands but it will not give you any long-time protection against them.

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


text:
What is the biological significance of k-mer counting?
There are many tools developed to compute the counts of k-mers present in a gene sequence. Jellyfish, Bloom Filter Counter, DSK Kmer Counter, KAnalyze, KMC 2 etc are some efficient software developed in last decade to count k-mers.
But in what purpose, these tools are used?
How they are serving biological community?

What we have used this approach for is to search for k-mers that are enriched, or over-represented, in one genomic interval (or intervals), while present at the expected, or anticipated, frequency in the rest of the genome. The hypothesis being that such k-mers may have a biological role, either in gene regulation, or chromosome structure and function. With a collection of these k-mers in hand, one can attempt to test the hypothesis. For example, if you had a list of human neuronal enhancers, you could ask if there are any enriched k-mers, etc.

@mdperry Can I also use what you said to detect repeat elements like copy-number variation?

I have not seen an application like that; but one could try. It seems to me that if you had two genomes, Normal, and Mutant, you could run the k-mer counts and compare them, to pick up repeated k-mers. However most of the CNV approaches I have seen in the literature have used micro arrays OR deep sequencing read depths.

The applications for counting the k-mer occurences in a sequence are: building de Bruijn graphs [1] for de novo assembly from very large number of short reads, produced by next generation sequencing, fast multiple sequence alignment [2], and [3] repeat detection.

Compeau PE, Pevzner PA, Tesler G: How to apply de Bruijn graphs to genome assembly. Nature Biotechnol. 2011, 29 (11): 987-991.
  10.1038/nbt.2023
Edgar RC: MUSCLE: multiple sequence alignment with high accuracy and high throughput. Nucleic Acids Res. 2004, 32 (5): 1792-1797.
  10.1093/nar/gkh340
Kurtz S, Narechania A, Stein J, Ware D: A new method to compute K-mer frequencies and its application to annotate large repetitive
  plant genomes. BMC Genomics. 2008, 9 (1): 517-10.1186/1471-2164-9-517

To be clear, here is the biological significance of each of these applications:

Sequencing any genomes (bacterial, plant, mammalian) has become very cheap and easy recently with the next generation sequencing technologies. As opposed to the Sanger sequencing (the first generation), these produce as a readout very short sequencing reads, which have to be assembled into longer ones, and subsequently, into whole genomes. Counting the k-mers is part of the assembly process and this is its biological importance.
In order to compare whether proteins might have similar function, and thus belong to the same protein family, a multiple sequence alignment is performed. This is crucial step when annotating new protein sequences and studying their biological functions.
There are many repeats in our genome, as well as in plants. Repeated sequences are also involved in neurodegenerative diseases such as Hungtingtons, so being able to identify them is of medicinal importance.

At first thank you for trying to answer me, but all these three things are known to me, because those are described in almost all papers of the tools I have mentioned like kmc2, jellyfish etc. It still not biological to me. I am seeking the last effect on biology. Say, on your answer, the question comes in mind is What is the biological significance of de Bruijn graphs, ast multiple sequence alignment and repeat detection? Thanks again.

These 3 applications are fundamental in biology. I gave short descriptions of each one. You can look them up if you want to know more.

@manetsus That should be asked in a different question. Plus, a question like "what is the importance of de Bruijn graphs in biology" is quite broad. You can have a look at Pavel Pevzner's review on how Eulerian path is used for genome assembly and ask a specific question.


text:
Can fireflies species be identified with their wavelength?
I was wondering if we could ID male fireflies using their wavelength? A bit like how we use UV light to ID species of scorpions.

This might be a bit broad; I don't know. There are many species of fireflies, with different flashing patterns and intensities; some male fireflies don't even bioluminesce. Though the luciferin may be slightly different among species, I would doubt (but have no evidence) that it is different among sexes of the same species. It's much easier to tell which are males by their location and flash patterns.

In short: Yes it should be possible, but probably not for all species and as @anongoodnurse said there are probably easier methods of species-identification.
Elaboration:
I know (but could not find a reference) that there are currently hyperspectral cameras that are able to capture bandwidths as small as 2 nm.
And there are differences in the emission spectrum of fireflies.
Firefly luciferase bioluminescence color can vary between yellow-green (λmax = 550 nm) to red (λmax = 620). ( https://www.ncbi.nlm.nih.gov/pubmed/2801227 ) There are currently several different mechanisms describing how the structure of luciferase affects the emission spectrum of the photon and effectively the color of light emitted. (https://en.m.wikipedia.org/wiki/Luciferase)
However, it is likely that there are closely related species of firefly that have no (or very small) differences in emission spectrum. These will not be identifyable with spectral imaging.

Do you think we could ID individual in one species using wavelength ? Putting a set-up of those camera and then use Capture-recapture model to estimate population size ?

@NicoCoallier I don't know but I doubt that the spectral differences within a apecies are large enough. But there is only one way to find out...

very interesting stuff


text:
Key points of Wagner's theory of innovation
What are the key points of Andreas Wagner's "theory of innovation" from his book The Origins of Evolutionary Innovations?
Specifically:

What is new in his theory?
What problems in evolutionary theory does it address*?

Wagner does not propose any new theory. He uses the word innovation to mean evolutionary adaptations that manifest qualitatively different traits. In fact, he has himself not defined it properly in the mentioned book. This is what he has written about the term innovation:

It may be difficult to define rigorously what an evolutionary
  innovation is [538,616]. However, these and countless other examples
  show that it is usually easy to recognize: a new feature that endows
  its bearer with qualitatively new, often game changing abilities.
  These may not only mean the difference between life and death in a
  given environment (just think of biosynthetic abilities), they may
  also create broad platforms for future innovations, as did innovations
  of photosynthesis and of complex nervous systems.

However the examples he cites in the introduction are not as obvious as he says. Lets say the evolution of nervous system. The innovation that would have led to evolution of nervous system could have been the evolution of electrically excitable cells.
Actually, throughout the introduction he does not actually clarify the meaning of innovation. In page-3 he does list some features of innovation but it is all still vague. Without a rigorous definition nothing is easy to recognize and classify (especially in theoretical terms).
I do not have the book and cannot look through the entirety of it. However, based on what I have read in some of his papers I can comment something about what he possibly means by innovation.
In certain dynamical systems, some parameter changes can lead to qualitative differences in the output (bifurcations). Steven Strogatz's book on Non-linear Dynamics and Chaos is a nice and easy read on this topic.
If you look at some of Wagner's research papers, you would understand this idea better. Some of these papers are about how some parameter changes can affect the overall outcome (which may be drastic). For example, in this paper the authors talk about how differences in cell division rates can affect the outcome of a cell differentiation event.
He also talks about metabolic innovations which refer to changes in metabolic reactions and network leading to new products/optimized growth etc. Details of this can be found in his lab's papers on Metabolic Flux Balance Analysis.
There is nothing new or drastically different about all of this. This is just an addition that was unknown during Darwin's time. All that he says is still quite in agreement with the current evolutionary theory. (But personally, I find the opening of the book too vague).
As far as empirical corroboration is concerned, you may have a look at his lab's research papers.

What is new in his theory? What problems in evolutionary theory does it address?

No major problems really. The problem he is claiming, or at least how it is portrayed, doesn't really exist. To borrow from my answer to your since closed question (see that answer for more):

"Wagner appears to suggest that Darwin's theory relies on novel mutation arriving after selection changes, which it does not.."

Put simply, selection acts on genetic variation. Novel selection can occur through two principle routes: acting on standing genetic variation or novel mutations. In the case of standing genetic variation, variants exist in a population and then the adaptive landscape changes, introducing selection (fitness differences) between the variants. In the case of novel mutations, there is a standing potential for fitness differences but there is no genetic variation underlying the trait, until a mutation arises.

Side note: examples of how standing genetic variation and novel mutation affect adaptation
Imagine that there is standing genetic variation for heat tolerance, but this variation is outside the normal range of temperatures (allele 1 allows tolerance of up to 30 C, allele 2 allows tolerance of up to 40 C, but the environment never exceeds 20 C). There may then be a shift in the environment which means that it sometimes exceeds 30 C. This means selection suddenly acts on the previously neutral standing genetic variation. It is not a new idea that previously neutral genetic variation can come under selection.

"Alternatively, a pre-existing neutral allele can drift to intermediate frequency and can later become advantageous when selection pressures change owing to environmental change or to colonization of a new habitat."

Conversely, imagine that higher sperm motility would increase reproductive output, but there is no genetic variance for sperm motility. In this case there is no selection on sperm motility (selection occurs only when there is genetic covariance with fitness), but if a novel mutation arises which does affect sperm motility, suddenly we have selection.

What Wagner's idea does suggest is that, because genes act in interacting networks (see epistasis), previously neutral standing genetic variation can be brought in to play for selection. If novel mutations arise in one gene that allow standing genetic variation in another interacting gene to affect fitness then selection acts on both loci. It's not so much a problem he is dealing with, just an additional idea of how genetic variation can accumulate in populations and allow rapid adaptation. It is this idea of harbouring genetic variation that can be brought in to play that is the novelty of the work.

"Wagner has emphasized how epistasis – interactions among genes that shape the adaptive consequences of mutations – allows neutral variation to modulate the effects of other mutations, producing a vast range of possible mutant phenotypes that may lead to an adaptive innovation."


text:
How to get taxonomic specific ids for kingdom, phylum, class, order, family, genus and species from taxid?
I have a list of taxids that looks like this:
1204725
2162
1300163
420247

I am looking to get a file with taxonomic ids in order from the taxids above:
kingdom_id      phylum_id       class_id        order_id        family_id       genus_id        species_id

I am using the package "ete3". I use the tool ete-ncbiquery that tells you the lineage from the ids above. (I run it from my linux laptop with the command below)
ete3 ncbiquery --search 1204725 2162 13000163 420247 --info

The result looks like this:
# Taxid Sci.Name    Rank    Named Lineage   Taxid Lineage
2162    Methanobacterium formicicum species root,cellular organisms,Archaea,Euryarchaeota,Methanobacteria,Methanobacteriales,Methanobacteriaceae,Methanobacterium,Methanobacterium formicicum   1,131567,2157,28890,183925,2158,2159,2160,2162
1204725 Methanobacterium formicicum DSM 3637    no rank root,cellular organisms,Archaea,Euryarchaeota,Methanobacteria,Methanobacteriales,Methanobacteriaceae,Methanobacterium,Methanobacterium formicicum,Methanobacterium formicicum DSM 3637  1,131567,2157,28890,183925,2158,2159,2160,2162,1204725
420247  Methanobrevibacter smithii ATCC 35061   no rank root,cellular organisms,Archaea,Euryarchaeota,Methanobacteria,Methanobacteriales,Methanobacteriaceae,Methanobrevibacter,Methanobrevibacter smithii,Methanobrevibacter smithii ATCC 350611,131567,2157,28890,183925,2158,2159,2172,2173,420247

I have no idea which items (IDS) correspond to what I am looking for (if any)

The same question was answered here

I'll copy/paste my answer from StackOverflow here also.
The following code:
import csv
from ete3 import NCBITaxa

ncbi = NCBITaxa()

def get_desired_ranks(taxid, desired_ranks):
    lineage = ncbi.get_lineage(taxid)
    lineage2ranks = ncbi.get_rank(lineage)
    ranks2lineage = dict((rank, taxid) for (taxid, rank) in lineage2ranks.items())
    return {'{}_id'.format(rank): ranks2lineage.get(rank, '<not present>') for rank in desired_ranks}

def main(taxids, desired_ranks, path):
    with open(path, 'w') as csvfile:
        fieldnames = ['{}_id'.format(rank) for rank in desired_ranks]
        writer = csv.DictWriter(csvfile, delimiter='\t', fieldnames=fieldnames)
        writer.writeheader()
        for taxid in taxids:
            writer.writerow(get_desired_ranks(taxid, desired_ranks))

if __name__ == '__main__':
    taxids = [1204725, 2162,  1300163, 420247]
    desired_ranks = ['kingdom', 'phylum', 'class', 'order', 'family', 'genus', 'species']
    path = 'taxids.csv'
    main(taxids, desired_ranks, path)

Produces a file that looks like this:
kingdom_id  phylum_id   class_id    order_id    family_id   genus_id    species_id
<not present>   28890   183925  2158    2159    2160    2162
<not present>   28890   183925  2158    2159    2160    2162
<not present>   28890   183925  2158    2159    2160    2162
<not present>   28890   183925  2158    2159    2172    2173


text:
How can a haploid plant be bisexual?
According to Wikipedia:

Meiosis is a specialized type of cell division that reduces the chromosome number by half. This process occurs in all sexually reproducing single-celled and multicellular eukaryotes, including animals, plants, and fungi Because the number of chromosomes is halved during meiosis, gametes can fuse (i.e. fertilization) to form a diploid zygote that contains two copies of each chromosome, one from each parent.

So it means that a haploid plant body will give rise to either a male sex organ or female sex organ that produces gametes to form zygote thus completing the alternation of generation.
We also know that chara a monoecious plant can be dioecious, which means that haploid plant body is producing both antheridia and archegonia which produce gametes by mitosis.
Coming to my question, "HOW CAN A PRODUCT OF MEIOSIS BEFORE FERTILISATION BE BISEXUAL?"
Does this implies that reduction division is not responsible of sex differentiation? If yes then what is responsible for sex differentiation in plants like chara where a haploid produces both gametes ?
Explanation will be appreciated

I am not sure I understand. You define male and female based on the size of the gametes. If the gametophyte is multicellular it can still produce gametes that are of different size. Isn't it?

@Remi.b          So ,there are no allosomes in plants unlike humans?

An allosome is a non-sexual chromosome. Yes plants have allosomes. Most species (of plants and animals) do not even have sex chromosomes but only have allosomes. I don't understand how it relates to the post though. Looks like something is unclear in your understanding of sex and sex determination system but I don't know what.

Meiosis does not determine sexual form. Eukaryotes use meiosis and fertilization to recombine genes to form new combinations.  Meiosis does produce haploid cells from diploid cells, but that has nothing much to do with the sexual forms involved.
In the case of the algal genus Chara, the organism's life cycle is entirely haploid except for the single-celled zygote formed during fertilization; this is called a haplontic life cycle.  Being haploid does not require an organism to be of one sex (or any sex), so there is no difficulty to being monoecious and having both male and female structures on a single organism.  The reason for having two kinds of gametes, sperm and ova, is simply practical: the specialized job of sperm is to move to another gamete, adn the job of the ova is to provide a maximum amount of nutrition for the future zygote (which means larger size and hence limited mobility).

Even Chlamydomonas.


text:
Is there any virus that contains both DNA and RNA in its genome?
It is known that viruses contain DNA or RNA- either one and not both.
I came across a question: Which virus contains both DNA and RNA?

RDHV virus. http://science.opposingviews.com/can-viral-genome-made-dna-rna-22901.html First google search result.

@GerganaVandova There is RNA "contamination" in genomes of complex organisms too (http://dx.doi.org/10.1038/nmeth.3259). This is said to cause genomic instability. However, this is different from what OP is asking. I am not sure if the link you mentioned is trustworthy. I generally do not believe in science blogs. My guess is that it (if it really is true) is something like a RNA contamination in DNA because of a non-selective polymerase.

Here is the real scientific paper:https://biologydirect.biomedcentral.com/articles/10.1186/1745-6150-7-13

Here is the results summary of the study that describes the discovery of DNA:RNA hybrid virus:

Results
  Bioinformatic analysis of viral metagenomic sequences derived from a hot, acidic lake revealed a circular, putatively single-stranded DNA virus encoding a major capsid protein similar to those found only in single-stranded RNA viruses. The presence and circular configuration of the complete virus genome was confirmed by inverse PCR amplification from native DNA extracted from lake sediment. The virus genome appears to be the result of a RNA-DNA recombination event between two ostensibly unrelated virus groups. Environmental sequence databases were examined for homologous genes arranged in similar configurations and three similar putative virus genomes from marine environments were identified. This result indicates the existence of a widespread but previously undetected group of viruses.

And here is the link to the paper:
https://biologydirect.biomedcentral.com/articles/10.1186/1745-6150-7-13

Please forgive me if I'm missing something, but that group of viruses are still only DNA-containing. "...group of circovirus-like DNA genomes whose common ancestor appears to have incorporated a capsid protein (CP) gene known previously only in RNA viruses." They do not have both DNA and RNA; just very strong similarities to a group of RNA viruses. The OP asked if there were/are viruses containing both DNA and RNA. How does this definitively answer the OP's question?

@anongoodnurse. You are correct, these viruses contain only DNA as their genetic material. But they also contain this capsid protein found exclusively in RNA viruses. So technically, yes, it is a DNA virus. Evolutionary, it is probably a DNA:RNA hybrid virus.

Can modified vaccinia virus be considered as an RDHV? http://www.ncbi.nlm.nih.gov/pmc/articles/PMC189881/

Hepatitis B virus (and other hepadnaviruses) have mainly double-stranded DNA genomes, but include a short piece of RNA

Genome: The HBV virion genome is circular and approximately 3.2 kb in size and consists of DNA that is mostly double stranded. ... The other strand, the plus strand, is variable in length, but has less than unit length, and has an RNA oligonucleotide at its 5' end.

--What is HBV?

Unlike others, HBV virions contain both DNA and RNA. Moreover, some regions of the packaged genome can be single stranded, double stranded, or even triple stranded. These peculiar features are a direct result of the HBV genome replication mechanism which will be covered later in this chapter.

--Robert's HBV Page
However, this is just a short piece of RNA that's used to prime genomic replication.

Most virions have either RNA or DNA - never both. The exception to this rule is human cytomegalovirus (HCMV). In 2000, researchers reported that although HCMV contains mainly DNA, it also carries four pieces of RNA that are used to synthesize viral proteins.
Microbiology: An Introduction.
Barry L. Batzing

Can you add a link or an excerpt from the book that really says this?


text:
Is water vapour a product of fossil fuel oxidation?
In textbooks, while water vapour and carbon dioxide are said to be the greenhouses gases which are most abundant in the atmosphere, when a table is given showing the top greenhouse gases emitted by humans, water vapour is omitted (carbon dioxide and methane are the top two).
However, when methane is oxidised to release energy from fossil fuels, the products are carbon dioxide and water (i.e. water vapour), therefore, aren't humans responsible for the concentration of water vapour present in the atmosphere?
Why is water vapour generally omitted from the tables?

Most likely because our atmosphere contains already huge amounts of it. This is different for CO2.

Your title confuses me. Is your question if water vapour is produced by fossil fuel combustion (answer: yes) or if water vapour is a greenhouse gas (no, not really, see answer EdM)?

@RHA the terminology here is tricky. The ACS page I linked suggests that water vapor accounts for over half of the total greenhouse effect, so it should be called a greenhouse gas. It's not, however, a greenhouse gas that's being affected by human activity in a way that increases the greenhouse effect, unlike carbon dioxide.

I'm voting to close this question as off-topic because it is not about biology. It appears to be about climatology or some such subject.

Althugh water vapor contributes to greenhouse warming of the atmosphere, changes in atmospheric water vapor tend to follow rather than drive changes in temperature. Also, in the form of clouds, atmospheric water can have a cooling effect on earth temperature.
Clouds illustrate why water vapor, unlike carbon dioxide and methane, is not thought of as a driver of recent changes in earth temperature but rather is more of a follower. Unlike those other two gases, if you keep trying to put water vapor gas into the atmosphere it will convert to liquid water at some point, leaving only a constant level of water in the form of gas. That's what happens when a cloud forms; what you see and what can shield you from the sun is a collection of water droplets or ice crystals. Large amounts of water vapor are also regularly put into the atmosphere by evaporation of water from the earth's surface, dwarfing the contribution from human respiration. Eventually the atmosphere gets locally saturated with water vapor and it falls back to earth as rain or snow in the hydrologic cycle.
In principle methane and carbon dioxide could similarly condense out of the gas phase, but not at temperatures that occur in our atmosphere. You need to go far out into cold reaches of the Solar System to find naturally occurring methane lakes or solid carbon dioxide. There is no equivalent of rain to remove excess of those gases from our atmosphere. Carbon dioxide can dissolve in water to leave the atmosphere, but at the cost of acidifying the water. Ocean acidification is another serious result of adding carbon dioxide to the atmosphere.
The amount of vapor you can add before conversion to liquid water increases with the temperature. So as land temperature increases the rate of evaporation of water into the atmosphere can increase, and as atmospheric temperatures increases the amount of water vapor that the atmosphere can hold also increases. So in principle water vapor might thus serve to amplify the greenhouse warming from other gases, although its transition to liquid or ice in the atmosphere might tend to counteract that. This is a major issue being investigated in attempts to understand the interplay of factors that determine earth temperature.
A focus on carbon dioxide has an important practical aspect. If you control the excess release of carbon dioxide due to fuel combustion, you necessarily also control the associated excess release of water vapor.
In summary, human activity ends up having much less direct influence on changes in atmospheric water vapor than it does on changes in carbon dioxide or methane. That's why the latter two gases rightfully receive more attention as controllable greenhouse gases.
The American Chemical Society also discusses this issue.

The answer from the ACS foes not make sense. They contradict themselves in order to support the main party line that CO2 is the problem. Water vapor is a far more potent greenhouse gas than CO2.The ACS concedes it makes up 60% of the entire earth's greenhouse effect. According to the chemical reaction of combustion of greenhouse gases twice as much water vapor is created as CO2. Thus, if there was a substantial greenhouse effect at all it must be due to water vapor. The data does not support it at all so it is left out of all EPA, IPCC and other political discussions of climate science.
The two main contention of the ACS are invalid. First, CO2 rise also follows temperature, as they report is the case for water vapor. This is separate from anthropogenic sources of the gases, though! The reason is that CO2 solubility in the ocean decreases with temperature rise, thus the ocean releases CO2 into atmosphere from warming. The other claim is pure speculation that the water vapor saturates the air and forms clouds. They do not present any evidence of increased clouds due to combustion, which would actually cool the surface temperature by blocking sunlight, the main source heating the earth.

Water vapor has a positive and a negative green house effect. Clouds cancel out the sun. Additionally: The concentration of water in the athmosphere should be more or less constant, while the concentration of CO2 is rising...

Natural feedback mechanisms control the amount of water vapor in the atmosphere.  Added water vapor vapor becomes rain in short order, increasing sea level by a miniscule amount.  OTOH, CO2 is a driver because there are no feedback mechanisms that regulate its concentration, at least on any timescale relevant to humans.


text:
Clarification in the name "white cheeked barbet"
Everyday I was listening sound of the birs "white cheeked barbet". Then I was wondering how this name came to it? It should be by certain properties of them. In wikipedia it says

Barbets are named for the bristles at the bases of their stout, sharp bills.

But this statement I couldn't believe from picture, since I couldn't see bristles. The words "white cheeked" can be understood from photo clearly.  I then thought this may be due to some change during the migration, or anything else.
Can one help how this bird gates named "white cheeked barbet"?

It seems as though it is named for feathers below the beak that have a barblike appearance, rather than actual barbs. It may be clearer from these images:

India Nature Watch
Or in this photo: SivamDesign - Flickr


text:
Relative concentration of enzyme vs reaction product
I was reading a paper in which a recombinant protein (His-6 tagged) is expressed in E Coli (BL21 DE3). The yield of the enzyme isolated from the culture is reported as 10-30 mg per L of bacterial culture. (After purification by Ni-affinity Chromatography)
First, is this a reasonable concentration for an enzyme? I thought it was rather high.
Second, when they measure the concentration of the product of the enzymatic reaction that was found to be merely 1-3 mg/Litre of bacterial culture.
Is this typical or unusual for the product concentration to be an order of magnitude smaller than the enzyme concentration? I assumed that since enzymes were in catalytic amounts they ought to be at lower concentrations?
PS. They use SDS-PAGE followed by the Bradford method for determining the protein titres. How accurate is the Bradford method?

Remember that the concentrations you report are in mass units rather than mole units. If the protein has a mass of 40,000 Da, reasonable for many proteins, then 20 mg/liter means $0.5$ x $10^{-6}$ mol/liter. A typical small-mass product of an enzyme reaction might have a mass about 200, so its apparently lower mass concentration of 2 mg/liter is $10$ x $10^{-6}$ mol/liter, 20 times higher than the enzyme concentration in terms of numbers of molecules per liter. The mole or molecule ratios are what you should think about in terms of catalytic function.
Furthermore, from what you provide we don't know whether the enzyme was produced under circumstances that allowed it to express its activity; there may have been limitations on substrate availability, presence of inhibitors that would be removed in later purification, and so forth. In this scenario, evidently to obtain enzyme for downstream use, the emphasis is typically on getting large amounts of the specific enzyme regardless of whether some reaction product is formed. I don't find the enzyme concentration particularly high for something that the investigators are trying to over-express as in this case.
The Bradford reaction is a mainstay of standard biochemistry, as it's simple and straightforward. Different proteins can bind the reagent to somewhat different extents, so there is a second-order issue of whether the protein used for the standard curve and that being measured are similar enough in that respect. In practice, what's important is to provide enough information in the methods that are described so that someone could repeat the work to determine the relation between the Bradford measurement and some other more accurate method for this particular protein.

Ah! Yes. I blundered. Totally forgot about converting to molar concentrations. My bad!

Also, the enzyme  mass is approx. 60,000 Da & the reaction-product is MW=200. So your guesses were bang right on target! :)

Funnily, neither the paper nor the supplementary information seem to give any details about the method they used for enzyme quantification. Other than that they used the Bradford method.

@curious_cat, mass versus mole confusions are easy to make. They become less frequent with practice, but can still occur. For the Bradford method, I would generally assume that bovine serum albumin was used as the standard if it wasn't specified. If a particular manufacturer's version of the Bradford test kit was specified, the kit itself might have a standard protein that the manufacturer's information would disclose.

Thanks Ed. If I may ask two follow up questions: (1) What would be the more accurate (than Bradford) methods you refer to? & (2) Your answer seems to indicate that the conditions for max enzyme expression can be / are different than those for max product synthesis. Am I interpreting this correctly? If yes, can you comment in what way are these conditions typically different?

With respect to issue (1), the gold standard is to purify the protein in large amounts and weigh it, then use that batch of the protein as the standard for other assays whether colorimetric, mass spectrometric, or based on binding to an antibody (e.g.,ELISA). Stable-isotope labels can also be used along with combinations of liquid chromatography and tandem mass spectrometry for absolute quantitation of a protein that has been digested into smaller known peptides. See this Wikipedia page as an introduction.

For issue (2), it is in principle possible to express an enzyme in a cell-free system that contains no substrates for the enzyme. That's not as efficient as bacterial over-expression, but the principle is the same: you don't necessarily have to produce product from an enzyme just to get the enzyme itself expressed. In fact, a non-hydrolyzable mimic of an enzyme substrate, IPTG, has been used for decades to drive expression from the lac operon that naturally controls $\beta$-galactosidase production.


text:
Why does fever above 102 herald a cancer patient's death?
I was recently intrigued by a longtime hospice nurse's observation that her cancer patients die a different death than her Alzheimer's, multiple sclerosis, heart failure and COPD patients.
She stated that the cancer patients will typically develop a fever over 102 degrees during the last 48-72 hours of their life, something that is not normally seen in her non-cancer patients.
Any ideas on the underlying biologic reasons for this extinction burst phenomenon and how might this be related to the high fevers induced with Coley's Toxins?

Welcome to BiologySE - do you have some reference to that temperature and death? adding that would strengthen this question considerably

Only reference would be the data regarding Coley's Toxin used to induce cancer remission by causing high fever.

@TomBeautrous any citation is better than no citation at all (for the most part) - I would add this to your answer through editing

Maybe this low fever is the body's last attempt to kill the cancer cells, as previous attempts have been thwarted by the obsessive compulsion of doctors and patients to give antipyretics when there is a fever. Which, predictably, only hampers this protective method present in all vertebrates for millions of years that is a major defense against cancer cells.

@Gustavomolina - Too bad comments can't be downvoted. There is absolutely no scientific evidence to back up your statement.

@anongoodnurse why do you talk of scientific evidence, I couldn't even find sense in that comment :P

I'm not sure I agree with that, but if I had to support that assertion, I would say that while patients with COPD, CHF and neurodegenerative diseases may die of hypoxia (no fever there), patients with cancer more often die of opportunistic infections.
In patients being treated with chemotherapy (and for some time afterwards as well), myelosuppression - that is suppression of white blood cells vital to fighting infection - is a major risk factor, and is the major dose-limiting factor of systemic chemotherapy.
However, as I stated, I don't agree that fever is a predictor of end of life in cancer patients.
In one large study of terminally ill cancer inpatients, infection was the cause of death in only 15% of patients. More common causes included congestive heart failure (24%), renal failure (30%), liver disease (30%), cerebrovascular disease (30%), pulmonary embolism (25%) - very common in cancer patients - and lung disease. (Overlap exists because of comorbidity.)
Another study of hospice patients found the major problems in terminal cancer patients were the presence of cognitive failure, weight loss, dysphagia, anorexia and dyspnea to be independent survival predictors in this population (which somewhat supports the above study.)
The National Cancer Institute's Last Days of Life–Health Professional Version does not even list fever as a predictor of end of life (EOL).
Among a few others, the late signs found highly specific for impending death in 3 days involved instead signs of cardiac, cerebrovascular, respiratory, and renal failure.
Similarly, a study in the journal Supportive Care in Cancer found that according to palliative care experts (78 professionals, including physicians, nurses, and others):

changes in the following categories (each consisting of up to three phenomena) were considered highly relevant to clinicians in identifying and predicting a patient's last hours/days of life: "breathing", "general deterioration", "consciousness/cognition", "skin", "intake of fluid, food, others", "emotional state" and "non-observations/expressed opinions/other".

Coley's toxins have to do with treatment of cancer. I'm not sure that they have anything whatsoever to do with death from cancer.
Mortality, morbidity, and cost associated with febrile neutropenia in adult cancer patients
Invasive fungal infections in patients with hematologic malignancies in a tertiary care cancer center: an autopsy study over a 15-year period (1989-2003)
Last Days of Life–Health Professional Version
International palliative care experts' view on phenomena indicating the last hours and days of life.


text:
Does introgression require interspecific hybrids to be fertile? How is this possible?
Wikipedia says that Introgression, also known as introgressive hybridization, in genetics is the movement of a gene (gene flow) from one species into the gene pool of another by the repeated backcrossing of an interspecific hybrid with one of its parent species.
Does this mean that the interspecific hybrid is fertile? But is it possible, that an interspecific hybrid is fertile?

Does this mean that the interspecific hybrid is fertile?

Yes

But is it possible, that an interspecific hybrid is fertile?

Yes
You might be confused by the idea that by definition two individuals from different species should not be able to interbreed. If so, then you should have a look at How could humans have interbred with Neanderthals if we're a different species?.


text:
Why does sunburn cause fever?
Today I found out that sunburns can cause fever.
What I don't understand is how/why? In my understanding fever is the side effect of an immune reaction against an intruder, mainly bacteria (though I admit I can be wrong).
Google searches like "can sunburn cause fever" only bring up that it is possible, but not why.

Please don't comment I should see a doctor. I know. Also I had a hard time finding appropriate tags, feel free to edit.

Here is a good article on the topic.
https://www.nlm.nih.gov/medlineplus/ency/article/003227.htm
But it's most likely due to the fact that a sun burn is an actual burn on the skin that can cause inflammation, inflammation can in turn cause fever. Also having a really bad sunburn can open you up more to the possibilities of skin infections. If this happens then once again you might get a fever due to infection. If you really want to find out more on the cause of fever after sunburn you need to examine the pathophysiology of fever and why fever happens. I bet my money on fever due to skin inflammation after a sunburn, I guess the real question would be why does inflammation cause fever since sunburn = skin inflammation
Here is a good article
http://antranik.org/inflammation-and-the-pathophysiology-of-fever/

Mr Hons, you are right on the money; no need to guess. Here's a reference backing up your answer: Ultraviolet Light Induces Increased Circulating Interleukin-6 in Humans.


text:
Why do fishes have both a gustatory and an olfactory system?
I would like to know if there is a reason why fishes (and many aquatic species) have both an olfactory and a gustatory system. As far as I know, in all fish species the chemoreceptors, organs and neuronal pathways are different for taste and olfaction, but why is it an asset to have two distinct sensory systems for chemical compounds in an aqueous medium ?
For terrestrial animals it makes sense to separate information stemming from remote sources mediated by volatile molecules and from the oral cavity, where the molecules are everything one can find in food. But in aqueous medium this distinction is far less obvious, especially when one considers that in some species there are taste receptors located on the body surface (lips, barbels).
I've read a few articles and this thread describing the physiological and neurological aspects of this separation, but it's not answering my question (and it actually aroused my curiosity even more).

In addition to olfactory and gustatory, fishes have two more chemoreceptor systems, solitary chemoreceptor cells and free nerve endings (Finger TE 1997). Asking why do they have all these chemorecepor systems is 'little bit' difficult in the light of evolution. But we can definitely look at this question by using some comparative studies. Hence, this answer will not give you answer to 'why' but will give you enough information to understand roles of these systems.
Reference provided by you explains much of the mechanism of olfactory and gustatory system. I will highlight the important difference between these mechanisms.

In olfactory system, signal is directly detected and transmitted to Central Nervous System (CNS) by neurons of cranial nerve I (Liu and Zhang 2019)
In gustatory system, signal is first detected by specialized gustatory cells and then transmitted to CNS via cranial nerve VII (Purves D et al 2001)

As both of them have similar function, it has been difficult to assign specific function to specific system due to lack of robust behavioral assays (Hara TJ 1994)*
Nonetheless, there are following functions in different kinds of fishes are preferred by one system over another,

Hara TJ 1994 comment that spatial feeding behavior is supported by olfactory system in contrast to gustatory system which helps in consummatory feeding like turning, biting, snapping and mastication**
Morais s 2016 suggests, olfactory system is involved in kin-nonkin recognition, prey–predator interactions, and territory or homing recognition because it is less plastic while gustatory system only plays a role in feeding behavior.
Discrimination of Pheromones is done by olfactory system (Lastein et al 2014)

From reading all these papers, I can 'guess' answer lies in the physiology of these sensory systems. Following conclusion is mine and I am no expert to tell whether this is correct. So just take it with pinch of salt :)
Fish has to survive in the water which is filled with tons of different chemical signals. So it has to distinguish these signals from each other. Many functions might not need very careful separation of signal (e.g. searching for resources) while other might need (e.g. which resources to eat). Some functions might need quick response (e.g. presence of predator) while other can be delayed for short time (e.g. migration). If you give responsibility to one system to perform all these functions simultaneously, it might get confused when multiple important signals arrive. From this I can speculate that this would have put some selection pressure during evolution so that there are multiple chemosensory systems.
From the literature cited above it looks like, Olfactory is less plastic and less sensitive than gustatory and hence involved in functions where you need little sensitivity to distinguish between multiple signal. While gustatory is involved where you need more specific selection of chemical signal.
*I could not get any recent paper directly comparing these two systems in fish. My hope is now we will be in more favorable place to perform some complex behavior experiments. **I did not understand difference between these behaviors conceptually, but you can look it up if you are interested.

Nice, well referenced answer, +1. One comment I have is that I doubt "Olfactory is less plastic and less sensitive" -Though I have little knowledge about fish, there are fairly obvious ecological reasons for olfaction to be very very sensitive. I wonder if you really meant a different word here. Maybe less specific, in that the olfactory system is responding to a broader range of odorants versus just a few in the gustatory sense? Additionally the review you cite does say that about plasticity but also later says "showing low plasticity" about taste; I think the earlier statement is a typo.

@BryanKrause, yes. I also wondered first. But I thought maybe it is like this for aquatic animals. The review I cited did not go into those details.

Imagine what happens inside a fishes mouth after it has eaten an insect or another fish, It's the same if I eat a sardine... the sardine stays stuck in my mouth for a while afterwards. Then if i used my mouth to smell, I would just smell sardines everywhere, literally for an hour.
If the fish only used it's mouth to sense the water, it's sense of smell would be impaired for a while after it has crunched a meal. So it hunts a lot better if it has the ability to check healthy and moldy food through taste, and also sense pristine water for other meals.
The scientific research states that the precise function of the olfactory system is not totally known, it seems to aid behavioral functions not related to eating, for mating and prey detection.
This research is very well written and it's recommended reading.
https://www.tandfonline.com/doi/full/10.1080/23308249.2016.1249279
Ultimately, a different olfactory receptor repertoire confers specialization towards different tasks. Take a shark's ability to detect blood, it makes sense to have a receptors to detect chemicals that are abundant at close range, it's specialized sensing abilities which are geared towards different peak detections and that guide responses in different zones of the brain.
Fish don't have as many receptor genes as mammals, so the evolution pressure is apparently less strong in water, i.e. mice and frogs have 1500 receptor genes versus 50-100 for fish.
catshark: 65 genes
elephant shark: 54 genes
zebra fish: 176
lamprey: 56
frog: 1500
elephant: 1900
stickleback: 159
platy: 98 ( https://academic.oup.com/gbe/article/doi/10.1093/gbe/evp003/597551 )
mammals: 1000 ( https://www.a.u-tokyo.ac.jp/english/topics/2014/20140812-1.jpg )
https://www.google.com/search?ei=Hz89XaK2JuCGjLsP4rGJoAk&q=receptor+repertoire+size+fish+gustatory

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


text:
How do high-throughput/NGS sequencers calculate quality scores?
I am confused as to how quality scores are actually calculated by DNA sequencers like Illumina. For each base call, some quality predictor value is computed, based on various properties of the sequencing machine, like intensity of light during the read.
Do we know exactly how these quality scores are computed? Exactly how many factors go into computing these QUAL values?

only have experience with Illumina platforms here's a link to the basics Illumina quality info More detailed Illumina info Take a look at the refs in that document to go deeper. (Am assuming you don't mean variant call quality scores which, in the pipeline I use, is all handled post sequencing)

@user3234810 Thanks. But I was looking for more information than that. There's some relationship between "signal-to-noise" and quality scores. How exactly Illumina calculates these, I don't know.

The quality score calculations are different for different types of machines. Specifically interested in Illumina?

@WYSIWYG Actually, any sequencer would do. I just mentioned Illumina as a starting point.

@ShanZhengYang I would suggest that you restrict your question to one kind of machine (or kinds of machine with same base calling technique). You can stick to just Illumina. Moreover, even for illumina there are different base calling approaches.

@WYSIWYG That's reasonable. Let's keep the discussion focused on base calling with Illumina.

@ShanZhengYang You can have a look at my answer

I'm restricting this answer to Illumina. Even then, I don't know about the exact details of the raw data analysis (it is a proprietary software).
Basically Illumina records the sequence based on photographic images. Each nucleotide has a distinct fluorescent label. In a cycle, a nucleotide is pumped and unincorporated nucleotides are washed off (this is repeated for all nucleotides). A laser excites the fluorophore and the emitted light is recorded in the form of a photograph. The template DNA is present in the form of clusters of strands (at a given location), which enables easy visual identification of the fluorescence.
Base calling is done using image analysis. Each image is analysed for intensities of different colours and based on this the quality score is calculated. The quality score is basically the log likelihood of a occurrence nucleotide at a given position (based on its colour intensity) compared to other nucleotides.
This is the most simple explanation of how Illumina does base calling. There are different kinds of errors and biases and there are different statistical approaches to correct for them.
Have a look at following references for more details:

Ledergerber, Christian, and Christophe Dessimoz. "Base-calling for next-generation sequencing platforms." Briefings in bioinformatics (2011): bbq077.
Illumina MiSeq Imaging and Base Calling course
Genome Analysis Wiki


text:
How many people in the world have bad eyesight?
I was watching this ted.ed episode and heard it was around 500,000 but that didn't sound right-- does anyone know?

Depends on how you define bad eye sight? Visual function is not either good or bad; it's a range.

I do know that the TED Ed episode linked (at 3:50) actually says that 500 million people have myopia or hyperopia, which is 1000 times what the question says, and which seems more reasonable for a world of 7.4 billion people (skewed towards the young).


text:
How exactly are gaps defined in genomics?
My understanding is that when sequencing a genome, "gaps" refer to fragments which were not sequencing in the sequencer.
Is this correctly? What are there other meanings to the term "gap"?

You're not wrong but gap can mean more than that. A good recent reference is this paper: Genetic variation and the de novo assembly of human genomes.
Essentially, a gap occurs if something happens in our genome that can't be explained by uniformity. Since our genome is highly complicated, you can expect gap is also more than just mis-sequencing. The gap you mention is the sequence-coverage gaps mentioned below.
This paper has a section about the types of gaps.

1. Sequence-coverage gaps
Sequencing gaps occur, under the simplest condition, where no sequence reads have been sampled for a particular portion of the genome.
2. Segmental duplication-associated gaps
Over one-third (206/540) of the euchromatic gaps in the human reference genome (GRCh38) are flanked by large, highly identical segmental duplications.
3. Satellite-associated gaps
These include short and long runs of tandem repeats designated as short tandem repeats (STRs; also known as microsatellites), variable number of tandem repeats (VNTRs; also known as macrosatellites) and Mb-sized centromeric satellite repeats.
4. Muted gaps
Muted gaps are defined as regions that are inadvertently closed in an assembly but that actually show additional or different sequences in the vast majority of individuals
5. Allelic variation gaps
Some regions of a genome also show extraordinary patterns of allelic variation, often reflecting deep evolutionary coalescence.

The word ‘gap’ can be used both loosely and in specific genomic contexts, as listed by @Student T. The usage that seems to relate to your question — Sequence Coverage Gaps — is quite nicely illustrated in the Wikipedia entry on ‘Contig’. I reproduce, below, a modified form of a (public domain) illustration from it.

The sequences of the ‘contigs’ (see legend) are known completely as the ‘reads’ (solid blue arrows in legend) overlap, even though the ‘fragments’ (see legend) contain unsequenced regions. However because the length of the fragments can be determined roughly (e.g. by gel electrophoresis) — here fragment 5 is the key — the two contigs can be assembled into a ‘scaffold’ with a gap of (approx.) known length. I have marked this as ‘Gap’ in green.

Thanks for the explanation. Please also check my answer.

Nice categorization @Student T! I've modified the opening para of my answer to relate it to yours. I think it's worth keeping as it goes into more detail on sequence coverage gaps and introduces some other relevant terms.


text:
Why do viruses last longer on hard surfaces, like glass, than porous ones
All the papers I've read about survival of viruses outside of the host refer to longer survival times on hard surfaces without explaination. As a layman I would have thought that a virus (who's main environmental dangers are things like UV would survive better on rough or porous surfaces, where they are protected and can hide from the light and weather, not the other way round.
For example, one paper I read recently (although it's an old paper) showed Ebola virus surviving for 50 days on glass but not even 2 on rough materials. Can anyone enlighten me as to what it is about glass that makes such an ideal home for viruses to extend its lifespan by over 25 times?
More scientific papers would be helpful, but the medical community does seem to think that hard surfaces in general preserve viruses better than soft ones. The Mayo Clinic and UK NHS web sites both make that claim, without explanation.

Can you link some of the papers? That might be helpful.

Sure - the paper I mention is - Piercy, T.J., Smither, S.J., Steward, J.A., Eastaugh, L. and Lever, M.S. (2010), The survival of filoviruses in liquids, on solid substrates and in a dynamic aerosol. Journal of Applied Microbiology, 109: 1531–1539. at link

Is it about roughness or material? Does it change between a flat glass and a rough glass surface? Because I think that the fact that glass is, in general, much less reactive than metal surfaces, for example, could explain why viruses survive better on it.

My first (purely hypothetical) thought is that porous materials would allow for ionic transmission in any direction, thus if water, ions or other bacteria would come in contact with the virus, it may affect it in a negative way. Glass is fantastically inert and impermeable.

The paper you cited is not about survival on smooth versus rough surfaces; it does, however, mention discrepancies in survival on metallic versus non-metallic surfaces.
From the article you cite (Piercy et al., 2010):

The lack of recovery of virus from metal substrates may be attributed to several factors; previous work (Sommer et al. 1999; Pawar et al. 2005) has shown the binding of micro-organisms to metal surfaces to be poor because of the high surface energy, high electronegative and hydrophilic properties of metal. Other research has also shown that positively charged metallic ions such as copper and silver have a high bactericidal activity (Friedman and Dugan 1968; Bitton and Freihofer 1977; Slawson et al. 1990) and hence by extrapolation may also have a high virucidal activity.

In short, it isn't exactly clear why viruses in particular might have poor survival on metal, but the electrical and chemical properties of metallic surfaces, as well as biological activity of metallic ions that are constantly leached from alloys like steel are all candidates.
The claim may also not apply to all viruses, and the results are not consistent across labs. For example, Sagripanti et al. 2010 find no effect of surface material (aluminum alloy, rubber, or glass) on Ebola, Venezuelan equine encephalitis, Lassa, and Sindbis viruses.
References:
Piercy, T. J., Smither, S. J., Steward, J. A., Eastaugh, L., & Lever, M. S. (2010). The survival of filoviruses in liquids, on solid substrates and in a dynamic aerosol. Journal of applied microbiology, 109(5), 1531-1539.
Sagripanti, J. L., Rom, A. M., & Holland, L. E. (2010). Persistence in darkness of virulent alphaviruses, Ebola virus, and Lassa virus deposited on solid surfaces. Archives of virology, 155(12), 2035-2039.
Bitton, G., & Freihofer, V. (1977). Influence of extracellular polysaccharides on the toxicity of copper and cadmium toward Klebsiella aerogenes. Microbial ecology, 4(2), 119-125.
Friedman, B. A., & Dugan, P. R. (1968). Concentration and accumulation of metallic ions by the bacterium Zoogloea. Dev. Ind. Microbiol, 9, 381-388.
Pawar, D. M., Rossman, M. L., & Chen, J. (2005). Role of curli fimbriae in mediating the cells of enterohaemorrhagic Escherichia coli to attach to abiotic surfaces. Journal of applied microbiology, 99(2), 418-425.
Slawson, R. M., Lee, H., & Trevors, J. T. (1990). Bacterial interactions with silver. BioMetals, 3(3), 151-154.
Sommer, P., Martin-Rouas, C., & Mettler, E. (1999). Influence of the adherent population level on biofilm population, structure and resistance to chlorination. Food microbiology, 16(5), 503-515.

Maybe I should have been clearer in the title question, my mistake. I read and understood the effect of metals, my main question is in the final paragraph, why glass, so much smoother than all the other materials which are rougher.

@Isaacson Do you have a paper that shows that glass specifically is best, or that says it is better because it is smooth? Most likely it is because it is quite inert, unlike metals. If you are comparing glass and metal, though, it doesn't really matter which you focus on. You could say "survival on metal is shorter because it does X, Y, Z" or you could say "survival on glass is longer because it doesn't do X, Y, Z": the answers are the same because it's a matter of comparison. Or am I still misunderstanding your original intent?

(also note the point I made at the end of my answer, which was a reference to a paper that showed for several viruses no difference between glass, rubber, and metal)

Yes,thanks. I don't have the papers to hand at the moment I will have to look them up again (this question is quite old) but it's mainly that all the papers I read on the subject seemed to cite a few days survival and then suddenly there was this one 50 day survival time on glass. I presumed it was the glass because I had read elsewhere that viruses like norovirius survive longer on hard surfaces too, but maybe it was nothing to do with the glass.

Ah okay - I didn't initially notice the age of the question because it just got bumped - I did see April but forgot we are in 2017 (this is really easy to do as an academic in the US, I might add). The paper you linked did show the longest hard-surface survival on glass, but that was just one sample with just one of the viruses, and they didn't try to conclude statistically that it actually survived longer than the plastic, just that it was clear that both those surfaces were much better than metal. If you find something else I'm happy to amend the answer as best I can!

No, that pretty much answers it, if you think it's most likely to be just an odd result and unrelated to the substrate, that's pretty much the answer, unless I can remember what I read that made me think it was more of a general trend.

Just to clarify, I don't think it's unlikely that glass could be a nice place for a virus to rest, I just don't think it is a magical home that provides any sort of order-of-magnitude increase in survivability over other surfaces that are also fairly inert, regardless of their actual microscopic texture.

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


text:
Cell biology books
I'd like to know, what is the best list of books for non-biologist to understand, how signalling between organels is organized inside of eukaryotic cells. I really want to get how cell as separate system works until apoptosis happen.
Of course, any useful online courses (like MIT ocw) are appreciated.

BOOKS

If you want to learn about cells in detail from scratch to advanced level I recommend you two books:

Molecular Biology of the Cell, 6th Edition. 2014. Bruce Alberts, Alexander Johnson, Julian Lewis, David Morgan, Martin Raff, Keith
Roberts, Peter Walter
http://www.garlandscience.com/product/isbn/9780815344322
Essential Cell Biology, 4th Edition. 2013. Bruce Alberts, Dennis Bray, Karen Hopkin, Alexander D Johnson, Julian Lewis, Martin Raff,
Keith Roberts, Peter Walter (This can probably be considered the
"light" version of the first book above)
http://www.garlandscience.com/product/isbn/9780815344544

Then if you really want to put everything you learn into practice and learn them in-depth, you can try the Problems Book of the first book mentioned above:

Molecular Biology of the Cell 6E - The Problems Book. John Wilson, Tim Hunt garlandscience.com/product/isbn/9780815344537

ONLINE COURSES

Crash Course in Biology -- on YouTube
Introduction to Biology - The Secret of Life -- available on exd.org
-- provided by MIT
Simply just search for "Biology" on coursera.org and you will find dozens of good courses

Finally, I highly encourage you to look into the first book I mentioned (Molecular Biology of the Cell, 6th Edition). It's a fantastic book and it will teach you much about biology and cells.


text:
Phototropism or Hydrotropism is a more important factor for trees beside the lakes growing bending to the water?
I see a lot trees beside the lakes are growing bending to the water and I wonder why. After reading this I think it might be a combined effects by:

Phototropism: the lake works as a mirror and sunlight are reflected
Hydrotropism: of course, Hydrotropism...

But which one is a more important factor? Phototropism or Hydrotropism?


text:
Choice of primers for PCR
This exercise was given by my professor but I am struggling to understand the solution.
A PCR is performed on the following sequence (in order to replicate the chain and thus have a greater quantity of DNA so to be able to analyze it):

The main sequence belongs to a horse and differences are indicated below with dna belonging to a cow.
1) Choose appropriate primers in order to analyze some lasagna, which is suspected to contain both horse and beef.
Given Solution:
The primers should be:

I understand how these primers would work in this case, but why not just have the second pair of primers which would make it possible for the whole chain to be analyzed at once?

Welcome to BiologySE - we have some specific home work question policies that you should look at when posting questions. Check this out and edit your question appropriately. http://biology.stackexchange.com/help/homework

You do need two pairs of primers one unique to each species as you need a positive result to be confident that the thing you are looking for (cow or horse) is there.
There is no limitation on them being in the same place (with a different last base).
Usually this would be analyised by gel-electrophoresis and not by sequencing so you don't have to worry about getting the whole thing. This is because you are only looking for the presence or absence of PCR product.
When you do the PCR you will have 4 reactions, one which amplifies horse only, one which amplifies cow only and their negative controls (adding water instead of lasagna DNA extract). After the PCR you take a small amount of your PCR product and run it on a gel (gel-electrophoresis). If you see amplification in the negative controls then you have contamination and can't trust the result. Otherwise if you see amplification by the cow primers then cow is present in the lasagna and if you see amplification by the horse primers then you probably don't want to eat the lasagna. If you used both options for the first forward primer you suggested (blue) then all your bands would be the same size, if you used both the first (blue) and second (yellow) then you would get different band positions on the gel due to the different sized products which makes you feel more sure that you didn't make the mistake of adding the same primer pair to both tubes (it happens).
In the end it's simply a matter of style.

I'm not quite clear what the question is asking, as far as I can see, one pair would be enough..  Since your primers don't include the distinguishing base (and it would be dicey to e expect a PCR reaction to totally fail because of a one base difference) I assume you are going to do sequencing or digest after the PCR to distinguish between the species?


text:
Why is the probability of fixation of an allele equal to its frequency?
Introduction
In a panmictic population, the probability of fixation of an allele at a neutral locus is equal to its frequency at that time. I will refer to this probability of fixation as calculated at time $t$ as $P_{fix,t}$.
If $p_t$ is the frequency of the allele $A_1$ at time $t$, then the probability of the allele $A_1$ to reach fixation (rather than disappearing) is $P_{fix,t}=p_t$. Typically, the generation when the mutation occurred, the probability of the new allele to get fixed is $P_{fix,0}=p_0=\frac{1}{2N}$, where $N$ is the population size.
Question
This simple and classic result makes very good intuitive sense to me. However, I would fail to provide a mathematical proof.
Can you please demonstrate that $P_{fix,t}=p_t$?

Several proofs are given here (p. 9). My favorite comes from the genealogical argument:
Consider the situation where there are $2N$ alleles: $A_1$, $A_2$, $A_3$ ... $A_{2N}$.
By the genealogical argument, we may state that at $t = \infty$, all alleles at this locus will be direct descendants of one particular allele present at $t = 0$.
Allelic variants at this locus are selectively neutral, so $Pr(A_{1fix})$ $=$ $Pr(A_{2fix})$ $=$ $Pr(A_{3fix})$ $= ... =$ $Pr(A_{2Nfix})$. For any given allele present at $t = 0$, the probability of fixation is therefore $\frac{1}{2N}$.
Now define allelic variants $A$ and a as complementary, non-overlapping groups of the initial alleles, such that $n_A$ + $n_a$ $=$ $2N$. From the above, the probability of fixation of an allele within group $A$ is $n_A * \frac{1}{2N} = \frac{n_A}{2N} = p_0$.

Sorry for digging this topic after 2 years. I am studying evolution these days and was reading basics from the book by Hartl and Clarke. There, this proof is given using the Markov chain approach. However, the way it is proved doesn't make sense to me (also shown in the slides that you have linked). In the Markov chain approach the probability is a vector with each element denoting the probability of having i number of alleles in the population. Can you, if possible, please show how to prove this result using the Markov chain approach?


text:
Is the birds' decision to fly away congenital or learned behaviour?
I see two possibilities how could the birds know what to do every fall:

The birds' migrations are driven entirely by the vertical memetics and today it is just a custom transferred from parents to offsprings.
There is a gene that causes birds to decide to fly to the warmer areas every fall, activated when it is appropriate time

Which of these hypothesis is closer to the truth?

The first hypothesis seems very unclear. I think you just mean that migration direction/distance/timing/etc.. could be a learned behaviour. However, you phrased it weirdly. You seem to poorly use the term macroevolution as well.

@Remi.b That's the original meaning of "macroevolution", isn't it? The process of preserving of successful families, packs and species. So this is exactly what should be responsible for the spread of this custom. But it is'nt entirely needed for the question.

@Probably I'm not the only one that finds discussing memes in this sense a pseudoscientific endeavour (Wiki of the criticisms). I think "learned behaviour" is a better term.

I think the question is clear now (+1). You might want to clarify that this is a nature vs nurture (or learned vs innate) question. The answer will likely depends on the species though.

This example proves IMHO that migration is largely nature and not nurture:
In the Netherlands, white storks were bred / reintroduced. A large part (about one third?) of the reintroduced birds do not migrate, but their offspring usually does migrate see. They couldn't have learned it from their parents, that's for sure.

Does it mean, that they have a circaannual biorhytms or do they detect the factors of changing weather such like temperature (if so, we could try to put them into a cold environment and see wheter they would fly south (or north in case of the southern-hemisphere birds)?

@Probably I thought your  question is if the behaviour is learned or genetic. What triggers migration is a totally different question.

I'm just interested how does it work. The mechanism is a direct consequence of the genetic code. But I agree I could find it in the quoted article.


text:
Is diarrhoea advantageous to the microbe?
Diarrhoea is a common side effect of many feco-orally transmitted bacterial infections. How does diarrhoea help the pathogen? Should it not have a selective evolutionary advantage? Do all symptoms of the disease need to have a selective advantage for the pathogen? All I can think of is that a more liquidy stool would lead to further ease in feco-oral transmission. Is this true?

It would increase the overall transmission rate, I guess. Diarrhoea is not just liquidy stools (which may be better for dissemination of the bacteria) but also frequent stools (high transmission) + low digestive potential of the gut (which also protects the bacteria). You can have a look at some of the epidemiological models for cholera.

@WYSIWYG "low digestive potential " Not sure that changes anything for the bacteria since gut pathogens are adapted to live in that environnement. Unless I misinterpreted the way it could help them.

Other than that you are totally correct and it is the actual answer to the question

Vibrio cholera for example is actively causing diarrhoea, by stimulating the CFTR channel to excrete chlorine ions, which will attract water from the gut tissue.
The answer of the function seems obvious: to promote dispersal in the environment and as such infect/find new hosts.
See also: extended phenotype (Richard Dawkins): how genes in one organism (mostly a parasite) influence the behaviour of another organism (mostly the host of the parasite) to increase the (reproductive) success of the gene/parasite.
Also: numerous (some horrifying) examples in Parasite Rex (by Carl Zimmer)

Welcome to Biology.SE! Please provide references to your claims (best would be peer-reviewed articles or, for well-known concepts, something like Wikipedia) so that others can check your answer and also for further reading. Additionally, please write comprehensive and explanatory answers and do not just throw hints for what to look for (take a look at guidelines here). Your answer as is might be down-voted. Thanks!


text:
Do only large birds float?
So, I've noticed a pattern in water fowl (here meaning birds who can take off and land on water, who float in the intervening time) tend to be larger birds.
The smallest I know of are gulls.
Are there any smaller water fowl? Anything the size of a partridge? Or a wren?
If it is only large birds, why is this?

baby swans/ducks/geese?

Many ducks are about the size of a partridge.  And indeed, about the (body) size of gulls, though gulls seem to have a longer wingspan.

There are many seabirds smaller than partridges. The smallest seabird (according to the National Trust of Scotland) is the European Storm Petrel, which weighs in at an average of 28g. That's not quite as small as the European Wren (6 - 10 g), but it definitely counts as 'small', nonetheless.
Being seabirds which spend their life at sea except during breeding, storm petrels float well.
Below is a European Storm Petrel weighing in at less than 35 grams in Fig. 1.

Great answer and hope you appreciate the edit. Feel free to remove as it clashes somewhat with your average weight of the bird.

I'm OK with the picture staying in, but I would make a couple of clarifications. Judging from the fluffy down on the underside, that's an unfledged young bird taken from the burrow. As such, that particular individual may not yet be waterproof. Also, it is common for tube-nosed seabird parents to feed their young until they weigh more than the adults just before fledging (Miskelly et al (2009) Biological Conservation 142(10):1965-1980). This way, they have some fat reserves while they learn to forage.

The Cotton Pigmy Goose for example is about 26 cm long and weight about 160grams (smaller than a grey partridge) can take off and land on water. Have a look at this video for example.
As @WYSIWYG said, any young of "water fowl" species are small and are still "water fowls".
I would also bet that if you put a dead hummingbird on standing water, it would float! It obviously wouldn't be able to take off though.

Perhaps the hummingbird would float, but could it then take flight? ;)


text:
Could there be some safe, hypothetical way of turning on and of thermoregulation?
This is something I thought of with the whole artificial gill concept.  Could a modification to the brain/nervous system allow a human to turn off their thermoregulation in air/water of the right temperature range, so they wouldn't have to expend as much oxygen?


text:
Flower identification (Singapore, April)
I saw some flowers growing by the roadside today, and was wondering about the species of this plant.

The plant also appeared to be fruiting, and it produced small fruits that formed small clusters.

Looks it belong to subfamily Mimosoideae under family Fabaceae

the long red rays seems their stamen

This is called "Red Powder Puff" or botanically Calliandra haematocephala. See the images (from the Wikipedia article):

What you identified as the fruit appears to be the buds:

Some more information can be found here.


text:
How do I "reinoculate" a petri dish with new bacteria?
Hypothetical question, intended to find a general procedure rather than case-specific recommendations:
I have a petri dish full of growth medium with a large population of gram-negative, anaerobic bacteria of numerous types growing in it. How would I go about replacing the existing population with lactobacillus and streptococcus strains?
Rules:

The growth medium cannot be washed out of the petri dish
The petri dish cannot be treated with anything a human body can't handle, i.e. no blasting with bleach
After the procedure is complete, the original bacteria should have little to no chance of returning, even given months or years in the petri dish

Why would you want to do this? In the lab, you would simply throw the plate away and make sure it is autoclaved and you set up a new plate with the bacteria of interest.

Don't worry @Chris, I'm not running low on plates. The lab exists for the very purpose of modeling the real world, and yet in the real world you can't autoclave the environment. I can't for the life of me figure out a good way of replacing the bacteria in a real-world environment, so the purpose of this question is to discover how a trained biologist with years of experience and a touch of creativity would go about this. Think of it as a thought experiment

Ah, ok, I wasn't sure of the purpose, thats why I asked.

Nobody has tried a procedure like this. Perhaps you can wipe the surface clean and wash it repeatedly with an antibiotic solution (a bactericidal one like streptomycin) + hydrogen peroxide (since the bacteria are anaerobic). I think all answers will be based on guess.

@WYSIWYG wiping the surface isn't allowed, as that wouldn't be possible in the equivalent real-world environment

@TheEnvironmentalist then washing would be allowed right? Depending on what the tissue is wiping might be feasible.

@WYSIWYG imagine the surface as something between a sponge and a rubber pad. Not very wipeable, unless you're being particularly creative


text:
Thickness / size / volume of a macrophage
What is the thickness of a macrophage? From some available literature it looks like a macrophage has a 'circular' shape of radius ~10 microns. But I need the thickness to calculate its volume.

volume is a function of r?

BioNumbers is a good database for different values (numbers) in biological systems. From BioNumbers*:
Volume of an alveolar macrophage ( Homo sapiens ) = 4990 (±174) µm3
Diameter of an alveolar macrophage ( Homo sapiens ) = 21.2 (±0.3)  µm
So, your thickness should be (assuming a circular shape of the cell):
Volume/(pi×(0.5×diameter)2) = 14.15 (±1.52) µm
Apparently, the size of the alveolar macrophages varies a lot between different species.

The AM from humans were significantly larger (p < 0.05) than those
  from all other species studied, corresponding to a 4-fold larger cell
  volume of human AM (4990 +/- 174 microns 3) compared to hamster (1328
  +/- 123 microns 3) and rat (1166 +/- 42 microns 3) AM

*
The paper that BioNumber refers to is this:
Krombach, Fritz, et al. "Cell size of alveolar macrophages: an interspecies comparison." Environmental health perspectives 105.Suppl 5 (1997): 1261.


text:
Can both the overlapping genes (in opposite strands) produce proteins?
I have recognized that both the forward and reverse transcripts from a genomic location code for protein products. Both do occur/express in the tissue of interest. In order to eliminate by chance probability, I have screened my entire list of genes and there are 6 different examples. I would appreciate if anyone having the knowledge about such exceptions could guide me further.
Is this phenomena of protein being coded from both directions (of a given genomic location) possible? Are there any known examples?

Maybe this can help you? It is about what regulates the directionality of a gene and they seem to include 9% of the genes are translated in both directions. Although it is hard to say without knowing about the organism you are talking about (seems to be eukaryotic, since you mentioned splicing).  http://www.sciencedirect.com/science/article/pii/S1097276514010077

Many thanks, I have read this paper and its really helpful

While overlapping antisense RNAs are quite well known, there are very few examples in which both the RNAs from the pair can code for proteins. However, it is not impossible. I can cite one validated example: RU2S (DCDC2) and RU2AS (KAAG1) pair.
While RU2S is constitutively and ubiquitously expressed, RU2AS is specifically expressed in kidney, bladder, liver, and testis. It is also expressed in certain tumours (Peltz and Dougherty, 1999).

 Peltz SW, Dougherty JP. Antisense Translates into Sense. The Journal of Experimental Medicine. 1999;190(12):1729-1732.