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What do blue cone cells add to visual function?
First of all, I saw this other question in the SE sites with a good answer, but I didn't find an explanation about the blue cones specifically.
So most human beings have 3 types of cones (cells specialized in color sensing : blue, green and red).
While it may seem obvious that the red and green-sensing cones are an evolutionary advantage (given our natural environment and how we ate for millenia), for instance to locate fruits and differentiate ripeness, I can't find a clear advantage in having the blue cones. Blue doesn't seem to relate to anything like food, predators, sexuality. Am I missing an obvious utility ?
Let's try to imagine what happens if we remove blue cones :

The sky would look gray. I don't see a survival issue there.
We wouldn't be able to make a difference between yellow and white (white = green + red in this case). Is it a big deal ?

I have the reflex to think "if a character is widespread, there must be a good reason". It seems I should rather say "there must be an explanation".
So I'm trying to think differently, and here are other possible approaches to address this question :

I read that dogs have only blue & yellow cones. Maybe our ancestors had only two cone types, including blue, then a third type appeared and blue stayed just because it wasn't a problem to keep it ?
What we call visible spectrum is in fact the only part of the spectrum that can go through air and water (in the eye) without being absorbed (link). Blue cones would be there just because "hey there's something to see" ?
For a long time we had only fires to look at, at night. No TV or screen with Q&A sites to consult. Is it possible that some of our ancestors stared for too long a hot fire, losing green and red cones ? Those with blue cones were not totally blind and managed to reproduce ! (this one is... almost a joke)

Sadly these approaches don't really convince me.
ADDITION : here is a visual example to see what happens if we remove blue information from an image (original image taken here). The image without any blue (middle) is confusing because it makes you think we could see yellow (while yellow wouldn't be different from white). That's why I added the image on the right, containing only information from red and green channels (the blue channel is replaced by min(Red,Green)). I think it illustrates well that blue isn't important, at least for vegetables and fruits !

Just a quick correction: this and other Stack Exchange sites are not "forums". Instead, they are question and answer sites. Please take the [tour] to learn more. There is actually quite a significant difference.

I used "forums" as a generic word, I'm not confusing the two systems. I didn't know it was better to avoid this word here, thanks. Or... are you talking about how I wrote my question, too "forum-way" ?

Water is blue (though only in some cases). I would love to find blue water from a distance.

@AnubhavGoel That's an interesting idea ! As you say, water only appears blue in some cases but that may be enough to be a convincing explanation. This image illustrates a case where it's easier to see a lake if we see the blue tint in the middle of green trees.

So you solved your own question!!! Just change it into a nice answer☺

The sky is also blue. I could imagine (but this is pure speculation) that, for tree-living species, blue can help to distinguish the background sky from foliage and branches etc., which would be useful for climbing and jumping. Ground-dwelling animals, on the other hand, don't need to distinguish the sky from other objects.

@StephanMatthiesen I don't find any clear advantage in seeing the sky as blue instead of grey in a green environment : it seems we can distinguish it anyway. That's what lead to my question in the first place. So far the only circumstances I can think of that require distinguishing blue specifically are seeing a river in a grey environment or seeing blue veins (note that veins appear blue only due to the absorption characteristics and depth of skin).

@GhislainBugnicourt Not sure I understand that. What is "grey" with two colours? Wouldn't the blue sky stimulate the green cones more than the red, so it would appear greenish rather than "grey"? The blueberries in your transformed images are much closer to the green vegetables.

Short answer
Primate color vision started off with photosensitive cells detecting medium to long wavelengths (M/L cones detecting greens and reds) and short wavelengths (S cones most sensitive to blue). By neurophysiologically weighing their relative contributions the full spectrum (red, orange, yellow, green, blue and indigo) can be detected by dichromats. Addition of a slightly different M/L cone and generating separate M and L cones increases the resolution of color vision in the medium and long wavelengths, which is thought to enhance color discrimination useful for foraging fruits. Indeed, blue in itself is not needed for this task. However, missing the blue cones would eliminate a large proportion of the visual spectrum.
Background
Evolutionary spoken, primate vision started off with dichromatic vision. These early dichromats had retinas with one type of cone sensitive to medium-to-long wavelengths (M/L cones) and one type sensitive to short wavelengths (S cones) (Jacobs, 1996). This organization determines the dynamic range of color vision, i.e., to see colors from short wavelengths (greens and blues) to long wavelengths (red and yellows). Weighing their relative contributions by neural networks in the retina allows the intermediate wavelengths to be resolved.
Later in evolution, some diurnal species had a gene duplication on their X chromosome, generating a M/L duplicate gene (Jacobs, 2009). Small mutations in these genes eventually paved the way for two closely related M/L opsins, namely one a little more sensitive to longer wavelengths (L opsin) and one to slightly shorter wavelengths (M opsin). The dynamic range of color vision still depends heavily on the S opsin in the blue cones, as the M and L opsins have absorbance spectra much closer to each other (Fig. 1). The benefit of two opsins with nearly identical absorbance spectra is a higher color discrimination ability (higher color resolution) in the medium to long wavelengths. High discriminating power in the red-yellow-green part of the spectrum is thought to be beneficial for diurnal fruit foraging primate species (Jacobs, 1996). Note that cones need a lot of photons to operate; nocturnal primates are typically dichromats and they will not benefit anyway from another M/L cone.
For fruit foraging alone, the L and M cones do a pretty good job, as your example shows. However, there is more to the eye than food alone. Eliminating the blue cones would substantially narrow down the dynamic range of color vision. Further, evolution started off with S and L/M cones and added another M/L cone to that existing system. Evolution didn't start off with a blind ape and the goal to generate the perfect fruit forager; no it started off with a dichromat and over time improved its ability to seek food during daylight.

Fig. 1. Absorbance spectra of the different opsins. source: Kevin MD
References
- Jacobs, PNAS (1996); 93: 577-81
- Jacobs, Philos Trans R Soc Lond B Biol Sci (2009); 364(1531): 2957–67

Very informative, thanks ! I'm still intrigued about the fact that dichromatic primates had blue S cones and not something around cyan-green : what objects of the environment did they need to distinguish at such low wavelengths ? So far the only lead I have is water as proposed by Anubhav Goel in comments above.

Very interesting. I've been wondering/speculating if blue helps tree-living species to distinguish the background sky from branches and foliage, which would make climbing and jumping easier and safer. The Jacobs papers are a bit vague on possible adaptive value, mostly discuss fruit although they mention other uses (like distinguishing skin colouration), and so far I haven't seen the sky mentioned. Do you know or have an opinion about that?


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Animals walking backward?
Have you ever noticed that we humans can walk forward and backward but animals don't walk backwards?I guess this is true with most of the animals.What is the reason behind this?

Most animals can walk backwards if they really want to, or if you make them. The reason they, and we, tend not to walk backwards most of the time is that most animals and people don't have eyes in the back of their heads, and would risk running into things or falling off cliffs. You might try walking backwards all day and see what is the result, but please do not hold me liable if you end up in hospital.

I'm voting to close this question as off-topic because it's based on a false premise.

Sorry but I never noticed them do so.Anyways thank you

Your premise is incorrect other animals can and do walk backwards. Like humans, other animals do most of their walking forward both for biomechanical reasons and for the obvious reason that it is easier to see where you are going when walking forward.

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What are hiccups?
What are hiccups?How are they generated and are they involuntary?Does it happen when we eat something tart?Or is there any other cause?I tried to find the solution but I always got different answers

This can be answered by a simple Google search. https://en.wikipedia.org/wiki/Hiccup

It is essentially the phrenic nerve being irritated and as such the diaphragm (innervated by the phrenic nerve) contracts when involuntary signals are generated as a result of the irritation.
This irritation can occur for a variety of reasons.

Overall great answer; however, it is highly recommended that you add some references, otherwise the answer may be downvoted and/or removed.

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How to determine continental ancestry group (race) with transcriptome data obtained with RNA microarray?
Say I have a whole genome expression data (transcriptome) for some sampled human tissue. Is this data sufficient to find out the continental ancestry group of a donor?

If you can call genomic variants from your data, depending on your coverage of the genome, you should be able to map ancestry. For example, if you have sequencing reads, you can align your reads to a reference genome and then call variants using existing pipelines.
Once you have variant calls, you could use ancestry-informative markers to infer the ancestry of your sample directly.
Or you could use existing software to map the ancestry of your sample in relation to other samples of known ancestry, using a program like ADMIXTURE, STRUCTURE, EIGENSOFT, or just principal components analysis. For reference samples, you could use a publicly available data set like HapMap 3 or the Human Genome Diversity Project.

Thank you @leekaiinthesky for answering. Do you mean whole genome sequencing reads or just short reads of protein-coding sequences by "sequencing reads"?

I meant RNA-seq reads. But it was just an example. It depends on what kind of data you're starting with.


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Where do I find standard tissue and cell names?
I am developing specialized database on some desease microarray experiments. The initial data is retreived from NCBI and ArrayExpress databases. The problem is that sample attributes sometimes specify similar or same things but in different manners: as cell and tissue names, desease names, age, ethnicity of donor, ect. Where do I find conventions for naming experiment sample attributes?

I doubt there are many. There are some conventions regarding naming cell types corresponding to what surface and internal markers are expressed (or not), but to my knowledge those are in early stages. In papers, authors generally define their own naming conventions, which may or may not match up to others. The problem is there's a lot of argument about how to name things, with each lab or institution having their own preferences. As a simple example, tuberculosis is also known as Koch or Koch's Disease. You'll probably need to pull from a lot of individual databases, and just use synonyms.

Also there can be conventions without controlled vocabulary ( http://www.ncbi.nlm.nih.gov/geo/info/MIAME.html )

It turns out that ArrayExpress itself uses various ontologies (dictionaries structured as trees) available at Ontology Lookup Service when it processes users' search queries. Experimental Factor Ontology is the precisely one I was searching for.
Medical Subject Headings (MeSH) dictionary turned out to be handy as well.


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Biomedical consensus on human aging and lifespan
Medical technology is improving quickly. Unless there is a global disaster and human progress is set back significantly, e.g. by an asteroid or a global nuclear war, there will come a day when humans can live indefinitely. This does not mean infinitely- people will still die in vehicle accidents, get murdered, etc. Also, at least at first, access will be prohibitive due to costs and possibly outright selection/rejection of patients.
Based on trends in the progress of biomedical research, what is the consensus in the biomedical research community for approximately what year will the average person vs. a very elite person be able to get treatment to live indefinitely?

This question is being voted to be closed as "primarily opinion based" because 1. your premise "...there will come a day when humans can live indefinitely" is strictly opinion and not currently substantiated by any major research that I know about, and 2. your question about the consensus of the biomedical community (which there likely isn't one due to there being no way for us to know) will likely only lead to answers "almost entirely based on opinions, rather than facts, references, or specific expertise".


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Does capillary blood pressure have any effect on how much oxygen or nutrient gets distributed to tissues?
From what I have read regarding blood pressure and blood flow, I've come to the conclusion that, apart from the osmolarity of blood, the only determinant of how much oxygen/nutrients the tissues get per unit time, is blood flow.
Does blood pressure (not systemic, but within a theoretical capillary) have absolutely no effect on this, and if so, why? Intuitively, it seems to me that if the force by blood on the walls of a capillary increases, that would imply a higher number of molecules touching endothelial cells, and thus a higher likelihood of molecule transport per unit time.
Or is it perhaps that they both have positive effects on oxygenation/nutrient transport; but blood flow's effect greatly excels that of blood pressure?


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How are antibodies specific for a disease detected in the blood if everybody produces a different antibody for the same antigen?
To break the title down into parts:

There exist serology tests that detect the amount of an antibody (Ab)
against a specific pathogen/antigen.
Every human produces their own Ab for a specific antigen by
(relatively) random combination of different gene segments in their B
cells, until one that recognizes the pathogen is found and produced
in massive amounts.
One portion of every Ab is constant, whereas the portion that
recognizes the antigen is variable. Even for antibodies (in different
humans) that recognize the same antigen, albeit to a lesser degree.

What exactly does an antibody titer/serology test detect in the blood so that it can accurately measure the amount of antibodies against a specific antigen? I am assuming they use antibodies against the antigen-binding/variable portion of an antibody. But if the variable region differs from person to person, how can a universal antibody (to be used in serology tests) against it be generated?
Is the variable region not that variable, so that any lab-generated antibody against any functional antibody against a virus works well enough for an accurate measurement of antibodies against that virus? But even so the concept sounds hard to believe since even a single antigen can have multiple epitopes, and one person might have an Ab for epitope 1 of antigen X, while the other would have an Ab for epitope 2 of antigen X. And they would still be immune to the same virus, while a universal Ab titer test for the virus would be unable to detect antibodies from one of them.
Do they perhaps employ multiple lab-generated antibodies against most of the possible variations of human-generated antibodies in the tests?

Specific antibodies are typically detected using ELISA.
The way you make a test for an antibody to a particular pathogen is not by using secondary antibodies to the specific part of the target antibody, but by using the antigen.
Different kits work differently, but the general idea is that you have antigen stuck to a surface, you put the sample on that surface. If there are antibodies to the antigen, they stick to it. Then you wash everything away and add a tagged antibody that binds to generic human antibodies.
See also https://www.sciencemag.org/news/2020/03/new-blood-tests-antibodies-could-show-true-scale-coronavirus-pandemic

ohh, using an antigen-coated surface makes a whole lot more sense. I don't know why I had such an extreme roundabout way of thinking.

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Personal Genomic Data Samples
a quick question. I am looking for complete personal genomic data of human individuals. The only requirement for the genomic data is that it contains the complete set of SNPs of a human individual. So far I found only one, a hispanic female.
Are there any similar personal genomic data available on the web?
Any database I can access with a collection of SNPs per individual?

Here is the link to the 1000 Genomes project, all the data is available for download. They already have a comprehensive list of SNPs as well.
It is not the only project around but it is definitely the one with more accurate data on so many genomes right now.

Another source would be the Simons Genome Diversity Project published by Mallick et al. in 2016. This set covers way more populations than the 1000 Genomes, and therefore includes more overall human genetic diversity, but also has only few individuals per populations (and populations do not overlap with 1000 Genomes as far as I know).
Which database is better for you depends on the actual question.


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Is there variability in genetic combination from the same sperm and egg combination
Given a single sperm and a single egg, is there more than one resulting DNA combination they can form given the same human process of combining that genetic material. That is if I have the  DNA off an egg sequenced and the DNA off a sperm sequenced, can I programmatically determine the DNA of the child formed by that egg and sperm?

@AlwaysConfused, I'm approaching this from the point of view of calculating a genome from the supplied materials. I listened to a ted talk where a process could - accurately - predict a persons face from only their DNA and my immediate thought was "Could you do the same thing prior to conception".

Assuming we know the haplotype of the ovule and the haplotype of the spermatozoid, then the genotype of the future egg is perfectly deterministic. This is true to the extend that none of the following rare events occur:

mitochondria could be inherited from the father as well
mutations in the broad sense (see here for definitions) may occur outside an event of mitosis or meiosis
The egg might pick up random sequence floating in the environment

Of course epigenetics elements might vary but this is another discussion.

There will be any number of combinations that can result during recombination and chromosome separation no?

Recombination and segregation occurs during meiosis, that is before the formation of the gametes (spermatozoid and ovule). Once we take we consider the haplotype of a specific spermatozoid and the haplotype of a specific ovule, the genotype of the egg is deterministic (except above listed rare events).


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How to convert between Kunitz units and Enzymatic units?
I've googled around and there has been the common answer of 1.5 U = 1 Kunitz Unit, but none of those answers have come from a reputable source, so I am really doubtful. :(
The enzyme I use comes in 723 Kunitz units per mg protein, but I need 600 U per mg of DNA being used in my procedure. I do not know how to properly determine how many Kunitz units equivocate to Enzymatic Units, and vice versa.

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What is meant by "a codon codes for an amino acid"?
What is meant by "a codon codes for an amino acid"? Does it mean in order to build that amino acid you must combine those three nucleotides?
Does it mean anything more than provides the instructions for manufacturing that amino acid.

It does not means "provides instructions for manufacturing an amino acid".  How could three little letters encode so much?
A codon is a three nucleotide sequence that matches the anti-codon of a t-RNA molecule capable of carrying one kind of amino acid.  The GGG codon, for instance, binds the t-RNA that binds to glyceine.  So the codon GGG in an mRNA ends up amounting to "put a glyceine here in the amino acid chain"

I'm not sure this kind of question should be answered. I know it's easy to toss off a quick answer to help the OP, but should this not be closed instead of posting an answer? Maybe a comment if you want to help? I would liken it to asking for a dictionary definition on EL&U... OT due to lack of research.


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Recovering DNA from an RNA-extraction/purification kit
We are extracting RNA from single insects with the later purpose of performing RNA-seq. We are using the RNeasy Plus Miniki from Qiagen, which involves the use of eliminator columns as you can see here page 7.
However, we would love to be able to recover some DNA to perform a PCR which would help us confirm the insect species we are dealing with. Ideally, we would like to do this without losing any RNA-containing material. We were therefore wondering whether it was possible to retrieve some DNA from a column, which would otherwise be discarded ? Does anyone have experience with this ?

Have you looked to see if there is DNA in your RNA extraction?

We have run it on a gel yes, there was none after the DNA removal step.

Test it with a PCR; gels are about the least sensitive method of looking for DNA. almost every RNA extraction contains some DNA. So long as you didn't add DNase that is.

The idea however is that we would use material which would be otherwise discarded, we are reluctant to take away some of our pool of RNA.

The procedures for DNA and RNA extraction are almost identical; the difference is a small change in pH. You could try collecting flow through from the sample binding step and then put it through a DNA column or DNA extraction procedure (precipitation). Surely the cDNA generated in the RNAseq will result in something you can use for ID of the species; even the RNAseq results should tell you that.

We would rather not use the cDNA generated in the RNAseq process because we are extracting from single small insects, and we might have just enough for RNAseq.
The DNA/RNA separation step happens on a column : the DNA will bind to the eliminator column while the RNA will flow through. Then the RNA is placed on an other column to be further purified and eluted. Which is why w would like to recover the DNA from the previous column.

Simple - don't use the eliminator columns... Note that most RNAseq preps use in the fmol range of sample loaded and have a PCR amplification step to help you get there.


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How does transcription end?
In rho-dependent termination in prokaryotes, how does RNA polymerase “know” that it has reached the end of a gene and that it has to stop so that the rho-factor can bind mRNA’s rut site? Is there a termination sequence on the template DNA that “signals” the end of a gene?
And consequently, how does the rho-factor “know” when to bind to mRNA?... how does rho-factor recognize that the RNA polymerase has stopped so it can start its ATPase activity to dissociate the transcription complex from DNA and release the mRNA?

You ask about stop codon?

The stop codon ends translation of mRNA to polypeptide, not transcription of DNA to mRNA (which is what I’m asking about).

There's a corresponding stop codon on the DNA

Doesn’t the stop codon end amino acid elongation during translation? So... is the stop codon also the terminator sequence during transcription?

https://en.m.wikipedia.org/wiki/Rho_factor

This question is very similar and has a pretty good answer.

Termination  of  the synthesis of  the RNA molecule in bacteria is also signaled by  a sequence in the template  strand of the DNA molecule.
This sequence of nucleotide in the template strand is the RNA polymerase pause site. When the RNAP continues its transcription it reaches this site and pauses it's transcription activity over here. The longevity of this pause can also be affected by various factors like high $Mg^{2+}$ ions in some cases.
Meanwhile, rho factor which after binding to rut-site, continues it's translocation along the mRNA (supposing mRNA is synthesized here) in 5'-3' direction using its ATPase activity. The rho factor utilises this opportunity when RNAP has paused it's transcription activity at the RNAP pause site to reach this ternary transcription elongation complex. When it had reached this complex it starts it's ATP dependent helicase activity which separates the RNA-DNA hybrid helix, causing the release of the mRNA.

In prokaryotes you have transcription and translation happen almost simultaneously. Downstream of the translational stop codon, there exists a C rich site on the mRNA called the rho-utilisation-site (rut) and another site called transcription-stop-point (tsp).
Rho-dependent Termination of Transcription Is Governed Primarily by the Upstream Rho Utilization (rut) Sequences of a Terminator
How does RNA polymerase know it has reached the end?
RNA polymerase pauses at the tsp site during transcription. The rut site functions as an mRNA loading site and it also works to activate the rho-factor. The activated rho-factor travels down the mRNA while still attached to the rut site and catches up with the paused RNA polymerase. Contact with  the RNA polymerase leads to RNA polymerase to dissociate from the transcriptional complex You can read about the dissociation here, the article is behind a paywall though.
I think I answered the "when does rho know?" too. Read the wikipedia article on this as well


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How do PrP mutations lead to prion disease?
My understanding is:
The PrP gene in human cells is expressed as both PrP-c (normal protein) and  PrP-sc (prion disease protein). This happens post transcriptionally, that is, the normal and the diseased protein are not distinguished based on genetic mutations, rather they are synthesized based on the same gene, but differ in their tertiary structures, which makes their functions also different.
If the amino acid sequence of both proteins is the same (same gene), then what determines whether the synthesized protein will take the disease-causing tertiary structure or the normal one? Is it due to post-translational modifications?
And finally (I apologize for advance for multiple questions): how do prions, which are void of nucleic acids (being proteins), integrate into the genome of a newly infected host by reverse translation, and become a familial disease?

If the amino acid sequence of both proteins is the same,
  what determines whether the synthesized protein will take the
  disease-causing tertiary structure or the normal one?

PrP-C and PrP-Sc do indeed have the same primary structure. However, they differ in secondary and tertiary structure. The protein can take more than one shape (conformation), where the likely conformation spaces taken by the protein are due to chemical and physical interactions. Many proteins can change their shape, often this is not well understood in detail. However, we know that the conformational space of some proteins allows for several, stable conformations of a single protein; the factors which stabilize it in a conformation or cause it to switch are difficult to understand in vivo.
PrP-Sc tends to accumulate in compact, protease-resistant aggregates. Circular dichroism shows that normal PrPC had 43% alpha helical and 3% beta sheet content, whereas PrPSc was only 30% alpha helix and 43% beta sheet. Although the exact 3D structure of PrPSc is not known, it has a higher proportion of β-sheet structure in place of the normal α-helix structure. The end of each fiber acts as a template onto which free protein molecules may attach, allowing the fiber to grow.
Prion proteins therefore propagate accumulation of more and more prion proteins.

Is it due to post-translational modifications?

No.

How do prions, which are void of nucleic acids,
  integrate into the genome of a newly infected host by reverse
  translation, and become a familial disease?

They do not enter the genome through reverse translation. The DNA sequence itself is mutated and the mutation drifts across generations for as long as it is being passed on through the germline.

In the first paragraph of your response, you said that “PrP-C and PrP-Sc do indeed have the same primary structure”, so how is it that you later say “the DNA sequence itself is mutated”? If they both result from the same gene, then shouldn’t something other than the “DNA sequence itself” be causing infection persistence through the gene line?

This paper here suggests that PrP-sc is physically passed on through cytoplasmic division of cells into daughter cells, so that the phenotype rather than the genotype is passed on, and if the phenotype is advantageous for survival, a mutation might incorporate it into the genome. https://www.omicsonline.org/open-access/revisiting-cricks-dogma-and-the-impossibility-of-reverse-translation-jtco.1000110.pdf

The protein is the infectious agent. The protein spreads through to new cells, causing the refolding of PrP-C. This does not occur in a DNA-dependent fashion. You are misusing the words phenotype and genotype, they do not refer to a protein/DNA dichotomy. Different protein isoforms can be made with a single gene. Mutations are not incorporated into genomes, they occur WITHIN genomes. Genomes are, colloquially speaking, records of mutations. Prion disease is a protein environment disease, it is not innately that prion proteins cause the disease (hence PrP-C, the healthy variant).


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Can experiments in ELISA kits be monitored via both fluorometry and photometry?
In my bioanalytics course slides, the professor has written at one point that in a heterogenous immunoassay such as ELISA, we use fluorimetry to measure concentration of an analyte. In another slide it is mentioned that we use photometry to measure UV-vis absorption. I am confused... is it one or the other, or can we use both methods depending on whether the marker enzyme on the antibody is given a fluorescent or chromogenic substrate?

can we use both methods depending on whether the marker enzyme on the antibody is given a fluorescent or chromogenic substrate?

This is essentially correct.
You can have the same ELISA work on different methods of detection. The most common ELISA is colorimetric, and works by binding a secondary antibody conjugated to some enzyme to your primary antibody. Fluorescent ELISA platforms are less-widespread but only because the colorimetric ELISA is reputed and "gold standard."
Horseradish peroxidase (hrp) is a common conjugate system utilized in sandwich ELISAs, and by adding TMB solution to the reaction wells, the resulting reaction produces a diimine that turns the liquid in the well blue, and does so in proportion to the amount of analyte captured. You stop the reaction by adding an acid, which turns the well yellow, and you read the OD at 450nm (they also recommend you subtract the OD at 510nm to account for the light scattering of the microplate).

Figure 1. R&D Systems Quantikine assays, HRP-streptavidin detection. https://www.rndsystems.com/products/quantikine-hs-colorimetric-sandwich-elisas-high-sensitivity
On the other hand, we know that we can also conjugate the antibody with a fluorescent molecule if we wanted to, like FITC or PE. All we need to do is excite the molecule with an appropriate light source or laser to get a fluorescent emission, and read with an appropriate system to read those signals. The fluorescent intensity would then be proportional to the captured analyte, based on a standard curve just like any ELISA.
So the real answer is we can use one, the other, or both, just not at the same time.
Just be cognizant that different platforms can yield different results, so you have to validate your two platforms, and correlate the two to ensure reproducibility. Most labs just try to stick with one or the other, though.

I should add that this can be made flexible by using a streptavidin-fluorophore conjugate. Then the process is almost exactly the same, with each detection molecule binding to biotin.


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Can a viable embryo develop from the fusion of two egg cells?
For a zygote to form, two haploid gametes undergo meiosis and fuse during fertilisation. Since two egg cells (or even two sperm cells) are both haploid, is it theoretically possible for them to make an embryo (via experimental manipulation)?
I’m guessing that if such a thing were possible, the two egg cells could each come from the same organism or two different sources.
Would there be any side effects, such as persistence of mutant alleles due to a lack of genetic variation if both egg cells originate from the same organism?

Related: Is ovum + ovum fertilization possible for human?

Yes, it is possible to make a zygote from two ovules. Other more complex scenarios are possible as well. You might want to read this cbc article. If the two ovules came from the same organism, then the baby will very likely suffer from a number of diseases due to very low heterozygosity (same mechanism that is causing inbreeding depression and problems of consanguinity).
It is likely not possible to get a zygote from two spermatozoids though because you would lack mitochondrial DNA (mtDNA). There is a little bit of mtDNA in spermatozoids but they are generally not transmitted. Through experimental setup I imagine it might be possible. Also, spermatozoids are very small and would lack many of the ressources necessary to start a zygote.

This pretty much answers my question, thank you.

You're describing chimerism (distinct genotypes in a single organism; in animals, this arises when two fertilized eggs merge). This article suggests that "microchimerism" can occur during pregnancy when small quantities of fetal cells migrate through a mother's body. You can find additional examples from humans and other species at my first link (the Wikipedia article), but here's one more from The New England Journal of Medicine in early 1998:

A 3.46-kg infant was delivered vaginally at term; he had a normal
  right testis and an undescended left testis, with otherwise normal
  male genitalia. At the age of six months, the left testis was palpable at the inguinal ring.  Surgical  exploration  at  the  age  of  15
  months revealed a hernial sac containing an abnormal gonad and
  vas deferens. These structures were excised; they proved on histologic examination to be an ovary with a fallopian tube attached to a horn of uterus. Karyotyping of peripheral-blood lymphocytes then revealed two cell lines, one 46,XX and the other 46,XY.

No, he is not describing chimerism.  He is talking about two unfertilized egg cells being fused to form a diploid zygote (instead of a sperm fusing with an ovum).

Did he ever specify that the egg cells couldn’t be fertilized? I’m struggling to see that in the original text of the question, and my answer is valid in the sense that it provides an explanation for how two eggs might combine to form “a viable embryo.” A mouse study showed potential for egg-egg fertilization but wasn’t sustained beyond ex vivo POC. For now, bi-egg organisms (especially humans) require sperm.

Yes, he indicated the egg cells (or sperm cells) were unfertilized by the terms he used: "For a zygote to form..." -- a zygote is a fertilized cell ready to divide into an embryo, being diploid (having a full set of paired chromosomes). "...two haploid gametes..." i.e. sperm or ova having half the DNA ",,,fuse during fertilisation. Since two egg cells are both haploid, is it theoretically possible for them to make an embryo?"

In that case, I’ve answered both parts of his question in my original answer and response to your question – the mouse study I linked is the only evidence I can find of an egg-only diploid, and otherwise it doesn’t seem to be possible without sperm.

Unrelated... but please stop assuming I'm a "he".

Certainly – and your point is well-taken (any further discussion will use your pronoun of preference, as specified) – but it’s important to keep in mind that there’s no maliciousness, assumption of gender, or any other subtext to the use of the word “he” here. At University, my english professors were always adamant that we not use the androgynous/singular “they.” Instead, I was taught to choose a singular (gendered) pronoun and use it, whether or not it’s specifically applicable to the group it describes. In this case, we were identifying/referring to a (functionally) anonymous user.


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Can the central dogma work in reverse?
Theoretically, is it possible to obtain the original gene from the protein’s amino acid sequence as its “template”, as in, the reverse of how gene’s codons were “templates” for the amino acid sequence of the protein?
I’m curious to know if it’s possible to use enzymes such as reverse transcriptase to obtain DNA from a protein in a reversed central dogma model.

What do you mean by "theoretical"? As in could a cell do it if it wanted to, or if they are even capable of doing so? Or do you mean can we realistically envision the chemistry that would be requires for that to happen?

This can be answered in both senses, which are very interesting.

I say “theoretically” because I am not sure if it has been done before, and I am not sure if that is because of the practical impossibility of the idea. Therefore, I guess what I mean is the last phrase you proposed.

what kind of googling have you done? Have you heard of protein sequencing?

Let’s first consider what the Central Dogma[1] actually says. It is precisely summarised in the following figure[2]:

solid arrows represent transfer of information that has been observed directly; dashed arrows represent potential, not yet observed, transfer of information

In the time since the original formulation of the Central Dogma in 1958, we have been able to contribute evidence for one of the dashed lines: RNA→DNA is performed in vivo via reverse transcriptase. By contrast, note the absence of any arrows originating from “protein”. The idea of the Central Dogma was that proteins were an information transfer sink: information could only flow in, not out.
And Crick and his contemporaries had good reasons for assuming such an information sink: translation from RNA to proteins is lossy  because the genetic code is degenerate. A given amino acid can be encoded by more than one codon.
This doesn’t mean that polypeptide chains couldn’t be reverse translated into “a” RNA representation. But it wouldn’t necessarily be the original RNA. Stated like this, it’s obviously possible: we can in fact take a polypeptide chain, sequence it, and synthesise a corresponding RNA.
However, this doesn’t happen in nature — at least, it hasn’t been observed so far, and there are good reasons to assume it doesn’t happen at all. In fact, Crick’s paper[1] explains:

The transfer protein→RNA … would have required (back) translation, that is, the transfer from one alphabet to a structurally quite different one. It was realized that forward translation involved very complex machinery. Moreover, it seemed unlikely on general grounds that this machinery could easily work backwards. The only reasonable alternative was that the cell had evolved an entirely separate set of complicated machinery for back translation, and of this there was no trace, and no reason to believe that it might be needed.

The “complicated machinery” Crick mentions here consists of two distinct parts: On the one hand the ribosome, and on the other hand the aminoacyl tRNA synthetases (aaRSs, singular aaRS). The latter is essentially the physical embodiment of the genetic code in the cell. The former is the machinery necessary to decode RNAs using the codon adapters (= tRNAs) charged by the aaRSs.
Crick correctly notes that, in order to allow the transfer protein→RNA, the cell would require a system analogous to the ribosome and all the aaRSs, redundantly encoding the exact same information. And it would need to ensure that these two distinct encoding systems (translation and reverse translation) never get out of sync with each other.
It’s worth contemplating, briefly, why the cellular translation process isn’t simply reversible, given that it’s an chemical process, and thus pretty much by definition reversible in theory. The reason for this is that translation happens in two entirely distinct, and physically separate, stages: the charging of individual tRNAs with their corresponding amino acids by an aaRS, and the actual mRNA translation by the ribosome.
Simply reversing the ribosome activity would result in a polypeptide being digested from one end, yielding individual amino acids. However, the ribosome actually has no facility for capturing these amino acids, they would simply diffuse away without being attached to a tRNA, let alone the right tRNA. A successful reverse translation would have to physically couple each type of aaRS in turn to the ribosome to ensure that terminal amino acids would pair with the correct tRNA, which, in turn, would pair with a codon. There are two fundamental objections to it, which render it impossible:

Codons, which could be combined into mRNA chains, don’t swim around individually. In fact, short RNA chains are highly unstable and are quickly degraded. By contrast, individual ribonucleotides can be combined into chains — that’s what polymerases do all day, after all. But the ribosome doesn’t possess polymerase activity, and the tRNA anticodon would not provide sufficient physical support to enable a polymerase to dock to it and start synthesising a secondary strand.
Steric hindrance prevents the aaRS enzymes from interacting with the tRNAs while they are being held by the ribosome: the ribosome and the aaRSs would have to physically overlap.

It’s hard to get definitive answers in science purely from theoretical considerations, but this one’s as certain as you’re likely to get: cellular translation using the ribosome is a non-reversible process. Reverse translation, if it existed, would therefore require a separate machinery.

My answer explicitly omits the discussion of the transfer protein→protein, as this is a topic all of its own, and would increase the size of the answer unduly.

Contrary to my belief, it may be possible.
The main concern we must look at is Protein to RNA, as we know RNA to DNA can be done through reverse transcription.
Some evolutionary scientist believe that reverse translation may be a process that could have occurred naturally during the process of evolution to create the central dogma we know today. Hence, there still lies the possibility that there is a mechanism for the process that remains undiscovered. Just because we do not have proof of it does not mean it does not exist.
There is also a product under development called PeplicaTM that claims to be able to convert protein to RNA, which can then be amplified with conventional PCR. Though, I can not find much information regarding it making me a little hesitant on suggesting whether it actually works.
The following is a little bit of a review on the topic that further outlines some points I mentioned. If you are interested, do read it.
https://www.omicsonline.org/open-access/revisiting-cricks-dogma-and-the-impossibility-of-reverse-translation-jtco.1000110.php?aid=24768

+1 for finding that article, it’s certainly … interesting. And by that I may or may not actually mean that it’s absurd. At the very least it’s probably the most uncharitable treatment I’ve ever read of Crick’s work, and it provides an intellectually dishonest caricature of his arguments so that the author can dispatch them.

The key underlying concept in Francis Crick’s so-called Central Dogma of Molecular Biology is that the genetic information to create a new cell (or organism) is encoded in a cell’s DNA, and therefore it is the DNA that gets replicated when a mother cell divides to give two daughter cells, and it is the same DNA that has to be equally partitioned, or transmitted, to each of the daughter cells for life to continue.
The primary information encoded in that DNA is the sequence of all of the proteins that the daughter cells might need to make to stay alive.  And so we have:
”DNA makes RNA and RNA makes Protein”
Where the messenger RNA is a transient intermediary between where the genetic information is stored, and where the genetic information is decoded (on the ribosomes, where protein synthesis occurs).
Reversing the central dogma would be a situation where the proteins of a cell contain the genetic information that gets replicated in the mother cell and then gets partitioned, or transmitted to the two daughter cells.  If proteins could be reverse translated into a genetic mRNA (this has certainly been done in a test tube where the primary sequence of a protein has been used to create an oligonucleotide primer (admittedly made of DNA) (this required a human who could read the universal genetic code table—also assembled by humans)), then in theory that RNA could be converted into a DNA copy by RT, as you described.  But then we are left with an incomplete scenario where it is the DNA sequences which have to provide the enzymatic, structural, and regulatory roles of the resulting cells (i.e., all of the roles that proteins currently provide).
DNA does not possess any enzymatic activity (as far as we know), so at this point the model you propose does not seem viable.
You also are ignoring the fact that the genetic code is degenerate such that there are up to six different codons that can encode one of the 20 common amino acids, so any reverse-translatase would have to be imprecise.
Consider this question: where is the genetic code table stored inside a cell?

I think your answer erects a partial straw man: there’s no necessity in this model for DNA to have an active role: It could conceivably act as a passive intermediate molecule. This is in fact exactly what happens with retroviruses.

I think you make a valid point (straw man), and I like the thoroughness of your answer. I am thinking of deleting mine now.

Let's consider the following theoretical possibility of of a molecular mechanism for information transfer from protein to RNA or DNA. One can imagine having "adapters" (either protein or RNA or even DNA) that bind with high affinity to a specific protein fold. There are estimates of about 4000 possible distinct protein folds, of these ~2000 so far demonstrated) (Govindarajan et al. https://pubmed.ncbi.nlm.nih.gov/10382668/). So one could imagine ~2000 different adapters, some of which could bind simultaneously to a protein and be brought to a linear register by means of flexible linker regions of variable lengths. One then imagines that at the other ends of this flexible region is a 3-letter codon (or anticodon). Imagine then a polymerase that either polymerizes the registered array of codons (or which nucleates a growing RNA strand on the noncovalently arrayed anticodons). This fantasy is physically plausible but is rather unlikely to exist in competition with the forward transmitting of genetic information. However, in an exoplanet life could have evolved to transfer information from polymers with irregular shapes to polymers with regular features for safe storage. In other words, it is possible to imagine information transfer from complex to simple encoders, in contradistinction from the more elegant solution of transfer of earthly biological information from simple to complex encoders.

Why 2000 adapters rather than ~20 (one for each amino acid)?

This does not provide an answer to the question. Once you have sufficient reputation you will be able to comment on any post; instead, provide answers that don't require clarification from the asker. - From Review


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IBD-value in pedigree with inbreeding
I have a question about IBD. Please see the figure below. How many pairs of alleles are IBD for X and Y, or what is the IBD value for X and Y. Is it four (4)? I have seen it to be maximally 2, but then we assume that no inbreeding occurs, right?

An Identical-By-Descent (IBD) value is the number of alleles which are the same because of descent from a common ancestor.  Since each (diploid) individual has two alleles for a given (autosomal) gene, the number of them that are IBD with another individual can only be 0, 1, or 2.
In your example, X and Y inherit each of their alleles from A2, so their IBD value is 2.  Inbreeding is just an extreme form of descent from a common ancestor; it causes on average greater probability of high IBD values than when comparing less-inbred individuals. See the passage here for more detail.

Thanks for answer @mgkrebbs. I am still a little bit confused. This is due to the following excerpt from Thompson: Pedigree Analysis in Human Genetics, 1986, The Johns Hopkins University Press, page 28: "Consider now a pair of relatives, neither of whom are inbred, although their parents may be. Since neither of the two individuals can carry two identical genes, there are only three possibilities of gene identity (figure 11): the individuals have two genes in common, or one or neither." Does the IBD value relate to only one person or to the two individuals under consideration.

Hmm. I see three possible solutions: 1) the individuals share 1 allele IBD, the a allele 2) the individuals share both of their alleles IBD so that IBD=2 3) all the alles are IBD, so that IBD=4 (you can make 4 different pairs of IBD alleles). It looks Thompson and the excerpt you provide look at the two persons at the same time; i.e how many alleles do two persons share . It looks like they do not look on the individual level (i.e how many of the alleles of.one person does the individual share with the other.)

If we assume that @mgkrebbs' solution is correct, what would the IBD-value be between R and X if R had genotype ca instead of cd? Now R has one allele in common with X, but X has two alleles in common with R.

IBD (and IBS) is a characteristic of the relationship of two persons' genes, not a characteristic of a gene or allele itself.  So the only possible relationships  are: no alleles are the same, one pair of alleles are the same and one different, or both pairs of alleles are the same.
If R' is ca, then R' and X have IBD (and IBS) value of 1 -- they have one  pair the same.  The alleles are unordered - you choose the pairings between individuals' alleles so as to maximize the IBD count, having chosen one pair, the other pair is also determined, being the only pairing that can then exist.


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Identical twins' biological sexes
Can identical twins have different genders (as in biological sex)?
I thought they should have absolutely the same genes. If they can, what caused it? I'd assume it MAY be because of errors in cellular division at conception.
Thank you.

Note that your question, and the accepted answer, seem to depend on the use of the term "gender" to mean "biological sex". You might consider rephrasing for clarity here, since "gender" is a rather more complex and nuanced social construct.

Done. Could you clarify what you mean by that? Or is it better if I post another question?

@WajihAziza These might get you started: http://en.wikipedia.org/wiki/Gender http://en.wikipedia.org/wiki/Transgender

Identical twins occur when a single egg is fertilized to form one zygote, which then divides into two separate embryos. Thus, identical twins are always the same sex unless there has been a mutation during development.
However, two identical twins expressing different sexual phenotypes does happen in some extremely rare cases due to environmental factors, deactivation of different X chromosomes in females, or aneuploidy. This is normally because an XXY Klinefelter syndrome zygote has split unevenly.
You are correct though, in that identical twins usually have hundreds of genetic differences early in fetal development which can be attributed to mutations in the DNA. But usually these differences do not result in twins with different sexual phenotypes, though it is possible.

There can also be many epigenetical differences between twins.

So theoretically, it's impossible to happen unless it was caused by an "error". That was enlightening. Thank you.

@WajihAziza Biology isn't at all my field so I may be off base here, but wouldn't the twinning event itself be considered an 'error' as that is outside of the normal?

Perhaps you want to rethink calling everything outside the norm an error.  It's needlessly pejorative.


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How are dental cavities different from body injuries?
I always had this question why dental cavities cause pain. I stumbled on this question on the reasons why dental cavities are painful. I have a followup question on how dental cavities are different from bodily injuries. I was under the impression that pain causes inflammation which in turn triggers something like mitosis that causes healing. Why does the same not happen with the dental cavities? Why are they not treated like the bodily injuries?

I disagree with some of these statements. Dental cavities are injuries and are treated like injuries warrent.
Unlike maybe trauma or cancer, dental cavities are a injury caused by decay of the enamel (the protective hard shell of the tooth). The decay is a result of the proliferation of bacteria, streptococcus mutants which releases an acid and breaks down the tooth.
When you have perforated enamel, other particles like food can get caught in the tooth and give rise to the growth of other bacteria. At this point you have a cavity.
Infection, the presence of certain toxins, and trauma all causes inflammation, a type of non specific immune reaction characterized by increased blood flow to the site of injury (which causes swelling, pain, redness).

Can you be specific on where you disagree?

You did not explain The increased blood flow and trauma happens to kickin healing processes in other parts of the body. Why does this not happen in the mouth?

@koya it does happen in the mouth. My disagreement was in reference to your mention that oral injuries did not induce inflammation. After re-reading your question I'm going to delete mention if that and edit some content.- I think I have a clearer idea what your asking.


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Can one talk about deacetylation of a promoter rather than associated histone?
I am confused on a detail in a paper I am reading and am not sure whether I am misunderstanding the wording or misunderstanding the concept.  I am including the whole abstract of this paper for background:

Epigenetic regulation of uterine biology by transcription factor KLF11 via posttranslational histone deacetylation of cytochrome p450 metabolic enzymes.
Zheng Y, Tabbaa ZM, Khan Z, Schoolmeester JK, El-Nashar S, Famuyide A, Keeney GL, Daftary GS.
Abstract:
Endocrine regulation of uterine biology is critical for embryo
receptivity and human reproduction. Uterine endometrium depends on
extrinsic sex steroid input and hence likely has mechanisms that
enable adaptation to hormonal variation. Emerging evidence suggests
that sex steroid bioavailability in the endometrium is determined by
adjusting their metabolic rate and fate via regulation of cytochrome
(CYP) p450 enzymes. The CYP enzymes are targeted by ubiquitously
expressed Sp/Krüppel-like (Sp/KLF) transcription factors.
Specifically, KLF11 is highly expressed in reproductive tissues,
regulates an array of endocrine/metabolic pathways via epigenetic
histone-based mechanisms and, when aberrantly expressed, is associated
with diabetes and reproductive tract diseases, such as leiomyoma and
endometriosis. Using KLF11 as a model to investigate epigenetic
regulation of endometrial first-pass metabolism, we evaluated the
expression of a comprehensive array of metabolic enzymes in Ishikawa
cells. KLF11 repressed most endometrial CYP enzymes. To characterize
KLF11-recruited epigenetic regulatory mechanisms, we focused on the
estrogen-metabolizing enzyme CYP3A4. KLF11 expression declined in
secretory phase endometrial epithelium associated with increased
CYP3A4 expression. Additionally, KLF11 bound to CYP3A4 promoter GC
elements and thereby repressed promoter, message, protein as well as
enzymatic function. This repression was epigenetically mediated,
because KLF11 colocalized with and recruited the corepressor
SIN3A/histone deacetylase resulting in selective deacetylation of the
CYP3A4 promoter. Repression was reversed by a mutation in KLF11 that
abrogated cofactor recruitment and binding. This repression was also
pharmacologically reversible with an histone deacetylase inhibitor.
Pharmacological alteration of endometrial metabolism could have
long-term translational implications on human reproduction and uterine
disease.
Citation:
Zheng Y, Tabbaa ZM, Khan Z, Schoolmeester JK, El-Nashar S, Famuyide A, et al. Epigenetic regulation of uterine biology by transcription factor KLF11 via posttranslational histone deacetylation of cytochrome p450 metabolic enzymes. Endocrinology. 2014;155:4507–20.

My question is on the fourth-to-last sentence of this abstract specifically:
"This repression was epigenetically mediated, because KLF11 colocalized with and recruited the corepressor SIN3A/histone deacetylase resulting in selective deacetylation of the CYP3A4 promoter."
This sentence seems to say that SIN3A/histone deacetylase is deacetylating the CYP3A4 promoter itself (i.e. it is deacetylating a region of DNA directly).  However, shouldn't a histone deacetylase be deacetylating a histone, not a region of DNA?  Am I misunderstanding the mechanism?  Or is "deacetylation of the CYP3A4 promoter" really a short-hand way of saying "deacetylation of a histone that is associated with the CYP3A4 promoter"?
Thanks in advance for your help!

The promoter sequence is wrapped by histones, which a modified (look at figure 3). "KLF11 binds distinct nuclear cofactor complexes that posttranslationally modify promoter histones to epigenetically alter the chromatin state, gene expression levels, and activity"

Thanks @GerganaVandova.  Just to make sure I am understanding the wording correctly:  is it always ok to refer to a histone modification as a modification of the corresponding gene (as the authors seem to do in the abstract)?  For example, if we were talking about histone methylation, it would be confusing to phrase a statement as "methylation of XYZ123 promoter" (since DNA methylation and histone methylation are two separate phenomena).  Is it acceptable in the case of histone acetylation, since there's no such thing as DNA acetylation (as far as I know)?
Hope this question makes sense!

I would say yes, it is probably acceptable, but I agree that the authors should have been more clear by stating that changing the acetylation state of the histones wrapping the promoter affects the expression of the gene from that promoter.

@Georgana Vandova. I've edited the title of this question, deleted my own comment and turned it into an answer. That way the question can be answered and eventually taken off the unanswered list. As your comment is more extensive you might like to do likewise (and perhaps reconsider your attitude to the acceptability of the statement).

The authors obviously meant to write that the histones associated with the promoter become deacetylated. They cannot mean the promoter itself as that is DNA.
What they wrote is not shorthand or acceptable alternative usage, but just a mistake — published papers often contain typos and mistakes of this sort. Probably the authors meant to write the technically correct form of words but lost a phrase. Or perhaps they had exceeded the limit to the number of words allowed in the summary, and so they went through trimming, but trimmed too much.
Why didn’t the referees pick this up? Of course they should have, but they were probably more concerned with the contents of the paper and whether the experiments described by the authors justified their conclusions. They are busy scientists and probably doing the job voluntarily.
In conclusion, scientists are human, scientific writing is difficult, and everyone makes mistakes. But we should still try to convey our ideas as clearly as possible, and certainly not copy something that is technically incorrect or ambiguous, just because it has made it into print.

This is all about DNA-Protein interactions.
The promoter region of the DNA is interacting with the Histone modifications, which are controlled by other proteins.


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Is bi-allelic gene expression random?
Supposing we have the genotypes “Aa”, “AA”, and “aa”... which are not mono-allelic (not imprinted and not X-inactivated). Does the dominance of the “A” allele over “a” allele affect which gene is transcribed, or are both alleles transcribed and the allelic dominance only determines the observed phenotype?
I’m guessing it’s the latter, but that makes me confused as to what the concept of allelic dominance would mean for mono-allelic expression, where only one allele is always expressed and observed.

I guess this answer might help.


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Do all bacterial cells have a double membrane?
I’m reading that gram positive and negative bacteria have an inner plasma membrane surrounding the cytoplasm, then a periplasmic space, then an outer membrane.
How does this compare to my general knowledge of bacterial cells having one plasma membrane surrounded by a cell wall?!

Do all bacterial cells have a double membrane?

No. There are a number of bacterial membrane and cell wall structures. Some of them have a double membrane, some of them don't.
In microbiology, we often make the initial distinction between two groups of bacteria based on whether or not they take up an iodine based stain called a Gram stain. Gram negative bacteria have an inner membrane, a rigid cell wall, and an outer membrane around the cell wall, so they don't take up that stain. Gram positive bacteria have an inner membrane and a rigid cell wall, without the outer lipid membrane, so they do take up that stain.  There are other bacteria that don't stain well with either the Gram stain or its red counter stain (typically safranin), but most medically important species of bacteria fall into one of these two categories (gram positive: blue, no outer lipid envelope, or gram negative: red, has an outer lipid envelope).

You can read about gram-negative and gram-positive bacteria on Wikipedia, but it's surprisingly technical. This biologywise post might be a more approachable introduction.

How does this compare to my general knowledge of bacterial cells having one plasma membrane surrounded by a cell wall?

When the concept of prokaryotes and eukaryotes is introduced, you're taught about key distinguishing features between the two. One of the key distinguishing features of (most) prokaryotes is a rigid cell wall. This is present in both gram negative and gram positive bacteria. They just didn't tell you about the outer lipid envelope in gram negative bacteria. At that point in your education, the idea is to introduce you to the concept of prokaryotes vs. eukaryotes, not to catalogue or understand all the different kinds of prokaryotes.
The more you learn, the more you'll see that life is quite varied. Many eukaryotic cells are coated in a layer of complex sugars and proteins that is in some ways similar to the cell wall of prokaryotes. It just doesn't provide rigidity against an osmotic challenge like prokaryotic cell walls. On the prokaryotic side, mycoplasma don't have rigid cell walls.


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How many different chemical substances are there (on the average) in a human cell?
How many different chemical substances are there (on the average) in a human cell?
I saw of an estimation of ~ 1 billion (10^9) in sci-pop books.
Is there any reliable estimation rooted in the scientific community?
There is this question, but it does not have any answer. It only states that modern researches use (model) only a very limited number of chemicals within a cell. But what is the estimation of the real complexity of a problem.

Why do you care? This is Guinness Book of records stuff, that went out of science two centuries ago.

For the scope of the question, it will largely depend what elements should be considered. All chemical substances would include atoms, molecules, basic chemical substances (for example amino acid, nucleic acid), supra molecular substances (peptide, protein, DNA molecule), and complexes. When considered from this point of view, any pair of amino acid or nuclei acids is a new entity. With all the possible building blocks that makes a huge combinatorial list. So the answer will largely depends at which "level" of details the question should be asked.

I think that the sci-pop books will be as reasonable as any other estimation.


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gene expression of tumor with different percentage of infiltrates
I'm performing differential gene expression analysis on rnaseq of  tumor samples that might have different amounts of immune infiltrate.
Tumors are extracted from patients that respond/not respond to immunotherapy
In my lists I found several immune response related genes significantly modulated but i suspect that this could be related to the different amount of immune infiltrate.
In order to highlight the genes that are induced by the tumors and not by the different amount of immune cells... it could be appropriate to normalize the raw reads counts (on which is based my analysis) on the basis of CD3 gene?

Consider that while a fair portion of your immune infiltrate will be T cells, that you can also have dendritic cells, macrophages, B cells, NK and NKT cells, and other cell types. I like to use this figure to demonstrate that fact, and also make note that the relative abundance of immune mRNA by cell type differs by indication (figure 1).

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4852857/
Also consider that for T cell markers like CD4 or CD8, these are expressed by antigen-presenting cells, as well.

Thank you very much You are right . If i correctly understand it is not easy to separate the mRNA that came from the immune fraction from the mRNA that came from tumors also because some genes are expressed from apc as well.

the best that i might do is estimating the fraction of immune cells present in my samples (with cibersort) and evalute if the amount of immune cells is comparable between samples

@GuidoL I'm not 100% sure the method to delineate your gene signatures but a common issue I'd run into with mac/mono contamination, for example, is you'd see this huge p < 0.005 IL-8 expression, but the common cell that produces a lot of the IL-8 are macrophages. And IL-8 is also secreted by other cells, so you can't link the expression back to a single type of cell, either.


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What is the adaptive significance of temperature dependent sex determination?
Why do some reptiles have TDSD ?  Is it because one of the genders is healthier than the other that only they, can survive high temperatures?

Please google search with "Temperature dependent sex determination". The search will bring up an excellent Wikipedia page on this complex topic that addresses your question. Several scientific references are also cited there as well.

To my knowledge, it is still mainly unclear what are the enviromental factors that would promote Environmental Sex Determination (ESD; incl. TSD) vs Genetic Sex Determination (GSD; incl. with and without sexual chromosomes).
Environment variability and Climate change
Generally speaking it is thought that in variable environment, GSD might be more beneficial as an ESD mechanism could lead uneven sex-ratio and hence lower fitness (Pen et al., 2010).
Climate change can be very detrimental to species that use ESD. A sudden climatic change can cause a population to have a highly biased sex-ratio to the point where persistence is not possible anymore (Boyle et al., 2014).
Differential fitness variance among sex
On the other hand, ESD can allow parents to decide the sex-ratio of their offsprings (Randy, 2005).
Consider for example a case where sexual selection lead to a much high variance in fitness among, say, males than among females. Note that parents fitness and offspring fitness is correlated (because an obvious genetic correlation but also because some environmental correlation). In such case, parents that have a low fitness would prefer to produce females (that despite being unhealthy / ugly will still manage to have a decent fitness) while parents with high fitness would prefer to produce males (because very healthy / good looking males will have a very high fitness).
Charnov and Bull model
In Charnov and Bull (1977) own words (taken from their abstract)

We propose that labile sex determination (not fixed at conception) is favoured by natural selection when an individual's fitness (as a male or female) is strongly influenced by environmental conditions and where the individual has little control over which environment it will experience. Our argument also applies to sex expression in hermaphrodites

According to wikipedia, there are a number of evidences for this model in the literature. I let you go through the cited papers for more information about what is the logic behind this hypothesis!
Evolutionary constraint
Changes in sex determination systems has not evolved that many times (in Reptilia at least; Jansen and Phillips, 2006; see this post for definition of Reptilia). It can be hypothesized that there might be a strong evolutionary constraint (see also phylogenetic signal) and hence looking for adaptive reasons for its evolution might be a moot point.


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Difference in frame rates of normal and peripheral vision
I recently encountered an incident in my laboratory. It was evening and the sunlight entered the lab through a window with exhaust fans. So the ray kept flickering at fixed intervals.
I noticed that the flickering was more noticeable when it was viewed through the side of my eyes.
Is it a fact that the frame rates of the two visions are different?

Vision doesn't have frame rates.

I believe the persistence of vision puts an upper limit for the no. of distinct images that can be seen in a second. That is what I meant by the frame rate of vision of human eyes.


text:
Degree of identity by descent with egg donated from a sibling?
If a woman becomes pregnant with an egg donated from her sister, what is the degree of identity by descent (IBD) between her and the child?
A pair of siblings have the following expected IBD probabilities:
P(IBD=0)=0.25

P(IBD=1)=0.5

P(IBD=2)=0.25

My solution therefore is:
So if we assume that recombination occurs at random so P(recomb)=0.5 and per haplotype there would be P(IBD=1)=0.75 (because one half is IBD=1 one quarter is IBD=2).
Then the result would be:
P(IBD=1) = P(IBD=1)*P(recomb) = 0.375.
So the result is the child and the mother would be:
P(IBD=0)=0.625

P(IBD=1)=0.375

P(IBD=2)=0.0

Is my inference correct?


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How much energy does active transport require in phosphorylation?
I know that active transport requires ATP in order to go against the concentration gradient.
But I somehow can't seem to find information on how much energy it needs.
So, my questions are:

What quantities does the energy required for active transport depend on? (If so, is there a formula for evaluating them?)

How much energy is needed for active transport in Oxidative phosphorylation and Photophosphorylation?

Thank you in advance.

Please edit the question to limit it to a specific problem with enough detail to identify an adequate answer.

Welcome to SE BIology. Please finish reading the [Tour] to find out how the site operates. We'll know when you have done that by the badge that appears against your name. Your question is not totally clear because it does not indicate what is being transported. Do you mean the transport of protons at three stages of the electron transport chain? If you do, please edit your question to indicate this. Then reflect on the fact that this process is used to set up an electro-chemical gradient to generate ATP, and revise the question to eliminate what you thought you knew.


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Drinking River Water Unsafe?
I've read that drinking river water is unsafe. Did people in the past drink water from the well exclusively or did they deal with diarrhea constantly?

This is not really a question about biology. I am not sure which SE site this may belong, though; perhaps [history.se] but even then these factors vary geographically a lot. I am afraid this question would be considered too broad in [history.se].

Which river? Unsafe how?

It depends how far in the past you're looking. Post-agriculture but pre modern sanitation, yes diarrhoea is a major problem. Pre-agriculture, however would have been a different matter. The majority of pathogens in river water are derived either from agriculture (e.g. cryptosporidium, giardia) from large human populations (cholera) or rodents associated with human populations (leptospira). There would, therefore have been far fewer disease causing organisms in river water Pre-agriculture. Add to that the effect on the immune system of Post-agriculture diet and lifestyle and it would seem unlikely that the cleanliness of most river water would have been a major problem.

It very much depends on the river and location along that river. if there is a city upstream who is defecating into the river, you'd better not drink from that river. But drinking from the same river upstream of this city could be totally fine.
Disease transmitted through the faeces were very common in the the 19th century especially in cities that had no system of evacuation of wastes. Now, of course the prevalence of such diseases depends on the type of society and therefore on the era and location.
Generally speaking, it is always best to carry tap water (or bottled water) on you. If you have to drink from a river, be cautious, talk to local people, think of what could live upstream (people, cattle, ...) and always use a good filtration system before drinking from any river.


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How and why did bats and dolphins develop echolocation?
By how and why, I mean, what factors pushed them to develop echolocation and how did the intermediate stage (before a full-fledged echolocation system was developed) look like?

There should be echo locating birds, but they perhaps don't have the right vocal and auditory structures. For dolphins, perhaps their eyes can't point forward while swimming fast, plus they stir sand and hunt in dark and low visibility waters. water's awesome transmission of high frequency sound is a factor. All animals can echo locate, like blind people do, evolution just has to increase high frequency hearing and chirps. Mammals tend to be nocturnal prior ot KT boundary and have good vocal and auditory structures by default.

@com.prehensible Is that an answer disguised as a comment ;-)

echolocation likely evolved very differently in each group you may have better luck spitting this into individual questions.

There are many conditions in which echolocation has evolved, and bats, dolphins, and even some birds (oilbirds) have evolved the ability to echolocate with different anatomical structures. Echolocation is a great example of convergent evolution, where a very similar feature is developed through very different stages in different taxa. Stephen Rossiter (from Queen Mary University of London) has uncovered that both bats and dolphins have similar mutations in a unique protein called "prestin", that increases hearing sensitivity. This could be a key step in developing the ability to echolocate.
Before a fully fledged echolocation system developed, fossil odontocetes seem to have developed high frequency hearing and sound production structures (for more details see research by Travis Park, Erich M. G. Fitzgerald, Alistair R. Evans http://rsbl.royalsocietypublishing.org/content/12/4/20160060 DOI: 10.1098/rsbl.2016.0060).
Instead of anatomical limitations (eyes on the side of the head) driving the development of echolocation, it seems to have evolved because it gives predators a competitive edge over visually oriented predators.

Simple echolocation is fairly widespread and varying levels of quality exist
This specifically addresses what the intermediary forms look like.
Mammals posses some nice preadaptations for echolocation. external ears for gathering sound, a three bone middle ear which creates an amplifier which means mammals can hear both weaker and a wider range of sounds. It also means the brain has to be able to do more processing of sound due to distortion and frequency shift. Even humans can perform very limited echolocation with training due to this.
Old world fruit bats don't use full fledgedly echolocation like other bats and dolphins. First the sound is created by their wings not their vocal cords, it is a side effect of their wing beat. Second it is functionally rather poor not giving a very detailed image, as noted in this study they cannot detect small objects or judge distance very accurately unlike other bats. The study also have a lovely table showing how many other animals have primitive forms of echolocation, including shrews, rats, and swiftlets.

re: mammals possess some nice preadaptations for echolocation, here's a human mammal example. The voiceover is incorrect when it says this is the only example of a person who sees with echolocation. There are others.


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Why is Lamarck's evolutionary theory considered incorrect?
Many sources postulate without much argumentation that Lamarck's evolutionary theory is "obviously incorrect". A classic example provided in such sources is the one with giraffes, in which Lamarck argued that the necks of these animals became long as a result of continually stretching to reach high foliage. This mechanism for adaptive change in response to the environment is considered wrong.
Now the counterargument to Lamarck's ideas comprises modern findings in genetics. So it is stated that organisms pass down traits through predetermined genetic information, not based on environmental adaptations during their lifetime. Furthermore, genetic research shows that living organisms cannot alter their genetic material as needed.

Doesn't the latter contradict the evolutionary theory itself, which states that nature (i.e. environment) shapes species through natural selection in the environmental milieu? If it is not the environmental/natural factor that is responsible for genetic evolution, then what is?
If genetic material were to be unchangeable, then how would adaptation to the environment and consequent evolutionary change would ever be possible? The genotype (following this logic) would remain the same.
And lastly, maybe giraffes do not develop long necks at such a rapid pace (as Lamarck probably thought) by simply stretching their necks in one generation; however, what, if not neck stretching, is responsible for their consistently longer necks throughout thousands or millions of years? Hadn't the environment gradually shaped their genotype? Similarly, if I run more often, maybe my children will not become more fit, but isn't it just a matter of time (thousands of years) that if all of us consistently run a lot, then our offspring will eventually become more fit? Wouldn't our voluntary efforts eventually enhance our genetics? I do not see any problem with Lamarck's logic at all, except probably the time frame.

PS I became inspired to ask this after reading this, this, and this, plus after consolidating a few of my own memories from bio classes

Welcome to Biology.SE. Your question could be summarized into "How does evolution work?", which is a broad question which answer can be found at many different sources online. I would recommend that you have a look at Understanding Evolution (UC Berkeley) which is a short and very introductory course to evolutionary biology.

You can have a look at plenty of very introductory posts on Biology.SE as well such as the answers to this post for example.

In science theories are tested by experiment evidence and, as scientific knowledge progresses, how they can be accommodated in the framework of knowledge. In brief, there is no evidence to support Lamarck’s idea (Lysenko is notorious for his falsification of such evidence during the Soviet era to fit with Stalin’s philosophy), and the subsequent discovery of the molecular basis of heredity provided a requirement for the theory to show how changes in somatic cells could affect the DNA of the germ cells. No such evidence has emerged.
It is true that there are epigenetic effects, but none so far support Lamarckian postulates of the giraffe neck variety.
Finally, a word of advice. Don’t waste your breath on this list with arguments of the sort “Doesn't the latter contradict the evolutionary theory itself”. This is not a philosophical debating society, but community that is concerned with the factual basis of science. If you have never studied molecular sciences, stay away — or ask questions in the course of genuine attempts to acquire knowledge in this area.

I think you misunderstand both Lamarckism and other descriptions of evolution such as the modern synthesis (Darwinism with Mendelian genetics and a few bells and whistles). Both theories accept organisms have heredity with occasional changes. Neither Darwin nor Lamarck knew about genes, so I'll explain what their ideas boil down to in modern language.
In the modern synthesis, frequent changes called mutations may increase fitness (we call these beneficial), preserve fitness (we call these neutral) or decrease fitness (we call these deleterious). Mutations happen because DNA isn't perfectly copied or maintained; there's no bias in favour of beneficial mutations. However, as generations pass beneficial mutations proliferate, deleterious ones disappear (unless continually generated by mutation asymmetries, and even then they'll be rare in the population), and neutral ones' frequency in the population "drift" at random.
In Lamarckism, mutations are preserved based on beneficial acquired characteristics, which would require a way for bodies to identify which acquired traits are useful (injuries aren't!), reverse-engineer the genetic changes that would achieve them (which is basically impossible because DNA is more of a recipe than a blueprint), then update gametes with these changes. There is a lot of evidence that supports Darwinian evolution ("natural selection") but not Lamarckian evolution. For starters, Lamarckism couldn't explain novel biochemistry.
Biologists such as Richard Dawkins (see e.g. Darwin Triumphant, a chapter of A Devil's Chaplain) have pointed out that, even if there were life that could do what Lamarckism requires, it would not only still be susceptible to natural selection, but could only perfect a viable Lamarckism mechanism of discriminating good changes from bad by the action of natural selection. In other words, even if Lamarckism happened it would be an emergent property of Darwinism, not an alternative to it.

Nice answer, but you should also add some references in your answer for further reading by anyone interested.

@another'Homosapien' Partially addressed in my edit.

"there's no bias in favour of beneficial mutations." I wonder though, is this based purely on the theory, or is this an inference from empirical data. Because theoretically it is not impossible for positive mutations to get favored (via genetic interactions).

@rus9384 You can think of it as an assume-fewest-empirically-required-entities version of theory. If someone discovers a gene tomorrow that biases mutations in its organism to be favourable, that'll become an oh-all-right-then footnote.


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To what extent is excretory control a learned vs. instinctive behavior?
Human babies are clearly not born knowing whether/how to hold in urine and feces, and teaching them to do so requires a nontrivial (really nontrivial...) amount of work on the parents' part.  But once this skill is learned, it becomes so effortless that one does it automatically in one's sleep.  I can't think of any other learned behaviors that are either (a) performed while unconscious, or (b) controlled by the parasympathetic nervous system, both of which are true for excretory control.  The fact that, once learned, excretory control becomes so "automatic" seems to suggest to me that it's not entirely a learned behavior.  If no one ever actively taught a baby to control its bladder and bowels, would it eventually learn to do so on its own (suggesting that excretory control is actually an instinctive rather than learned behavior)?  Presumably this experiment has never been performed on a human baby, but are non-human animals born knowing how to control their bladder and bowels, or is this a learned behavior?


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What is the difference between silent and synonymous mutations?
Several sources all caution that silent mutations and synonymous substitutions are not the same thing and should not be confused. But they seem to draw different actual distinctions between the terms:

This Wikipedia page and this biology dictionary entry define a silent mutation as a point substitution that replaces a single codon by another codon that codes for the same amino acid, and therefore does not directly change the amino acid sequence that is coded for. It defines a synonymous substitution as a silent mutation that occurs in an exon. Under these definitions, a synonymous substitution is a special case of a silent mutation.
This Wikipedia page and this blog post define a silent mutation as any mutation that does not have any phenotypic effects, and defines a synonymous substitution as a point substitution to a degenerate codon (anywhere in the genome, as far as I can tell). It points out that such synonymous substitutions can still have indirect phenotypic ("nonsilent") effects by affecting translation and transcription. Under these definitions, a silent mutation is a special case of a synonymous substitution (namely, one that doesn't have any indirect phenotypic effects).
This Wikipedia page uses similar definitions to the one in #2, except it explicitly requires that a synonymous substitution occurs in an exon.

Clearly these definitions are not all compatible. (#2 and #3 are very similar and could perhaps be excused as minor variants on the same definition, but they clearly conflict strongly with #1 - they disagree on which of "silent mutation" and "synonymous substitution" is a special case of the other!) Is there a standardized distinction in the biology community between these terms, or is it just the case that everyone uses conflicting definitions and we should ask people to clarify the senses in which they're using these terms?

Silent mutations are those which have no phenotypic effect and it seems important to note that these could occur in coding regions and non-coding regions alike. Synonymous mutations, on the other and, are confined to coding regions. Because these mutations, by definition, do not change the amino acid sequence, they are nominally silent. However, due to codon bias, etc.,, a synonymous mutation may not always be silent. Therefore, my non-authoritative opinion is that it is not entirely accurate to classify one as a subset of the other. All you can really say is that silent mutations have no phenotypic effect, and synonymous mutations can be silent or not.

"Silent mutations are those which have no phenotypic effect".. the definition should have ideally been so. However, the existing definition pertains only to changes in amino acid sequences. In fact, you can have non-synonymous mutations that are "silent".

@WYSIWYG I seemed to remember, for some reason, that silent mutations need not necessarily refer to mutations in a coding sequence, but I struggled in vain to find more than a few papers that used it this way. Your answer certainly captures its actual usage better than mine.

Your definition does make real sense but unfortunately the real definition is a bit obsolete.

I would say that silent mutations, as they have been defined, are a subset (or perhaps even same as) of synonymous mutations. However, the term, "silent mutation", is not used so much these days. Almost every research paper that I have read pertaining to this topic has always used the term "synonymous mutation" irrespective of whether or not it has a phenotypic effect. It seems that the term, "silent mutation", is confined only to textbooks.
If you consider silent mutations are mutations that are not reflected in the phenotype then there some points that you should consider.

As canadianer mentioned, these mutations can be present in non-coding region. However, mutations in non-coding regions can also affect the phenotype. Moroever, as they mention, synonymous mutations can cause changes in translation rates because of the codon bias which in turn can lead to phenotypic differences (Kimchi-Sarfaty et al, 2007; Waldman et al, 2011; Buhr et al, 2016). These phenotypic differences can arise due to altered protein concentration or altered folding states. So a synonymous mutation is not essentially "silent"
A non-synonymous mutation may not affect the phenotype (neutral mutation).

I would say that this definition should not be used unless the majority of the scientific community agrees on redefining the term. Till then, you can possibly use the term, "neutral mutations", to mean mutations that do not affect the phenotype. Remember that neutrality of "neutral mutations" is defined with respect to fitness. However, if your measure of fitness pertains to the molecular function of the gene then this definition works.

I don't understand your last paragraph, I thought that there's a standardized definition that "neutral mutation" only means neutral with respect to evolutionary fitness, not to phenotype. What do you mean "your measure of fitness pertains to the molecular function of the gene"?

@tparker Fitness is a relative term. If you are selecting for the molecular function of a gene, lets say an enzyme, then the enzyme activity is your fitness. Check this out.

Oh, I thought that "fitness" always refers to reproductive success.

@tparker Let's say in a lab you want to engineer an enzyme with high activity and you are selecting the E.coli cells that show high activity of this enzyme. In that case the fitness (under the selection) is proportional to enzyme activity (unless there are pleiotropic effects). In fact there are (many?) research articles that have used the term in the context of molecular phenotypes.

I meant to say that I thought that "fitness" always refers to reproductive success under natural selection. But I suppose that if you also include reproductive success under artificial selection, then indeed any trait (even normally "bad" ones) could improve fitness.

But the following sites (Nature and Science) use the "silent mutation" as synonymous mutation.
https://www.nature.com/scitable/definition/silent-mutation-10
https://www.sciencemag.org/news/2006/12/sound-silent-mutation

Please provide more ocntext in case your links go dead. If possible, please include the formal citations of each article you link as well as a quote or page number where you are pulling from. Thanks.


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Are there any phenotypically visible examples of gene linkage in humans?
Are there any examples of two "visible" or "obvious" phenotypic traits in humans that are a priori unrelated, but which tend to be inherited together (i.e. their inheritance probabilities are correlated) due to genetic linkage from their proximity on a chromosome?
I know that peas' flower color and grain shape are genetically linked, but are there any similar examples in humans?

Sex-linkage would be the canonical example.
In other words, people with phenotypically male or female sex characteristics have non-random genetic predilections towards specific X-linked traits such as hemophilia, color-blindness, Duchenne dystrophy, etc.
However, other classic examples would include linkage between blood group antigens and peptic ulcers.
For a general review of how linkage has been used historically in human genetic research see here.

The blood groups/peptic ulcers paper linked is from 1954 and behind a paywall. Given that peptic ulcers' cause wasn't sorted out for another 40 years or so and isn't a gene, I don't think it really fits the question here.

Sex linkage certainly counts, but I think there's a big difference from genetic linkage of genes on non-sex chromosomes. If I understand correctly, chromosomal crossover is fairly common between homologous chromosomes, so genes are faraway loci on the same chromosome are inherited fairly independently because there is a high probability of a chromosomal crossover occurring between those loci, so gene linking is the exception rather than the rule on non-sex chromosomes. But chromosomal crossover is much less common between and X and Y chromosomes because they aren't homologous (except at the ..

pseudoautosomonal regions). So if I understand correctly, gene linkage is more the rule than the exception for genes on the sex chromosomes, so it isn't as surprising, but it's more the exception off of the sex chromosomes.

@tparker The ballpark genetic length of human chromosomes is around 100 centiMorgans so very roughly two genes on a given autosome will have a fifty-fifty chance of being linked -- not so exceptional.

@Armand I'll note that the asker's post mentioned as an example phenotypes from peas that were discovered to be linked in 1905 (taking the linked wiki example)- it's not as if the mechanistic basis of those linked phenotypes was sorted out! Asker doesn't seem to be interested in burden of causal evidence here. Their prompt is "inheritance probabilities are correlated". Also, I have located on openly available version of the peptic ulcers paper, editing answer to include.

@MaximilianPress The pea phenotypes were in fact due directly to different but linked genes. Blood groups and peptic ulcer assocations seem plausibly to be due to the same gene, in which case genetic linkage would not be involved, but rather pleiotropy.

@Armand- interesting, I was not aware of the direct functional relationship. I'll look for some other examples.