Majority of transcripts are from sense strand? I am wondering whether majority of transcripts are transcribed from the 5'->3' strand? Because I encounter a lot of expressions like "anti-sense transcripts". Could anybody help clarify this? Thanks.

From my understanding sense and anti sense is contextual. If you are looking at a gene from 5'->3'(which is convention) that strand is the sense strand and the complement to the gene is the anti sense strand.

However further along the DNA there could be a gene on the 'original' anti sense strand, if you are discussing this new gene, there is a new context and it is now on the sense strand (oriented 5'->3'), and it's complement on the anti sense strand.

I hope that's clear.


Does DNA polymerase I require a $3^\prime$ end? DNA polymerase III adds nucleotides in the $5^\prime \rightarrow 3^\prime$ direction because it can only add nucleotides to the $3^\prime$ end of the previous nucleotide. This is why it requires a primer. However, does DNA polymerase I operate by the same criterion? Does it require a $3^\prime$ end of a previous nucleotide in order to bind successive DNA nucleotides?

If it does, then how can it do so for Okazaki fragments when each Okazaki fragment is unbonded to each other? It is the DNA ligase that finally catalyzes the phosphodiester linkage between the $3^\prime$ end $5^\prime$ beginning of two Okazaki fragments, isn’t it?

If it does not, then what’s the deal with telomeres? After each DNA replication event, the DNA gets shorter and shorter at the very ends because that final primer can be removed but not replaced by DNA via DNA polymerase I, correct? This suggests to me that DNA polymerase I requires a previous nucleotide's $3^\prime$ end to work with, and it has confused me regarding its action on Okazaki fragments in conjunction with DNA ligase.

DNA Pol I does require the 3' end of a previous nucleotide to initiate elongation.

Regarding Okazaki fragments, this is accomplished by the annealing of small RNA primers to the lagging strand part of a replication fork. DNA Pol I extends the lagging strand off of the 3' end of those primers, generating the Okazaki fragments. The RNA primers are later removed, leaving gaps between Okazaki fragments, which are later filled in through the combined actions of DNA PolI and DNA ligase.

In the case of telomeres, the final RNA primer can't be filled by DNA Pol I because polymerase requires a free 3' hydroxyl for the attachment of the first DNA nucleotide. After removing out the RNA primer, the first DNA nucleotide would need to be attached to the DNA nucleotide preceding it, which is not found in the case of the final primer on a telomere, since it's all the way at the end of the linear strand.

In this case then, DNA Pol I removes the RNA primer is removed by DNA pol I but cannot replace it with DNA, leaving a gap (step 6 in the following image).


To what extent does loss of neurons in the substantia nigra affect movement? There is a substance known as MPTP that is capable of crossing the blood-brain barrier. Once it does so, it is metabolized into a toxin called MPP+, which then selectively destroys dopaminergic neurons in the substantia nigra pars compacta of the brain, causing parkinsonism. This effect of MPTP was discovered when drug users were poisoned with it in the 1980s.

How much of an effect does this destruction of neurons have on movement? Were these patients completely paralyzed as a result, or did they retain some ability to move voluntarily?

Great questions!  Here's some quick answers, but I'll give an additional little recommendation at the end if you're interested:

How much of an effect does this destruction of neurons have on movement?

Answer:  A large effect.  The key term here is "Parkinsonism," meaning that the symptoms resemble Parkinson's disease. This often involves motor symptoms like shuffling gait, tremors, rigidity, and bradykinesia (which means slow movement).  While they typically don't result in total paralysis, these symptoms can be debilitating and require treatment, such as L-dopa.

Were these patients completely paralyzed as a result, or did they retain some ability to move voluntarily?

Answer:  Generally, these patients were still able to move, but they greatly struggled with controlled movements.  As stated above, Parkinsonism/Parkinson's disease is marked by many motor symptoms, but these do not result in complete paralysis.  Rather, they make voluntary movements more difficult and slower.  According to a paper entitled "The MPTP Story (doi: 10.3233/JPD-179006)" it appears that at least one patient was nearly (if not totally) catatonic and exhibited very little voluntary movement.

If you'd like to know why this is the case in Parkinsonism and Parkinson's disease, I'd encourage you to look up the direct and indirect pathways of the basal ganglia online.  There's likely a good lecture with helpful visuals on how these pathways work to facilitate (direct) and inhibit (indirect) movement by their effects on the thalamus and motor cortex.  Alternatively, you can let me know you're interested via a reply and I'll do my best to explain those pathways on here.  Hope this helps!


Identification: creepy dangling spiderthing Can anyone identify this creepy mess dangling from the cieling of my garage on a few strands of spidersilk? The thing is 5cm.

Should I burn down my garage and move to another country (Currently Belgium)?

It is probably a wasp mud nest with spider bodies (possibly still alive and paralyzed) used to house and grow their larvae.
See https://bugguide.net/node/view/560614
and https://ucanr.edu/blogs/blogcore/postdetail.cfm?postnum=28834
The wasps are commonly called "mud daubers" or "mud wasps."


Are the antibodies developed by differing vaccines still the same? If one person gets an mRNA vaccine that teaches their body to deal with a specific virus, and another person gets a similar but different mRNA vaccine, and another person gets a more "classic" vaccine with modified/weakened/dead virus cells, will there be any real difference in the antibodies developed by the three different people?
My gut instinct says that the antibodies/proteins developed by all of the people will be mostly identical, but I'm not a biologist.
I'm having difficulty finding articles/research on this. Full disclosure: this somewhat pertains to the SARS-CoV-2 and the varying vaccines, but it is also a more general question. I was hoping to find research on this, but it is proving difficult to google for such a verbose subject.

Due to the nature of the immune system, even people who receive the same vaccine will have a different set of antibodies.
Our immune systems generate a vast number of essentially random recognition combinations, unique to every individual. This leads to a polyclonal response to both infections and vaccines, involving multiple antibodies and the fine details of those antibodies differ based on the specific antibodies in the "library" that the person's body has generated.
Now, different antigens do result in different antibodies being selected for, so one might expect there to be additional differences due to getting an mRNA coding for a SARS-CoV-2 spike protein vs. getting a whole inactivated virus. There's a reason that the spike protein is the preferred target, however, in that its position on the outside of the virus leads it to be a focal point for the response to an inactivated virus.
Bottom line: the responses will differ, but will likely always have a varied set of antibodies targeting the spike protein in any case.


How does GTP help in the step of codon recognition? The anticodon of an incoming tRNA base pairs with the complementary mRNA codon in the A site.Hydrolysis of GTP increases the efficiency and accuracy of this step.
How does GTP do so ?

GTP based structural changes (even motor actions) are very common in biological systems. For e.g. G-proteins, Rab-GTPase (vesicular transport), Ran-GTPase (Nuclear export/import).

So all these GTP-bound proteins make use of an intrinsic or assisted GTPase activity to convert GTP to GDP. This conversion causes change in the structure of the associated protein. Going back to the GTP bound form requires proteins called GEF (Guanine nucleotide Exchange Factors).

So in the case of translation elongation, the elongation factor is a GTPase which changes confirmation upon GTP hydrolysis. This confirmational change twists the tRNA so that the bound amino acid moves closer to the peptidyl-transferase center (if P-site is in the left then the amino acid is bound to the rightward CCA tail of tRNA. The twist causes the amino acid to move leftwards- towards the P-site).

You can refer books like Genes by Lewin for details.


Does self replicating RNA occur in nature? Do self replicating, independent RNA strands occur in nature? They are often used in laboratory experiments but I have not heard of any wild populations. I mean independent of other organisms and able to reproduce on their own in the environment. I.e., not just viruses or transcription RNA.

They probably existed in the beginning of life (on Earth or somewhere else). But any free RNA now would be almost immediately devoured by bacteria or other organisms.

Bacteria are ubiquitous. That's one of the first things you learn in a microbiology course. We do this experiment a few times: open up a Petri dish far from a Bunsen burner, and in a few days you can see how many bacteria and/or fungus colonies have grown in the Agar. Any good microbiology book will show you this. I have none right now with me, but have just found a few links by  searching for "bacteria are ubiquitous" on Google: Understanding Bacteria, The Purple Phototrophic Bacteria, Bacteria in Agrobiology: Plant Probiotics and Public Health and Infectious Diseases.

As for the science studying the origin of life, I recommend The Fifth Miracle: The Search for the Origin and Meaning of Life, by Paul Davies.


Are there any motile plants? There are numerous examples of sessile animals (sponges, barnacles etc.) but are there any examples of motile plants? If not, why not? Surely mobility would have conferred an evolutionary advantage to some plant species. I am specifically thinking of locomotion here.

It depends how you define locomotion.

If you take it to mean moving from one place to another, then yes, almost all plants do this at some stage during their life cycle. Primarily seeds and pollen move around, and generally they do so by harnessing either natural forces like wind and rain, or by manipulating animals to do the leg-work, e.g.:

by recruiting pollinating insects
by having barbs which snag the fur of passing mammals
by producing tasty fruit so monkeys eat them, seeds included, and deposit them with a dollop of fertiliser somewhere else

If you take it to mean moving around under ones own propulsion, then yes, some plants do this. The example that springs to mind is the gametophyte generation of ferns:

The prothallus (i.e. the gametophyte) has rhizoids on the underside and uses them to slide around and find some space in which to start the next generation. I have seen this happen when fern spores are germinated on agar - when they reach the tiny prothallus stage, they start sliding around to avoid overlapping with one another. I can't find any references for this, but I'll keep looking.

Another example of self-directed locomotion in plants is the motile sperm of bryophytes. The male sex cells have flagella, which they use to propel themselves through water to the female sex cells (reviewed by Renzaglia & Garbary 2001).

Renzaglia, K.S. & Garbary, D.J. (2001) Motile Gametes of Land Plants: Diversity, Development, and Evolution. Critical Reviews in Plant Sciences. [Online] 20 (2), 107–213.


Have any genetically altered organisms actually become abundant in a natural environment? Most of the things that come up in Google and Google Scholar for this question have a mostly/completely speculative tone, or at best use models instead of measurements. This report describes some actual measurements in pollen transfer to neighboring fields from GM fields, though they all seem to have been one-off measurements at some unknown time after the GM plants appeared, rather than investigations on if the genes are becoming more common over time, which might imply the ability to become unavoidably common in some environments or even a weed/pest/parasite. This doesn't seem like an obvious problem to me, because the traits associated with those genes are always meant for the context of being farmed or raised by humans and therefore probably wouldn't contribute more to fitness in wild populations relative to the wild alternatives of those genes, but a few counterexamples would smash that belief to bits.

Many organisms including plants, bacteria, insects, fishes and even mammals have been GMed. Most of them have experimental purposes, but GM crops have been released for commercial purposes. Maybe the most amazing between them is triticale, which is a hybrid of wheat (Triticum) and rye (Secale). Triticale, BT Potato, BT Tomato, BT Maize (I am not sure), BT and Golden Rice and lots of other GM crops have been released in almost all lands in world. Almost all these GM crops suppose to have higher yield and higher resistance to pathogens and physiological problems and as a result they have higher chance of surviving (specially in natural environment).
A study published in Nature in 2001 reported that Bt-containing maize genes were found in maize in its center of origin, Oaxaca, Mexico. In 2002 Nature concluded that the evidence available is not sufficient to justify the publication of the original paper.  A significant controversy happened over the paper and Nature's unprecedented notice. Also there are safety concerns about modified gene transfer during pollination in GM Rice(s). Even some scientists think that that this would not be a problem because rice is a self-pollinating plant. Any way GM crops can become abundant and release their genes by themselves or through gene transfer to other organisms.


Are insects attracted to near infrared light? Do insects see near infrared light?  If yes, are they attracted to it at night, as they are to visible light sources?

I am building something similar to a home-made trailcam with a Raspberry Pi camera.  Currently I use an incandescent light source.  Obviously, it attracts lots of bugs.  I was wondering if the same is going to happen when I switch to an infrared light source.  This would be 850 nm or 940 nm, as these types of LEDs are commonly available.

In general, insects are most attracted to UV light. If you switch to a light source without UV-light, the amount of insects attracted will reduce to almost zero.
It has been hypothesized that this sensitivity to UV-light is because direct light sources (sun, moon) contains more UV than objects that reflect light. In this way, it may help insects to distinguish between open spaces and shelter.
It has long been thought that insects are blind to red and IR light. However, there is evidence that some insects do see, and are attracted to, IR light, at least up till 740 nm. However, red or IR light will attract far less insects compared to ypur incandescent light source.


What is this tiny lizard? This tiny guy stumbled into our house in the suburbs of Sydney. What species is it?

It's dark and has two yellow stripes going along the length of its body. They start on its head and go right above its eyes.

This looks like a Common Garden Skink (Lampropholis guichenoti)

Further information can be found here and here

The description is a quote from the first source:

  The colour of the skin of a common garden skink is mostly a brown-grey colour, and it usually has a black or dark coloured stripe down either side of its body and a copper coloured head. The diet of common garden skinks generally consists of insects and vegetation, and can include caterpillars, spiders, slugs, cockroaches, crickets, worms and ants, and fruit and vegetables. Small and enclosed spaces, such as rocks or trees, are the sought after home for common garden skinks, and they are commonly found in urban gardens, hiding in among plants or leaves. Common garden skinks generally grow to a length of 9 centimetres (3.5 inches), and they have five toes on each of their four legs, as well as a long tail. Common garden skinks can release their tails when caught by predators, such as birds, cats and larger reptiles like snakes.


SARS-CoV-2 : does vaccination provide a better immunity than being sick and recover? I recently read in the news that countries are thinking to offer a "green passport" based on the vaccination against SARS-CoV-2, allowing vaccinated people to do things with less restrictions than the non-vaccinated :
New York Times
BBC News
Bloomberg
IATA
If those passports are to be put in place, why do they not include people that were exposed naturally to SARS-CoV-2, this number being bigger days after days (60 millions people, 17/02/2021) ?
Does that mean that vaccines offer more immunity than being exposed naturally to SARS-CoV-2 and recover ?
My questions don't address the ethical aspect of implementing a "green passport", I'm only trying to figure out if vaccination offers more immunity than being exposed to the virus. A possible answer to this question can simply be "we don't know so far" because of the lack of feedback on a long term view.

As @MikeyC and @jamesqf pointed in the comments, vaccines are better documented than the actual cases, whereas qualifying the immunity conferred by having recovered from Covid-19 would require large cohort studies.
However, one can follow up thir argument in many ways:

It would be reallys urprizing, if large-scale cohort studies have not been udnerway or already available by now: while nationwide testing may still be lacking in many countries, masive and repeated testing campaigns in specific regions are not a rarity by now. (see, e.g., here and here)
Hospitalization is not a necessary requirement for attesting a covid case - one could test unvaccinated persons for the presence of the Covid-specific antibodies.
There is much still unknown about the vaccines themselves - particularly about whether the immunity conferred is a lasting one, and whether.
Moreover, the fact that many people might have lived light cases of Covid does not make it easier for attesting the efficacy of the vaccines. Public authorities openly warn that the vaccine might be inefficient and a vaccinated person might be still a carrier of the disease.

In other words, "we don't know" is the most likely answer.
As the OP, I forgo the ethical issues raised by the "green passport" - these are not only those related to the restrictions on the individual freedom, but also the discrimination against the individuals to whom the vaccine is counter-indicated (e.g., allergics, pregnant women, people with weakened immunity, etc.)


How many paraphyletic groups can be formed from a phylogeny? How many paraphyletic groups can theoretically be created from this phylogeny?

I found (2n)-2. Is this correct?
This is not homework nor exam, just a question about paraphyletic groups.

If we define a paraphyletic group as any group on a phylogeny that is not monophyletic, I count there to be 2^n - 2*n paraphyletic groups for a fully ladderized tree with n tips.

There are 2^n possible groups of n species. Of these groups, 2*n of them are monophyletic: n groups containing a single species, and n groups containing multiple species.


How many virus infections does the average human have? According to the WHO:

67% of the population  are infected with herpes simplex virus type 1 (HSV-1)

Presumably there are other viruses as well that infect a lot of people. How many infections does the average person have?

Ignoring short-term (acute) viral infections, so only considering persistent viruses, probably on the order of 5-10-ish.  There are 8 human herpesviruses known, of which 6 (herpes simplex I, EBV, CMV, VZV, HHV6, and HHV7) are very common in humans, generally infecting 50-90% of a population.  There are over 50 strains of human adenoviruses, but only a few are very common and persistent; hAb2 and hAd5 are probably the most likely.  Then there may be a human papilloma virus or two persistently infecting many people, though the prevalence is lower than herpes or adenoviruses.  So, it's reasonable to assume that most people have somewhere around 5-10 persistent viral infections.

If you add in acute infections, and ask about all exposures during one's life, you're probably looking at thousands or tens of thousands of viruses, but the questions about what's a different virus and what's an "infection" become trickier.


Sex biased gene expression in the X chromosome It has been shown that the X chromosome is frequently enriched for female biased genes, and has a deficit of male biased genes. For example in this paper, and this one.

However, I'm struggling to find papers which test the general distribution sex-biased genes. I am trying to find out if the X is enriched for sex biased genes, e.g. if the X hosts 20% of all protein coding genes, it would be enriched if it carried 30% of all sex-biased genes.

Are there any such studies?

I think I found an answer tucked in the methods section at the back of the Allen paper where 15% of sex-biased genes were X-linked, I'd suggest this means that 15.55% ($100 \times (\frac{1075}{1075 + 4938 + 4323})$) of sex-biased genes are X-linked - other examples are still sought:

  "Genes associated with chromosomes 2 (4,323 genes, 37%), 3 (4,938
  genes, 43%), and X (1,705 genes, 15%) were used in the analysis; these
  chromosomes accounted for 10,967 (95%) of the genes... a further 547
  (4.7%) of the genes ... were omitted"

You can answer this question for yourself using the modMine data warehouse for modENCODE datasets.  All you need is a list of female-specific genes (using your identifier of choice, although FlyBase FBGxxxxxxxx are the simplest). You can use their list tools to upload your own list of identifiers, and then there are a bunch of widgets that will tell you things like GO Term enrichment, PubMed references, and one is a histogram plot showing the chromosomal distribution of your genes, and a second histogram showing the "expected" distribution. Access to many modENCODE sites can be found at www.modencode.org

Okay, I went and did this myself.  modMine was quite slow, but fortunately the intermine server at FlyMine is working fine.  I downloaded Supplemental table 25 from Graveley et al., Nature, 2011 and cut and pasted all of the "Female Biased" IDs for those rows that had FlyBase Gene Identifiers.  This figure shows the chromosomal distribution of the 928 genes:

The Labels on the X-axis do not line up properly (for some reason), so here is a table with the Chromosome names and the counts:

Chrom     Actual    Expected

2L:     157      169

2R:     176      186

3L:     143      173

3R:     174      217

4:       0       10

X:     264      150


What ways are there to determine how big genera are? I want to look at genera as a whole, across the animal kingdom to determine the range of sizes of genera. I have examined species richness and genetic diversity (pairwise distance from sequence data sets), but I am looking to find more ways to look at 'how big is a genus?' in terms of biodiversity. Any ideas or comments are greatly appreciated!

Bearing in mind that the information is bound to be incomplete (as is the list of existing species), you could use the NCBI taxonomy database. For example, checking the page for the Drosophila genus will give you an idea of its size.

For more precise numbers, you can download the taxdump.tar.gz file from NCBI's FTP server (link), extract it and run the script below on the file nodes.dmp (a dump of the database info).

#!/usr/bin/perl
use strict;
use warnings;
use Getopt::Std;
my (%opts,%children,%ranks);
getopts('t:',\%opts) || do { print STDERR "Invalid option"; exit(1); };

my $taxid=$opts{t}||die "Need a taxid: -t\n";

sub getchildren{
    my $p=shift; ## The taxid of interest
        my $found=0; ## will be 0 unless we find a new kid
    ## For each child of this taxid
    foreach my $kid (keys%{$children{$p}}){
     ## Get the kid's kids
     foreach my $gkid (keys%{$children{$kid}}){
         ## If this one hasn't been seen before
         unless (defined($children{$p}{$gkid})) {
      ## Add it to the list of this taxid's children
      $children{$p}{$gkid}++;
      ## We found a new one, we need to test again.
      $found=1;
         }
     }
        }
        ## If we found a new one, run again
        getchildren($p) if $found==1;
    }
    while (<>) {
        ## Remove trailing newlines
        chomp;
        ## Parse the current line
        my ($name,$parent,$rank,$rest)=split(/\s*\|\s*/);
        ## Save the current taxid as a child of its parent
        $children{$parent}{$name}++;
        ## Save its rank (species, genus, order etc)
        $ranks{$name}=$rank;
}

## Recursively get all children of this taxid
getchildren($taxid);

# Count only species as children
my @kids=grep($ranks{$_} eq "species", keys(%{$children{$taxid}}));

# Print out the results
printf "Genus %s has %s members\n", $taxid, scalar(@kids);

Assuming you are on or have access to a *nix environment, save that file as genus.pl and run it on the nodes.dmp, giving the taxid of your genus of interest:

perl genus.pl -t 9257 nodes.dmp

The output of the above example (Ornithorhynchus) is:

$ perl genus.pl -t 9257 nodes.dmp
Genus 9257 has 1 members

If we try on Drosophila, we get:

$ perl genus.pl -t 7215 nodes.dmp
Genus 7215 has 738 members

This is realy not the most efficient way to do it (far better to do this in the script itself but I don't have the time to implement that now), but if you don't mind waiting, this will give you the numbers for all genera:

for i in $(grep -w genus nodes.dmp | awk '{print $1}'); do
        perl genus.pl -t $i nodes.dmp;
done


Why does our face get red during anger? My attempt: This site says that it is due to flight or fight mechanism, which results in more amount of blood being passed to face causing red face.

But isn't it wasteful for our body to send more blood to face than to our muscles for efficient action?

Also an answer to this question says quite opposite.

So, I think that first site maybe wrong.

So, what exactly is the reason for red face during rage(anger)?

Evidence for my claim:

  Several physiological studies have demonstrated that human facial color also varies with emotional states. The face often flushes during anger, or pleasure, and sometimes goes pale when experiencing fear or fear mixed with anger.

Source:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5259783/

The comments and answer so forth are mainly related to the visibility and possible social and evolutionary explanation of the 'red face'.

While not discussing the social or evolutionary factors, I can give an overview of the biochemistry involved.

Anger and associated feelings such as stress are part of the 'fight or flight' response. This response is regulated mainly by the release of epinephrine and norepinephrine (the same as adrenaline and noradrenaline) into the blood stream by the adrenal glands, and from neurons into the synapses.
Wiki:Fight or Flight response
(Hence, the signal is send out both in the whole organism, and locally between neurons).

These hormones/neurotransmitters have a number of physiological effects:

They trigger a combination of vasoconstriction and vasodillation  in different parts of the body, meaning that the blood vessels constricted and widened, respectively, in different tissues.
This allows for a more effective transfer of nutrients to the muscles and brain. Wiki: Epinephrine
They trigger the increase of blood sugar by breakdown of glycogen deposits. Again, the body is in a situation where it needs to use the available energy ressources.
The heart rate is increased. Again, this allows for more effective transportation.

As listed above, the hormones related to anger both trigger the constriction and dilation of blood vessels in different tissues. Thus, the routing of the blood through the system also changes.

However, the routing of the blood seems to differ, depending on the exact feeling, where blood sometimes are routed to the surfaces areas of the skin, and sometimes away from them (by means of vasoconsttriction and vasodillstion, respectively).

Intuitively, this is can be a way of controlling the body temperature, as the body can expose the warm blood to the surroundings to a lesser or greater extent.

I don't think it is entirely understood, what determines this, but a guess could be that in situations of anger, the body has to be able to effectively use the muscles and fight, and thus also needs to be cooled, in order for the systems to work properly.
In situations of fear you might to hide instead for a long time and preserve the body heat and energy (just speculations).

Besides, it also could have a social impact.

But when blood is transferred to the facial areas, including the brain which needs energy to think quickly, and the skin surface for cooling down, it can have an affect on the perceived color of the face.

As noted by others, the degree of visibility is highly personal, as it depends on several factors such as the degree of hormone release, hormone sensitivity, anatomical features of the face such as placement of blood vessels, skin color and so forth.


What are the good and bad cholesterol ? I have question about cholesterol, as I know we can get cholesterol using vegetables and meat, so what is good and what is bad ?

Original Answer (posted originally as a Comment)

It is now accepted that high cholesterol causes atherosclerosis. Cholesterol a major component of the plaques that block arteries. 'Good' and 'bad' cholesterol refer to the way cholesterol is transported in the bloodstream.

'Bad' cholesterol is cholesterol in the form of low density lipoproteins or LDL, and 'good' cholesterol is in the form of high-density lipoproteins or HDL.

Or at least that is how it used to be. It is still accepted that high concentrations of LDL in blood promote atherosclerosis, that is high levels of LDL may still be considered 'bad', but drugs that specifically raise the levels of HDL have had serious adverse effects.

Check out this great article: Cholesterol and Controversy: Past, present and Future by  Jeanne Garbarino, especially the section on "Deconstructing Cholesterol: “Bad” is still bad, but is “good” still good?". It is hard to know what the current position is. And check out the work of Brown and Goldstein.

Edit

Goldstein, in his Nobel lecture, famously said (see here)

  Cholesterol is a Janus-faced molecule. The very property that makes it useful in cell membranes, namely its absolute insolubility in water, also makes it lethal. For when cholesterol accumulates in the wrong place, for example within the wall of an artery, it cannot be readily mobilized, and its presence eventually leads to the development of an atherosclerotic plaque.

Cholesterol may be synthesized in the body, or obtained from the diet.  The site of biosynthesis is mainly the liver. Cholesterol and fats (triacylglycerols) are transported in the bloodstream as lipoprotein particles, which may be roughly described as a lipid core surrounded by a protein coat, and may be viewed as a mechanism for transporting insoluble fat molecules (by 'coating' them with a soluble protein exterior).

There are five main classes of lipoprotein particles (see, for example, Berg): chylomicrons, very low density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), and high-density lipoproteins (HDL)

Cholesterol (and fats) are transported from the liver to other tissues in the form of low-density lipoproteins (LDL).  High-density lipoproteins, on the other hand, pick up cholesterol and fats in the blood and from specialized cells and transport them to the liver. Hence the names 'bad' and 'good' cholesterol.  (In reality, of course, things are more complex than this simple scenario: for a very readable account, see Berg).

The ratio of 'bad' to 'good' cholesterol, ie the ratio of LDL to HDL may be used diagnostically, and a healthy LDL/HDL ratio is about 3.5 (see Berg), but in view of the studies cited by Garbarino a low ratio due to high concentrations of HDL (rather than low LDL) might not be so great either. In fact, if LDL is in check, there may be no benefit to raising HDL (Garbarino article).  But I suppose the physicians will always find a way to waffle (and to charge for the privilege).

It is a common misconception that plants do not contain cholesterol. (My original answer to this question attempted to promulgate this nonsense). In particular, plant membranes do contain cholesterol. However, the amount of cholesterol in plants is low compared to that found in animals (Behrman & Gopalan, 2005).  But it is certainly not zero. The nucleus of maize shoots contain significant amounts of cholesterol, for example (Kemp & Mercer, 1968).

This great reference, Cholesterol in Plants, by Behrman & Gopalan (2005) suggests that the following paragraph should be inserted into biochemistry texts.

  More than 250 steroids have been described in plants.
  Of these,  perhaps  sitosterol,  which  differs  from  cholesterol by an ethyl substituent at position 24, is the most
  common.  But  plants  also  contain  cholesterol  both  free
  and esterified. Cholesterol occurs as a component of plant
  membranes  and  as  part  of  the  surface  lipids  of  leaves
  where it is sometimes the major sterol. The quantity of
  cholesterol is generally small when expressed as percent
  of  total  lipid.  While  cholesterol  averages  perhaps  50
  mg/kg total lipid in plants, it can be as high as 5g/kg
  (or more) in animals.

A great generalization is the following (Behrman & Gopalan, 2005)

  Prokaryotes do not contain cholesterol

These authors also suggest that one of the reasons for the common misconception that plants do not contain cholesterol is "legalities of food labeling that allow small quantities of cholesterol in foods to be called zero".

I suppose we should not be too surprised that plants can make cholesterol. They can of course, make steroids, the Mexican yam being the original source of a precursor of a particularly important one.

A key enzyme in the biosynthesis of cholesterol is HMG-CoA reductase, which is the target for statins, and these drugs  may be used to lower serum cholesterol levels (but there may be side-effects).

One interesting thing about the biosynthesis of cholesterol is that the final cyclization step requires oxygen which has lead to much philosophical and evolutionary debate (see, for example, here).

Finally, another quote from Goldstein

  Cholesterol is the most highly decorated small molecule in biology. Thirteen
  Nobel Prizes have been awarded to scientists who devoted major parts of their
  careers to cholesterol. Ever since it was first isolated from gallstones in
  1784, almost exactly 200 years ago, cholesterol has exerted a hypnotic fascination for scientists from the most diverse domains of science and medicine


What are the requirements for a stable carbon cycle in sealed "bottle gardens"`? The most famous example of a sealed bottle garden is David Latimer's bottle with a Spiderworth plant, pictured below, which has been sealed for 40 years. My own attempt at a bottle garden is failing and I'm looking to "debug" what's going on.

My garden is a 2 litre glass jar filled with gravel, sand and soil, filling about a quarter of the jar. The soil is rather damp. I'm observing the following: When the bottle is sealed, plants such as moss, strawberry shoots and seeds thrive for a couple of weeks. They will then wilt and worms that had hitched a ride in the soil try to escape. When opening the bottle, there is a strong smell exactly like manure. The brief exchange of air when opening the bottle is enough to allow the plants to properly rot over the coming days, with mold only now spreading. (This proves that oxygen was depleted before I opened the jar) I removed the dead plants, sprinkled seeds on the soil and closed the jar. The seeds germinated and thrived for a couple of weeks until the process repeated.

At first look, it appears that when oxygen has been depleted, anaerobic bacteria take over, producing H2S, which I assume kill the plants. Or are they killed by changes in pH under high CO2 concentrations? Why does this not occur for all bottle gardens? Is the problem that there's too few plants to keep up the oxygen level which keeps the anaerobic bacteria at bay, is it the waterlogged soil or some other factor I'm unaware of?

Latimer did something right with his bottle garden, which started with a seedling and some compost.

The problem lies in soil bacteria.
There has been a project on a larger scale: Biosphere 2. After their initial trial they realised $O_2$ levels are getting much lower from what was predicted. The scientists team investigated the problem deeper and came to the conclusion that there was a lot of dead organic matter in the soil, which got consumed by aerobic bacteria. There were also other hypotheses: not enough sunlight and $O_2$ sequestration by concrete.

A solution for you would be to make sure there is little organic matter in your soil. Perhaps use inorganic "soil" like sand + some nutrients. And also make sure there is enough sunlight.
Start also with small plants - too large plants in the beginning might change $O_2/CO_2$ ratio to abruptly during day and night cycle. (remember that plants are also consuming oxygen at night).


What cells would have the CD3 marker on them (other than T-cells) Do you know of any peripheral blood mononuclear cells that would express any amount (beit low or high) of CD3 on their surface (other than T-cells)?

CD3 is initially expressed in the cytoplasm of pro-thymocytes, the
  stem cells from which T-cells arise in the thymus. The pro-thymocytes
  differentiate into common thymocytes, and then into medullary
  thymocytes, and it is at this latter stage that CD3 antigen begins to
  migrate to the cell membrane. The antigen is found bound to the
  membranes of all mature T cells, and in virtually no other cell type,
  although it does appear to be present in small amounts in Purkinje
  cells. This high specificity, combined with the presence of CD3 at
  all stages of T cell development, makes it a useful
  immunohistochemical marker for T cells in tissue sections. The antigen
  remains present in almost all T-cell lymphomas and leukaemias, and can
  therefore be used to distinguish them from superficially similar
  B-cell and myeloid neoplasms.

Source: http://en.wikipedia.org/wiki/CD3_(immunology)


How is trangender female different from normal female biologically? I have read in many places that transgender people are usually people who are born with typical male or female anatomies but feel as though they've been born into the “wrong bodies.” The thing that I am confused about is that how someone can not be considered as normal just because he thinks he should not be what he is? I met a female who looked exactly like a normal female and she was very beautiful. She didn't know that she was a transgender till her mom told her that she was transgender when she became adult. What is biological difference between a transgender and a normal male/female?

Remi gives a good introduction to the various terms and definitions you should know when learning about gender identity. However, he didn't really address your basic question:

  What is biological difference between transgender and a normal male/female[?]

Except for some likely genetic differences, which we aren't even close to beginning to understand, there is no biological difference between two persons born with $XX$ sex chromosomes, one of whom identifies as female (cis-gender) and one of whom identifies as male, or somewhere on the spectrum between female and male (trans-gender). There is no difference physically - both have the same organs, including sex organs, and both have the same secondary sex characteristics. One cannot tell the difference upon gross physical examination, X-ray, blood test, etc. Gender is a social construction, and while the majority of people in the West have a gender identity that matches their biological sex, some do not, for reasons that are not yet clear.


If mutations are random, why do antibiotics 'cause' resistance? Full disclosure: I am not a biologist and this is more of a general question about understanding antibiotic resistance of bacteria.

We are always told that careless antibiotics use is the cause of new more resistant bacteria, which can obviously devastate huge societies and even have global impact. At the same time from my knowledge it seems that bacteria mutates in a purely random fashion.

So, thinking about this concept probabilistically, the virus mutating and antibiotic consumption seem to be completely disjoint events such as:

$$P(M|A) = \dfrac{P(M \cap A)}{P(A)} =\dfrac{P(M) P(A)}{P(A)} = P(M)$$

Where $M$ is the event that the bacteria mutates and $A$ is the event of taking an antibiotic. I couldn't find any research online as to how $P(M)$ is actually modelled or what probability distribution it even roughly follows, but intuitively it would depend on time as the longer the bacteria spends inside the host the higher the probability of mutation would be. So from this train of thought it would seem that taking antibiotics would actually be a good idea as to eradicate the bacteria quicker and give it less chance to mutate down the line.

I am obviously not trying to discredit hundreds of years of research and understand that there must be a gap in my thinking somewhere. My question is, why are we told that antibiotics cause antibiotic resistance even though the mutations are described as 'random'?

(ELI5 explanations are preferred as I said I don't come from a biology background)

There are many models for mutation accumulation (Liò and Goldman, 1998). The simplest model (Jukes and Cantor, 1969) assumes mutations to be a Poisson process. With a given mutation rate, the number of mutations accumulated will follow the Poisson distribution.

This basic model has been extended to include non-uniform mutation rate across the genome and different rates for different kinds of mutations. You can check out the link and the works it cites to have a better idea.

However, the answer to your question does not pertain to how mutations happen. Although there is some evidence that some antibiotic treatment can actually increase mutation rate (Long et al, 2016; Meouche and Dunlop, 2017, Windels et al., 2019), the main principle pertains to selection and not actually the mutations. Improper antibiotic treatment can lead to some cells with moderate resistance to survive, which in turn can evolve strong resistance. Here, we assume that the infecting bacterial pool already has enough variation (or develops during infection) some little resistance. Moreover, there is another phenomenon called persistence (ability to survive antibiotic, Brauner et al., 2016). Windels et al (2019) report that persistence can increase resistance.


Can far-UVC light be safely used as germicide? (help understanding a paper) I've been trying to familiarize myself with the literature on far UVC light as a germicide.  My question mostly pertains to figure 4 of this paper. The paper investigates the efficacy of 207 nm light for killing MRSA without damaging human cells.  Figure 4 shows that you can get 4 logs of cell kill for MRSA with relatively little damage to human cells.  The authors treat this as a very promising result.  This is where I'm confused:  Yes 207 nm light kills MRSA selectively, but it still kills a lot of human cells: to get 4 logs of MRSA cell kill, you need a fluence that kills 80% of human cells.  Killing 99.99% of bacterial cells while also killing 80% of human cells seems obviously not good enough.  But the authors don't touch on this point: They just point out that it kills 5000x more MRSA cells than human, and interpret the result as promising.  What am I missing here?

This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology! I'm glad we encourage such questions from curious people who want to learn more.

There is another paper here that discusses using a similar frequency range of UVC radiation (207-222 nm) as a biocide:

  The biophysical reason is that, due to its strong absorbance in biological materials, far-UVC light does not have sufficient range to penetrate through even the outer layer (stratum corneum) on the surface of human skin, nor the outer tear layer on the outer surface of the eye, neither of which contain living cells; however, because bacteria and viruses are typically of micron or smaller dimensions, far-UVC light can still efficiently traverse and inactivate them.

Safety perhaps derives from the relatively exponential damage that far-UVC light can do to bacteria and viruses, while the layers and types of human cells that would get exposed are surface cells and mostly already dead or expendable. A 20% constant survival rate of vulnerable cells may be an acceptable trade-off, as those cells which are vulnerable would not typically be exposed (short of a wound or other exposed tissue, maybe), while the figure you cite suggests that you can raise the intensity of UV light linearly and kill exponentially more MRSA (or other disease-causing bacteria).


What is the attachment after this gene name, following the comma: SULF1,hCG18956? What is this part mean: hCG18956? Is it an alternate naming convention for genes? I am trying to read in a list of gene names using R, but I don't have an extensive biology background.

There are some rows where gene names is not listed. Only something like this: hCG1809003. Does that mean there is no appropriate gene name?

Here, hCG stands for "human Celera Genome". hCG-prefixed protein and gene descriptors are used as a last resort for genes which are found only in Celera's database.

See for example http://www.ncbi.nlm.nih.gov/protein/119619226 , the gene you referred to as "hCG1809003". As the entry says, this was submitted by Celera in 2005 as a putative gene, after being found by "conceptual translation", that is, scanning the Genome Project data for start and stop codons. It is likely this gene has yet to be found as RNA or protein - because the only references for that gene are Celera's submission and the Genome Project paper. Nevertheless, Celera's sequencing (and microarray!) software and chips still look for it.

Your two example genes eventually made it to GenBank. The first example even has a proper name and function assigned - sulfatase 1. Many genes remain in hCG limbo.


Frogs stop croaking at same time I know frogs start croaking at the same time to attract a female.

Why do they all stop at the same time?

Calling is a risky activity because it makes the frog conspicuous to predators. When calling in a group, the risk to any given individual is minimized to the point that the minimal risk is outweighed by the advantage of attracting a mate. However, a single frog calling on his own is assuming all of the predation risk. So, the frogs are playing a bit of game theory and when too few are calling simultaneously to make the risk worthwhile, they will all tend to stop.


What could independent investigators learn from the first (known) copies of the virus from Wuhan, if they had (physical?) access to these samples? RFI reports:

"You have to remember -- these labs are still open inside of China these labs that contain complex pathogens that were being studied. It's not just the Wuhan Institute of Virology," Pompeo told reporters.
"It's important that those materials are being handled in a safe and secure way such that there isn't accidental release," Pompeo told reporters.
Pompeo cited the example of nuclear facilities, pointing to the rigorous global inspections to ensure safety.
He renewed concerns that China has not shared a sample of the initially detected virus, known scientifically as SARS-CoV-2.
"We still do not have a sample of the virus, nor has the world had access to the facilities or other locations where this virus may have originally originated inside of Wuhan," Pompeo said.

(China has now rejected this US call as being "politically motivated" but they weren't terribly specific beyond that.)
Would China [physically] sharing "a sample of the initially detected virus" (which of course begets the question which sample is that precisely--but let's assume they share all 40 or so initial samples they reported/discovered back in Jan) have any scientific value? E.g. is [physically] sharing those samples (more broadly) likely to shed any additional light on the virus' origins? (In that regard, have Western scientists asked for those [physical] samples, or said they are important for China to [physically] share them, independently/before the US political leadership's involvement in the matter?)
For more context, a Yale med page from January says:

Two weeks ago, we didn't even know what the nCOV2019 virus was. Today, thanks to China’s quick public release of the initial nCOV2019 virus genome [...] To go from unknown pathogen to diagnostic tests so quickly is incredible! The scientists at the Fudan University, China CDC, Chinese Academy of Medical Sciences, Chinese Academy of Sciences, Zhejiang Provincial CDC, and the Thai National Institute of Health should be highly praised for making their data rapidly available to the public.

A bit later, Chinese researchers published a paper on 10 genomes from the initial outbreak in Wuhan. The (FASTA) data for those seems publicly available, although behind a registration page.
So, per comments below, if Pompeo means something else by "sample of the virus" (not physical sample[s]), what is that?

I'll take a shot at this. It's my impression that most of this is political rather than scientifically grounded.  There are reasons to want physical samples of viruses (rather than just genomic sequences), e.g. if you want to do experimental (in vitro or in vivo) studies on a particular virus strain. (It might be theoretically possible to edit the genome or reconstruct the genome of an earlier strain, but it's much easier if you have the desired viral strain in hand.)
Based on this Financial Times article (which may or may not be accessible without a subscription/accepting cookies)

Mr Pompeo added the Chinese Communist party had still not shared virus samples with anyone outside China, impeding efforts to understand how it emerged.
A researcher at Wuhan Institute of Virology, who declined to be named, told the Financial Times earlier this month that China had not shared samples of the live virus with the WHO as the country “had already published plenty of information” such as the genetic code of coronavirus.

It does seem that almost all of the research on the origins of SARS-COV-2 is based on genome sequences rather than on phenotypic studies (i.e., in vitro and in vivo studies of actual viruses).
I don't think viral samples would actually be very useful (that's why I said at the beginning that I think most of this argument is political rather than scientific). In principle I guess you could use the viral samples from an early stage  do experimental infections in different animal species, but I don't know that any researchers actually want to do that, and I don't think there's been enough phenotypic evolution in the last few months that the early-epidemic viral samples would behave that differently from current samples ... it's also likely that researchers could study the effects of particular mutations (observed in genomic sequence) by modifying viral samples they had in hand.
To take an example from an earlier pandemic, researchers have done experimental studies in mice to show how particular mutations influenced the virulence of earlier flu strains. This is an example where it's useful to have an actual virus rather than just the genome - but in this case the virus was actually reconstructed from knowledge of the genome ("two isogenic recombinant chimeric viruses were created with an influenza A/WSN/33 virus background containing the PB1 segment from the HK/156/97").


Are there species which is debatable if they should be classified as animals or plants? I'm watching a sci fi series and a character who is a biologist claims "even on Earth there are species which is debatable if they should be classified as animals or plants". I looked for examples of this and I couldnt find any. Is this true? Are there species which is debatable if they should be classified as animals or plants?

No, there are no such debates. Plants and animals diverged over a billion years ago. Animals are defined by the unique molecules that are secreted by the cells, and fill the intercellular matrix, like collagen. Plants have unique cell walls, chlorophylls a and b, and plastids. The unique characteristics of plants are given here: http://www.bio.miami.edu/dana/160/160S10_10.html
Although there may be animals like sponges that don't seem to move around a lot, or corals that have symbiotic relationships with algae, simply "behaving like a plant" does not make them plants. Similarly, there are plants that move and trap insects. But taxonomists would never confuse them with animals.


What does metal-dependent mean? I was reading about Cas1 and Cas2 and came across this excerpt:

  ...Cas2 was identified as a metal-dependent endoribonuclease that cleaves ssRNA or dsDNA...

What does metal-dependent mean in this context?

It means that these enzymes need a metal ion as a co-factor for their function. This metal ion is typically bound somewhere near or in the active center and helps stabilizing transition states.

Without these metals, these enzymes cannot function properly, that's why chelating agents are used in protein or DNA preparations to inhibit their function.

References

Information available at cut rates: structure and mechanism of
ribonucleases.
The Role of Metals in Enzyme Activity


Convert gene name to uniprot ID I have a list of gene name in a file

CHRNB2
EGR2
GCK
KRT14
LMNA
FGF3
TK2
ABCC8

How can I map them to uniprot ID ?
P.S I tried Uniprot "ID mapping" (from-"GENEID" to-"UNIPROTKB AC"), but it couldn't map.
Please suggest me what to do.

ID mapping
This is called ID mapping. It used to be a headache as programmatic access was the only real way, but it is pretty trivial these days.
As mentioned in the comments, by far the most popular and easy method is to use Uniprot's list uploader for mapping. The corresponding publication can be found here. You must convert from Gene name to Uniprot KB ID
Programmatic access
The Uniprot web user interface will work for thousands of IDs, but is like to result in errors for queries exceeding 10,000 IDs. In that case, programmatic queries are probably better. I've slightly modified this from the Uniprot docs so that the IDs are queried 1 at a time to avoid any errors in exceeding query size. The python code would be:
import urllib,urllib2

list_to_convert = ["CHRNB2", "EGR2", "GCK", "KRT14", "LMNA", "FGF3", "TK2", "ABCC8"]
url = 'http://www.uniprot.org/mapping/'

print "From To"
for i in list_to_convert:
    params = {
    'from':'GENENAME',
    'to':'ACC',
    'format':'tab',
    'query':i
    }

    data = urllib.urlencode(params)
    request = urllib2.Request(url, data)
    contact = "" # Please set your email address here.
    request.add_header('User-Agent', 'Python %s' % contact)
    response = urllib2.urlopen(request)
    page = response.read(200000)
    print page.splitlines()[1] #Ignores the header line returned by uniprot

The output from this looks like:
From    To
CHRNB2  A0A096MXS8
EGR2    A0A096P554
GCK     A0A021WXA1
KRT14   A0A024R1X6
LMNA    A0A096MQV4
FGF3    A0A096NXI3
TK2     A0A096NJ58
ABCC8   A0A088S7J5


Can multiple antibodies bind the same antigen? Given the size difference between small molecule antigens and antibodies is it ever possible for multiple antibodies to bind to the same antigen if they recognize different domains on that antigen? When the antigen is a protein rather than a small molecule is it more likely that multiple antibodies can bind?

Not only is it possible for multiple antibodies to bind a single antigen, when that happens, it's more likely to trigger a full immune response.

Here's a description of the concept from a company that sells antibodies for research. To help understand the quote, you'll need to know that the portion of an antigen that an antibody binds is called an epitope.

  Because an antigen can have multiple different epitopes, a number of antibodies can bind to the protein. When two or more antigen binding sites are identical, an antibody can form a stronger bond with the antigen than if only one of the antibody’s sites is bound. Antigens with multiple identical binding sites are called multivalent, and antibodies are able to bind it more strongly.

Here is an article that describes, among other things, the importance of clustering in B-cells when multiple B-cell receptors bind to a single multivalent antigen.


Are all phenotypes normally distributed Reposting from the stats stackexchange.
John Cook, in his blog https://www.johndcook.com/blog/2015/03/09/why-isnt-everything-normally-distributed/, writes that many aren't:

Adult heights follow a Gaussian, a.k.a. normal, distribution [1]. The usual explanation is that many factors go into determining one’s height, and the net effect of many separate causes is approximately normal because of the central limit theorem.
If that’s the case, why aren’t more phenomena normally distributed? Someone asked me this morning specifically about phenotypes with many genetic inputs.
The central limit theorem says that the sum of many independent, additive effects is approximately normally distributed [2]. Genes are more digital than analog, and do not produce independent, additive effects. For example, the effects of dominant and recessive genes act more like max and min than addition. Genes do not appear independently—if you have some genes, you’re more likely to have certain other genes—nor do they act independently—some genes determine how other genes are expressed.
Height is influenced by environmental effects as well as genetic effects, such as nutrition, and these environmental effects may be more additive or independent than genetic effects.

I have two questions regarding this. First, I can't come up with any obvious example of phenotypes that don't follow a normal distribution. Could anyone help me? And second, his claims seem to contradict this other paper: https://www.uvm.edu/~dstratto/bcor102/readings/4_Evol_of_Phenotypes.pdf

To understand the genetic basis of quantitative traits, it is important
to think about the effect of a particular allele, not simply its
presence or absence. A single locus can produce three discrete
phenotypes, but as more and more loci contribute to a trait the
phenotypic distribution comes closer and closer to a normal (bell
shaped) distribution

Who is right here? Does the fact that genes are digital rather than analog really make a difference? And what about the second argument that they aren't independent. Is that really necessary (second paper seems to indicate otherwise if I am understanding properly).

Many phenotypes might be normally distributed assuming a large enough population size and many QTL (Quantitative Trait Loci) as the normal distribution is a simple result of the CTL (Central Limit Theorem). If it is unclear to you, you should definitely have a look at the central limit theorem.

Typically, if the number of loci is too low, the phenotype may for example follow some kind of continuous approximation to a Poisson distribution. Of course, if the allelic effects are correlated among loci or if there is some linkage disequilibrium or if the phenotype is bounded or discrete, or nominal, you may not end up with a normal distribution of phenotypes but all of that is a discussion for another time.

  I can't come up with any obvious example of phenotypes that don't follow a normal distribution

As, the second quote says, think of any phenotype that is discrete. Here are a few examples

sex
right / left handed
eye color

Now if you want a quantitative phenotype that is not normally distributed, then height (which is the bad example of your first quote) is very slightly bimodal due to an average height difference between male and females (look at Are males taller than females in humans?). You can also think of any phenotypes that are bounded. For example running speed. Athletes will cause a very long right tail, while people in wheel chairs will make a big stack of probability mass in 0 km/h.

There is a lot of things to consider when trying to guess whether a is normally distributed or not in a population. It will take some good knowledge of statistics and good knowledge of the genetics of the population.


Can yeast in a primary fermentation of wine be used as a source of yeast for new fermentation? So if I were to pitch bread yeast, and get to primary fermentation, which as I understand it, is the point at which regular cellular respiration can no longer continue due to a lack of oxygen , which is needed for the electron transport chain. Therefore the yeast switch to fermentation, which produces my desired product, ethanol.

But as I understand it, at this state the yeast are no longer reproducing and are in a survival mode.

Therefore if I were to cut a 2$L$ bottle of my primary ferment in half, and then add more sugar and water to the now separate 1$L$ bottles, and oxygen (if possible), up to 2$L$, would I be able to have the same amount of ethanol produced/would fermentation even occur?

I feel there would be diminishing returns even if it was possible, since yeast can only reproduce asexually so many times, which happens during stressful times, which this process might induce?

Yes, it is possible to reuse yeast in both beer and wine fermentation - commercial brewers do it all the time for cost savings and batch reproducibility, and although I'm not as familiar with making wine, many sites including this one say it's perfectly fine, as long as the viability of the cells is high enough.

The yeast aren't necessarily in stress-induced survival mode during fermentation, they're just living (and metabolizing) anaerobically. They may no longer be reproducing, or doing it very infrequently, but they'll remain perfectly happy little buggers (that's a technical term) for quite a while. Give them more food (sugar), and they'll keep fermenting. What eventually stops the process with wine is the level of ethanol rising too high for their comfort. If you were to dilute the ethanol out with water, they'd keep going.

Now, I wouldn't recommend doing this indefinitely (some strains may exhibit genomic instability, etc.), but new batches can certainly be produced with existing pitches.


What separates gene loci? Introns are sections of noncoding DNA that separate exons within a gene locus. However, between different gene loci, I also would assume there to be noncoding regions of DNA. What are these regions called? (And if my assumption is wrong, then please correct me.)

These regions, if unannotated, are simply called intergenic regions.

Sometimes, if a large section of chromatin is regulated by an enhancer/silencer/locus control element, then there are boundary elements that demarcate this chromatin region and prevent the spread of the chromatin state to neighbouring regions.


What are the major steps of follicular B cell development This is a learning objective in my curriculum, and after having spent two hours trying to answer it for myself using official course resources (many of which are online, but some of which are behind paywalls and so may be inaccessible to other community members), it's clear to me that I need some assistance.

So I would just like to know what is the latest understanding of the major steps of follicular B cell development in mouse and human.

According to Basic Immunology - Functions and Disorders of the Immune System (3rd Ed.) by Abbas and Lichtman (Copyright © 2011 by Saunders), p.133:

  A majority of B cells are called follicular B cells because they
  reside in the follicles of lymphoid organs. These follicular B cells
  make the bulk of T-dependent, class-switched, and high-affinity
  antibody responses to protein antigens and give rise to long-lived
  plasma cells.

and in the caption for FIGURE 7-2:

  Subsets of B cells. Follicular B cells make T-dependent responses to protein antigens, and marginal zone and B-1 B cells account for
  most of the T-independent antibody responses. In mice it has been
  shown that B-1 B cells arise earlier in development, from progenitors
  in the fetal liver, and follicular and marginal zone B cells arise
  later, from bone marrow precursors. Comparable differences in the
  origins of these subsets have not been defined in humans. Note also
  that the distinctions in the type of response are not
  absolute—follicular B cells can make T-independent responses and
  marginal zone B cells can make some T-dependent responses. Ig,
  immunoglobulin.

(emphasis not in original)

From the sentence I emphasized, it seems to me that as of 02011, there is still a great deal that is not well-understood about the origins (and perhaps also development?) of human follicular B cells.

Interestingly, in the 4th edition of this textbook (Copyright © 2015 by Saunders), the details have changed slightly (as below):

  Subsets of B cells. Follicular B cells make T-dependent responses to protein antigens, and marginal-zone and B-1 cells account for most
  of the T-independent antibody responses. In mice, B-1 cells arise
  earlier in development, from progenitors in the fetal liver, and
  follicular and marginal-zone B cells arise later, from bone marrow
  precursors. Note also that the distinctions in the type of response
  are not absolute; follicular B cells can make T-independent responses,
  and marginal-zone B cells can make some T-dependent responses. Ig,
  Immunoglobulin.

Most interesting to me is the removal of the 3ed sentence: "Comparable differences in the origins of these subsets have not been defined in humans." Which leads me to believe that comparable differences in the origins of these subsets have now been defined in humans (in the past 4 years).

So I have a definition and description of follicular B cells, but I am unable to find anything else in either edition of this book on the development of follicular B cells (in either mouse or human).

Another reference in my course resources is Cellular and Molecular Immunology, 8th ed., 2014, by Abbas, Lichtman, and Pillai.

In it (Chapter 12: B cell activation and Antibody Production), I find the following about follicular B cells:

  Distinct subsets of B cells respond preferentially to different types of antigens ( Fig. 12-3 ). Follicular B cells in peripheral
  lymphoid organs primarily make antibody responses to protein antigens
  that require collaboration with helper T cells.

Which strikes me as yet another description of follicular B cells, but not a list of steps in their development (which is my learning objective).

The same textbook makes several other mentions of follicular B cells, but does not address their development. Although I should probably already know this (and this may be in some of my lectures but these are not universally searchable and I have precious little time to read), I do not know about either their progenitors or their progeny, and I think this is what is meant by this learning objective: the major steps in their development.

In the same chapter of the same textbook, I also see:

  Most mature naive B lymphocytes are follicular B cells (sometimes also
  called recirculating B cells) that constantly recirculate in the blood
  and migrate from one secondary lymphoid organ to the next in search of
  antigen. Follicular B cells enter secondary lymphoid tissues (spleen,
  lymph nodes, mucosal lymphoid tissues) through blood vessels located
  in the T cell zones, and then they migrate into the follicles, the B
  cell zones of these tissues. The movement into lymphoid follicles is
  guided by the chemokine CXCL13 secreted by follicular dendritic cells,
  the major stromal cell type in the follicle, as well as by other
  stromal cells. CXCL13 binds to the CXCR5 chemokine receptor on the
  recirculating naive B cells and attracts these cells into the
  follicles. As we will discuss later, the same chemokine-receptor pair
  is also important during immune responses because it can attract a
  subset of activated T cells to the follicle.

This seems like a great description of the follicular B cell that also delves into its function, but seems to include nothing about its development.

The same chapter of the same textbook also includes:

  Naive follicular B cells survive for limited periods until they
  encounter antigen (see Chapter 2 ). Follicular B cell survival depends
  on signals from the BCR as well as on inputs received from a tumor
  necrosis factor (TNF) superfamily cytokine called BAFF (B
  cell–activating factor of the TNF family, also known as BLyS, for B
  lymphocyte stimulator), which provides maturation and survival signals
  through the BAFF receptor. BAFF and a related ligand, APRIL, can
  activate two other receptors, TACI and BCMA, which participate in
  later stages of B cell activation and differentiation (and will be
  discussed later). These cytokines are produced mainly by myeloid cells
  in lymphoid follicles and in the bone marrow.

This paragraph briefly address a little bit of what seems like the development of the follicular B cell ("Follicular B cell survival depends on..."). And in chapter 2 I see that follicular B cells are a class of B lymphocytes (along with Marginal zone B cells), but I interpret this learning objective as about the development of follicular B cells after they become follicular B cells, not before this point in their development.

So this is the best answer I can find on my own after many hours of searching and reading relevant passages in recent textbooks on the subject. Yet this answer also seems incomplete to me. After all this reading, I still have no "steps (per se) of follicular B cell development."

So I could really use a more complete answer.


Is there a maximum limit of connections between a pair of neurons? As neurons fire and work together, their connections strengthen. I was wondering if there was a limit on how connected neurons can be. If these neurons were constantly connecting then surely there would be an overload of connections at some point?

There's several ways neuronal connections can strengthen: growing the spine, increasing the amount of vesicles that carry neurotransmitters at the synapse, sensitizing and increasing the amount of receptors and yes creating more spines and synapses also.

Roughly, neurons can make tens of thousands of connections to multiple neurons the size of each spine is estimated to be between 0.01 µm3 to 0.8 µm3.

You are correct in saying that as life happens the connection would tend to grow to max and not encode anything anymore, however the brain seems to re-normalize all of its connections during sleep through special membrane channels.

Check out:
https://en.wikipedia.org/wiki/Neuron (especially the connectivity part)

https://en.wikipedia.org/wiki/Long-term_potentiation

https://en.wikipedia.org/wiki/Long-term_depression

https://en.wikipedia.org/wiki/Ion_channel


What causes knuckle "popping" and the feeling of relief that comes from it? Many people like cracking their knuckles. I have always been curious about it.
What happens when we crack knuckles?

What creates the POP sound?

Why do we get a relief-like feeling after doing it?

Nobody really knows where it comes from. The currently most popular theory is that pulling the joint apart leads the gases in the joint's cartilage to accumulate and form a bubble which then pops when you let it spring back. The only thing that has been researched is whether it has an effect on the joint, but people who do it regularly don't seem to have any problems with their joints more than anyone else (I'll find the reference once I have time). Apart from that it's hard to get funding for this kind of research because it has little practical use.

Relief like feeling? That must be subjective to you, I used to do it every now and then but I don't remember getting any relief from it. In that case, it's probably the same relief as other people get from picking their nose, their ears, biting their nails, etc. It's called compensation reaction.


Can an upper forearm amputee correctly control the Median and Ulnar nerves I'm an engineer who is looking to build a robotic hand for people without their upper forearm(from center of forearm in direction of hand), controlled by the Thalmic Myo(an EMG sensor). I am first checking for the idea's viability.

I was wondering if one who does not have their upper forearm can still send the correct nerve impulses for a desired hand movement through their Median and Ulnar nerves?

Yes, severed nerves still convey neural responses from the brain.

In fact, nerve potential recordings in the ulnar and median nerves of the stumps of arm amputees have already been successfully applied to control arm prosthetics (Jia et al. 2007; Kuiken et al., 2007.


How would a herbivore's digestive tract differ from a human's? How would a herbivore's digestive tract differ from a human's? What are parts (organs, tissues, etc.) or enzymes that can't be found in one but is in the other? Also, is it correct to say that a herbivore's digestive tract would be more complex than a human's because herbivore diets tend to  contain a lot of complex carbohydrates to digest?

It depends on the method of digestion the herbivore utilizes and what they eat, grasses, leaves, fruit, or nuts . Ruminants are only one form of herbivore. A wonderful introduction to the various methods can be foundd here. http://vetsci.co.uk/2010/05/14/comparative-digestion/#
For comparison gorilla which are far more herbivorous than human have a much longer small intestines which is one reason they need a much wider trunk. They also of course need larger teeth with thicker enamel and much larger jaw muscles to chew the tough plant fibers. Not so much more complex digestive systems just bigger/longer.


What is dental health like in animals? Do animals suffer from tooth decay, such as cavities? Is it to the same extent as in humans, or do animal teeth decay more or less? If teeth decay in animals as well, are there natural strategies animals use to heal it? And, lastly, how do animals take care of their teeth?

If this is in comparison to humans, the animals are more or less free from the two common dental diseases by which teeth are lost in humans. These are dental caries (dental decay)  and periodontal disease (gum disease).

Common to both the diseases is the biofilm which forms on the teeth known as dental plaque.

If the plaque is colonised by acidogenic (acid producing) micro organisms cavities are produced in the presence of refined carbohydrates.

The gum disease is produced by bacterial toxins from the plaque causing inflammation of the surrounding gum resulting in loss of supporting structures of the tooth including bone resulting in loosening and loss of teeth.

In animals in the wild, plaque accumulation is effectively controlled by the coarse unprocessed diet which has a very good scrubbing effect. Besides wild animals are not exposed to refined carbohydrates like sugars.

Hence wild animals do not have these two diseases. However domesticated animals on human diet are prone to similar diseases.

In wild animals severe attrition (wear) and fracture of teeth are more common.

Wild animals will not survive long without adequate number of functional teeth.


Cloning of a sheep.. Dolly? Dolly the sheep was a clone. When she was born she was eight years old on her 1st day of birth, her mother (from which she was cloned) was also eight years old. What is a molecular reason behind this - that Dolly was eight years old when she was born?

If you look at the replication of end of chromosomes, you will see that one of the strand gets shorter every time. To prevent the genes from being disrupted, the ends of the chromosomes have repetitive sequences called telomeres which shorten with every replication but will prevent the disruption of genes.

As you can deduce from the above information, there will be a certain limit to how many times a cell can divide.So, it has been thought that any organism ages because of shortening of telomeres.

Gametes have the enzyme telomerase which will lengthen the telomeres to full length so that the zygote formed will have unshortened telomeres. But, in the case of Dolly the nucleus was taken from a somatic cell and so the telomeres did not lengthen. The age of Dolly at the time of birth was thus the age of mother from which the nucleus was taken.

See : Telomere


Can mexican salamander regenerate any organ? Mexican salamander or few other species of salamander can regenerate limbs, tail etc. Do they have HOX genes for vital organs like liver, heart, brain, kidney?

If brain is damaged, can salamander grow it's brain to normal functioning again ?

I'm going to assume you meant Ambystoma mexicanum also known as the axolotl. There are other kinds of salamanders that live in Mexico, but the axolotl is widely-studied and sometimes called the 'mexican salamander'.

The axolotl has exceptional regenerative powers, and although I suspect this ability is shared among salamander larvae(even if not the adults) there's not much research into phylogenetic distribution of regenerative capability. So in the absence of a more refined answer I'm going to hope axolotl results generalize to other salamanders.

Axolotls, as long as they don't die, can regenerate nearly any part of their brain. As a rule, as long as they don't die they can regenerate from any injury. There are a couple exceptions(it's very hard to keep an axolotl alive without a heart, so that hasn't been tested) like the eye but in general they can grow back nearly anything.

The Hox gene research I've found was done explicitly on worms and frogs, but I would feel safe concluding that axolotl regeneration relied on a similar mechanism, and that therefore they have Hox genes for internal organs. I mean, they had to grow them the first time, right?


Protein bands not visible after sds page coomassie dye stain I am working with cell wall protein of Candida albicans and cryptococcus neoformans but after protein extraction and run on SDS PAGE my bands are not visible after coomassie staining. Can anyone tell me how to concentrate the protein so that bands can be seen on coomassie stain.
I am using Ammonium Carbonate buffer for extraction of protein. Also, the bands are visible on silver staining.

The problem here is concentration. Coomassie Blue stain can only detect protein band greater than or near to 50ng, in this case, the concentration of your protein is too low for detection. If you want to stick with Coomassie stain, you can try colloidal Coomasie stain instead because it has a much lower detection limit than Coomasie blue (between 10ng to 20ng).
In addition, I think what causes such low protein concentration is the poor solubility of yeast cell wall. One way to get around this is to increase solubility is through chemical hydrolysis, for example using diluted sulphuric acid1-3. This will partially solubilize mannas-protein outer layer of the cell wall and help you to obtain soluble yeast cell wall products.
References:

Theodoro, S. D. S., Putarov, T. C., Tiemi, C., Volpe, L. M., de Oliveira, C. A. F., Glória, M. B. D. A., & Carciofi, A. C. (2019). Effects of the solubility of yeast cell wall preparations on their potential prebiotic properties in dogs. Plos one, 14(11), e0225659.
OGAWA, K., & MATSUDA, K. (1994). Characterization of Manno-oligosaccharides Containing α (1→ 2)-and α-(1→ 6)-Linkages Obtained from Saccharomyces cerevisiae Mannan by Controlled Acid Hydrolysist. Journal of Applied Glycoscience, 41(4), 433-437.
Peat, S. (1961). Polysaccharides of baker's yeast. Part IV. Mannnan. J. chem. Soc., 61, 29-34.


There aren't any animals like hornets that hunt large prey (like a rabbit, or even up to a deer), right? Why not? There aren't any eusocial animals (hives of wasps, ants, termites, etc) that hunt large prey, are there?

I'm thinking prey in the size range of, say, a rabbit, or even a deer.

I can't see a rabbit or a deer having any real effective way to defend against a swarm of hornets, especially if you supposed that the hornets' venom could easily be adapted to be particularly effective against such prey.

Intuitively, this seems like it would be a lucrative little niche.

Like:

A swarm could bring down a kill without risking losing too many members.
The return seems like it could be very high.
There shouldn't be too much of a risk of losing much of the kill to scavengers or whatever.
And after starting down the evolutionary pathway into such a niche, they could easily develop methods of preserving meat (I'm imagining a horrifying hive full of natural ham, here).
Protecting this ham-hive wouldn't be any more difficult than protecting a honey-hive from bears etc.

And such a niche doesn't seem that evolutionarily distant from where hornets already are.

Like:

They already do seriously hurt or even kill large animals that they perceive as threatening their hive.
They already do scavenge large animals they find dead, and even steal the occasional chunk of flesh from living animals.

But as far as I know, nothing like this exists, right?

Why not?

(And, like... maybe the most important question: How can we make sure it never comes into existence?)

They're not fast enough

A hornet has a top speed of around 40 kph, while a rabbit is only a touch faster, a deer can hit 75 kph (all figures from Wikipedia). In order to act as hunting insects they need to match the speed of these large animals in large enough numbers to surround and overpower them but these animals could easily match their speed or outpace them. Let's suppose they can overcome that limitation somehow and bring the prey down. They've now bagged a big lump of protein but it's a long way from the hive because they've had to chase it down first. That means that a long round trip is required every time they visit the kill and thus reduces the energy yield as well as increasing the chance of losing it to scavengers.

Against this you have the simpler option of eating smaller, easier to catch, prey as they do now.


How do antioxidants affect human metabolism? I'd like to know how antioxidants affect human metabolism and which ones are essential for metabolic processes.

This mainly depends on which kind of antioxidants you're talking about.

Vitamin A and E are antioxidants acquired from the food
Superoxide dismutase, Catalase and the Glutathione system are enzymes produced by the cell.

Antioxidants keep the oxidative balance of the cell and quench free radicals which are generated by the mitochondrial respiratory chain. Very simplified: Antioxidants are thought to be anti-ageing compounds because free radicals destroy cellular compounds, which can be related to the ageing process.

I would be very careful with products claiming to contain antioxidants and be therefore anti-aging. This whole anti-ageing marketing is far from being scientifically proven.


Attraction and hormones levels Why do we ignore all imperfections in people we fall in love with for a couple of months, but after a certain period we start noticing imperfections?

Can hormones - or any chemical - be used to influence someone to fall in love with you?

Yes. The chemical/hormone that causes attraction is called serotonin. That's what causes attraction between two people. Theoretically, chemicals can be used to make people fall in love with you, such as MDMA, which increases serotonin levels. If the "animal" (such as a cat or a monkey), was in the same room as you and you gave the cat MDMA and you were the only one in the room, the cat would bind with you and seratonin would be released.

This is why MDMA and methamphetamine are known to cause homosexuality and fetishism, for the drug tricks the human into thinking that serotonin is formed with a guy who he is hanging out with or what he is doing at the very moment.

Another hormone that is a "love" hormone is called oxytocin, but this chemical will only cause bonding once the love is formed.

In short, serotonin makes someone fall in love with you, while oxytocin will keep someone in love with you.


How did the genetic code evolve? The genetic code is redundant, there are 20 amino acids for 64 possible nucleotide combinations (triplet codons). Therefore some amino acid are coded by several different codons. While leucine is coded by 6 codons, tryptophan is coded only by one codon.

[I am aware that the set of codons that code for one given amino acid tend to look alike each other more than random. Usually it is only the last base that does not affect the amino-acid that is encoded.]

I therefore do not think that the genetic code can be entirely be explained by “it happened to occur that way the first time” (at the origin of life or in the last universal common ancestor) “and it never changed”.

So, my questions are:

Why are some amino acids coded by a several codons while others are coded only by one or two?
Specifically, why is methionine coded by only one codon — AUG — which has also to serve as a start signal?
In general, how (by what mechanisms, selective pressures) has the genetic code evolved to give this pattern of redundancies?

This question is closely related, and the fascinating link posted by @JohnSmith is a good read.

In short, with a four-base system, and a codon size of 1, you get four possible amino acids.  Silly system.  A codon size of 2 gives 16.  Not too shabby, but not a lot of room for growth, and not enough for those 20 amino acids.  Codons of size 3 gives 64 - plenty of room to work with and it covers all your forseeable amino acids, and then some, without being too wasteful.

The redundancy, known as degeneracy, is pretty straightforward.  There's room to expand, and any redundancy/degeneracy will only reduce the likelihood of errors.  That's a huge benefit.  For some amino acids, the first two bases are enough.  That third position can be quite tolerant to mutation, which is very beneficial to organisms.  It appears to be even more fine-tuned, to the degree that redundancy often not only reduces the likelihood of mutation but also reduces the damage caused when a base does mutate.  Swapping a hydrophobic AA for another hydrophobic one is less likely to cause aberrant protein function, and anything with a U in the middle is probably hydrophobic.  Convenient!  I'll also note that, while it's not perfect or even a significant correlation, the more popular amino acids tend to get more redundancy; tryptophan is traditionally the least common AA.

Finally, there are a few non-proteinogenic amino acids, so, as the linked question/answer above points out, maybe in the future there will be more amino acids.


Neutralizing TCA washes Trichloroacetic Acid (TCA) is commonly used for protein precipitation but the wash waste needs to be neutralized prior to disposal. What exactly is required to effectively neutralize TCA waste? Do I just add caustic?

A neutralization reaction occurs between Brönsted acids and bases to form a salt.

In this case, you have to add a Brönsted base to neutralize your acid. If the final pH is important, you should work out the exact quantity of base to add. Otherwise, just use litmus paper to check the pH of your solution, and add base until it's neutral.

EDIT

In view of the other answer proposed, I want to stress the following:

Do NOT dispose of your solution in the sink/sewer. Leave it in its plastic bin until a lab technician takes it to the furnace.

If the base you use is sodium bicarbonate (NaHCO3), there will be bubbling, caused by the decomposition of carbonic acid (H2CO3) into water (H2O) and carbon dioxide (CO2). You've successfully neutralized the TCA once there's no bubbling upon addition of NaHCO3.

It is indeed best to proceed slowly while adding your base.


Systems Biology of triacylglycerol (TAG) synthesis in Jatropha I need the genetic regulatory network of TAG synthesis (Kennedy pathway) of Jatropha plant??
Or is there any way to convert metabolic pathway into genetic regulatory network?

Triacylglycerol synthesis in plants is probably highly conserved.  The metabolic pathway is here.

The Jatropha genome sequence is also available.

Given this some effort has been made to figure out how these genes are regulated.  This is a microarray study of Jatropha focusing on fatty acid and TAG biosynthesis.   This gives some idea of how TAG genes respond to one another, but of course will not find the promoter sequences or the transcription factors themselves.

Having spent a summer going over fatty acid synthesis, I can only say that there has been a lot of wet lab work done on these pathways which would probably be conserved in the Jatropha plant.  The literature would be quite extensive.  Integrating all of that is more like a paper for publication than an answer on stackexchange.  This sort of outlines the procedure... do you have a more focused question?

I'll outline one way of approaching this - there are an uncountable number of variants if you tweak it.  There are other ways to get this, most notably looking for defective mutants, the method which is still used in plants quite a bit.

Anyway here is a genome based approach:

1) Identify genes in the pathway of interest. choose 10 or so genes that you think constitute your network.  This is an editorial decision. Ultimately if you start looking at genes regulated by the same transcription factors as being included in your network, you will eventually take in the entire genome and the work will be impossible to accomplish.

2) find candidate promotor binding sites. look at the upstream promotor regions for all these genes.  you can look at how these are conserved between similar plants by examining the same gene promotor regions aligned against each other.  This doesn't work very well.

2b) Another way of finding these is to do a pull down experiment where transcription factors are bound to DNA and a DNAse digestion is done and remaining fragments identify the binding sites.  All this somewhat assumes that you kind of know which transcription factors are responsible for each gene. That is probably not the case here.

3) find the transcription factors important for the plant pathway.  this is not easy - one way is to try knock outs of the TF genes.  I imagine this plant has 4000 + of these genes.  around 1-2% may be involved.

So far these methods have been use for the ENCODE project as well as some bacterial genomes.  a plant is a new scenario which will have issues of its own.


What are the distinct neurochemical components of sexual pleasure? Sexual activity is usually described as pleasurable.

What neurochemical systems does sex activate? Does the presence or absence of a partner make a difference -- say, in the activation of the oxytocin system?

Undoubtedly, sexual activity is salient, and so it surely involves dopamine. (Salient activities, whether painful or pleasurable, activate the dopaminergic system.)

What about these systems:

adrenergic
gabaergic
cannabinoid
nicotinic
opioid
serotonergic
cholinergic
glycinergic
histaminergic
glutaminergic

Sexual response is primarily related to nitric oxide and its products. All of the systems you mentioned play a role, however the core pathway is from touch stimuli, to oxytocin release, to nitric oxide and dopamine accumulation, to motor response (orgasm) followed by prolactin to counteract said neurochemicals and temporarily suppress sexual response.


Using BLAST for molecular replacement in structural biology This is my first time trying to do molecular replacement to solve a protein structure. I am using the NCBI blastp program to find suitable search models. When choosing a search model, I understand that sequence identity is the most important -- but should I also take into account e-values or query coverage (i.e, what % of my query sequence is in the alignment) or any other factors for the purpose of molecular replacement? Thank you for your help!

Identity, Similarity, E-value are the key numbers, for the prediction of the 3D structure of proteins. The Length of the query and selected results should also be close to each other.
E-value:
The first value to look at is indeed the E-value.
For the most accurate predictions, E-values less than $10^{-100}$ are of extreme importance While E-values ranging between $10^{-50}$ to $10^{-100}$ come as the second priority. E-values less than $10^{-20}$ or so, should not be trusted. (As you know the larger amount of E-value accounts for random hits which may not have any evolutionary background with your query)
Similarity and Identity:
The ranges for these amounts differ for each survey and should be assessed with other statistics. Needless to say, Identities below 5% for amino acid blasts and below 25% for nucleotide blasts are useless. For proteins identity above 25% is acceptable and 35-50% (and more) are of greater importance. Similarity plays a more important role in the overall shape and structure of the protein. "Total score" in Blast NCBI should suffice for these evaluations.
Length:
The sequence length of your results should be reasonably near to one another. For example, having a sequence of 600 amino acids as your query, the acceptable range for the selected results (to eventually predict 3D structure with) should be 600 $\pm$ 30. Five percent difference is usually enough. Deviation from this would result in extra 3rd and 4th structures induced by other subunits.
Other considerations: In the case that your organism is known, pick the sequences which share a common evolutionary history with your organism of interest See Tree of life. The number of subunits and Symmetry types might be useful in some cases. Avoid selecting ab-initio based 3D structures in your results all the time and focus mainly on X-ray diffraction-based structures. If you're using the PDB website for data retrieval, Refinement Resolution is also extremely important. Try both CIF and PDB formats as input, as the results may sometimes improve.
At last but not least, try blasting using curated databases. In blastp, refseq_protein , swissprot , pdb , refseq_select are ideal.
This is just a rule of thumb and should not be generalized as the exact numbers differ substantially from one query to another.