Are peppers on the same plant genetically identical? I'm a hot pepper growing enthusiast and on one unknown super hot cross there is significant variation in pod size and shape.

What causes significant variation of pod shape and size on the same plant? Environmental factors? Genotype/genetic factors?

Also, what is a hot pepper phenotype? What makes a phenotype a phenotype?

Appreciate any input!

Also, what is a hot pepper phenotype? What makes a phenotype a phenotype?

Phenotypes are the quantitative or qualitative characteristics that arise from the interaction of an organism's genetics with the environment.  For pepper plants, height is a phenotype, as are leaf color, average fruit weight, and pretty much every other characteristic you can measure. Capsaicin concentration (mass of capsaicin per unit mass of fruit) is a phenotype that is relevant to hot pepper enthusiasts.

  What causes significant variation of pod shape and size on the same plant? Environmental factors? Genotype/genetic factors?

It's hard to know.  There could be a genetic component that results in inequitable distribution of resources to individual fruits during plant development. There could be environmental factors that determine why one fruit is larger than another -- perhaps the larger fruit developed during a time when water and sunlight were plentiful to the plant.

  Are peppers on the same plant genetically identical?

See this excellent answer given by mgkrebbs to the question Are the seeds in a single capsicum fruit genetically identical?


Is a fatty acid a polymer? From my understanding, polymers are long chain molecules containing repeating units of monomers.

For example, proteins are polymers called polypeptides with repeating units of (different) amino acids. Therefore, a fatty acid, saturated or unsaturated, would classify as a polymer as they are long chain molecules with repeating units of alkyl monomers?

Fatty acids are usually not considered polymers.

From a biological viewpoint this is simply because there is only a very limited set of chain lengths that exists in nature (~2-20 or so) and also even numbered chains are much more common than uneven numbered ones. In contrast to this 'true' polymers can have an arbitrary length of chain length (of course there is still a limit in biology, but not a super strict one) and no specific lengths are favoured.

From a chemical viewpoint fatty acids are also not really a polymer: you can't just take a bunch of alkyl monomers and fuse them to one long fatty acid  chain, because simple alkyl monomers don't have chemical groups that allow this reaction to take place (making C-C bonds is chemically not the easiest thing to do).


If birds are dinosaurs, then are mammals reptiles? I'm just curious - it seems generally accepted that birds are dinosaurs. If that's the case, then can we call all mammals reptiles? Can we go even further and call humans amphibians? And since single-celled bacteria were the precursor of all life, isn't just anything a bacterium?

Reptile is not a clade - it is a paraphyletic group because it does not contain all descendants (i.e. birds) of a common ancestor. Humans are amniotes like birds and reptiles but while birds and reptiles are sauropsids, mammals are synapsids. Humans are not amphibians either because amphibia is another paraphyletic group which is distinct from amniotes. Possibly some amphibians and amniotes share a common ancestor. Amphibians, sauropsids and synapsids can be grouped together under tetrapoda. So both humans and frogs are tetrapods but humans are not amphibians.

However, birds are dinosaurs and belong to a very specific sub-clade of dinosaurs called theropods. Both dinosauria and theropoda are monophyletic groups - i.e. they contain all the descendants of a common ancestor.

Extending this to bacteria. Yes you would group all living things (eukaryotes and prokaryotes) and can call them cellular living organisms.
However, animals (or any other eukaryotes) are not bacteria (they have diverged a lot). Moreover, extant bacteria are not precursors for all life. The precursor is called Last Universal Common Ancestor but we don't know much about it (at the moment it is a hypothetical organism). Eukaryotic evolution itself is a big mystery. So it would be  preposterous to call all lifeforms as bacteria.


How can we calculate the minimum sustainable number of the panda population? I have a degree in Biology so I'm a little embarrassed that I never learned this, but...

How do we know 1600 Pandas isn't enough?

I know that we have historical numbers (although I couldn't find them) which show the population has declined, but we also know the usable habitat has declined and it would be foolish to not consider that when trying to replenish the wild population. It seems to me that if there's only 1600 Pandas in the wild, that's probably the right number. How do we know it's not?

I will accept answers about other endangered animals, if they show how we can calculate the approximate "appropriate" number for a species.

Minimum viable population (MVP) can be predicted in two ways.

Computer simulations.
Population viability analyses (PVA)

PVA is considered generally more common practice by ecologists and without a reference to the 1600 panda population you mention, my guess would be that this is what they did. PVAs work well for endangered species prediction.

A typical example of PVA was carried out on an endangered species Fender's blue butterfly an endangered species (Schultz et al., 2003). However there is currently no scientific standard on how a PVA should be done.

Schultz, Cheryl B.; Hammond, Paul C. (October 2003). "Using Population Viability Analysis to Develop Recovery Criteria for Endangered Insects: Case Study of the Fender's Blue Butterfly". Conservation Biology 17 (5): 1372–1385.


Henrietta Lacks and HeLa cells Why did Henrietta Lacks die when her cells didn't die? As I understand it only the cells from her cervix were immortal so perhaps the cervical cancer took her life and the cells never died.

The cells never died in the sense that they kept replicating, individual cells still died. They were safely cultured in petri dishes before Henrietta Lacks died. The cells came from a tumor that developed from her cervix. The cervical cancer cells had developed high telomerase activity. Telomerase builds telomeres on the ends of DNA, protecting the chromosomes. In normal cells, telomeres tend to get shorter as the cells divide, eventually the DNA is damaged and the cells die. HeLa cells are protected because their telomeres are well maintained.

There was nothing special about Henrietta lacks that made her tissues immortal, so digging her up wouldn't be worth it. Her family would probably get mad too.


Can sexual selection operate in temperature dependent sex determining organisms? Or more broadly, are distinct forms of genetic inheritance (ie. sex chromosomes) needed for sexual selection?

My thinking was that since there are no sex determining loci, there could not be linkage to mutations that are subject to sexual selection.

Given the large sexual dimorphism in crocodiles (wikipedia), I would expect sexual selection is acting in crocodiles, but how are those phenotypes heritable if there are no sex chromosomes?
I know the sexual dimorphism could be due to differences in gene expression, but that still leaves me with a chick-egg problem. What causes the differences in expression?
I'd like to know if there are any studies that have looked at this kind of question.

Can sexual selection operate in temperature dependent sex determining organisms?

Yes! Crocodiles are indeed a good example as the sex in determined by the temperature (ref) and they have some traits evolving through sexual selection (ref).

I think you went almost all the way to the answer in your thoughts. Let's categorize things a little bit and talk about Genetic Sex Determination (GSD) and Environment Sex Determination (ESD) separately; that might help.

Note that ESD and GSD are two extremes of a continuum present in nature. Note also that I will talk about sexual dimorphism only and not specifically about sexual selection. Of course sexual selection is one process that can yield to sexual dimorphism. You can replace "locus involved in sexual dimorphism" by "locus involved in selection selection" in what follows and that will work as well expect that we will lose some generality.

Genetic Sex Determination (GSD)

Physical linkage

Indeed if you have sexual chromosomes, then you can have loci sitting on those sexual chromosomes that are affecting only one sex and therefore have genders with different appearances.

Gene expression

As you noted as well, those genes causing sexual dimorphism can also be sitting at different position in the genome and be regulated (directly or not) by the sex determining locus.

Environment Sex Determination (ESD)

If there is no genetic variance for sex but the whole variance is exclusively environmental (ESD), then phenotypic differences between males and females are just determine by whatever environmental variable (temperature for example) is used. In other words, you can have loci being under antagonist selection pressure between the two sexes that is regulated (more or less directly) by the temperature.

In short, you can have sexual dimorphism in ESD just like in GSD that...

the causal agent of the sexual dimorphism is not the sex determining locus but some environmental variable.
sexual dimorphism cannot occur through physical linkage (as there is no genetic variance to determine the sex) but only through regulation of expression.

I recommend this book (although a little expensive).

Do males of all sexual species have Y chromosomes is a somewhat related post but might be too introductory for you.

Here is a nice figure from Bachtrog et al. 2014 that offers an idea of the diversity of sex determination system (thanks @rg22)


What kind of snake is this? Seen in Peru along the Inca Trail I have been searching so much to find out what kind of snake this is. It looked black with white stripes. We found it on the Inca Trail to Machu Picchu in Peru. It was about 2500 m above sea level.

EDIT: Apparently M. medemi only exists in Colombia, not in Peru. Thus, as I'm not sure about the below ID. Instead of deleting the answer (users with <10k cannot see it), I just turned this into a community wiki, so I don't receive any RP.

By the shape of the head and the structure of the rings, it seems to me that this is a Micrurus.
Of course, the lack of yellow/red rings excludes the most common coral species, like Micrurus peruvianus. So, I'd guess this is a Micrurus medemi.
Here is another picture of it, for comparison:

Source: http://www.planetscott.com/speciesdetail/10840/coral-snake-micrurus-medemi
Some M. medemi specimens have white rings (like in your photo) while some have red rings.
They are venomous, but they are not dangerous: all Micrurus species I'm aware of are not aggressive, and bites are not common. As Wikipedia correctly says:

When confronted by humans, coral snakes will almost always attempt to flee, and bite only as a last resort.

The problem with this ID is that there are reports of M. medemi in Colombia and Ecuador, but not in Peru. I'll keep researching this and update this answer when I find a record (or delete it if I don't).


Exact location of E. coli in human body E. coli lives in lower intestine. But exactly where can we find E. coli, and where is there none (or a really small amount) of it?
I need the exact names of parts of the lower intestine where we can find E. coli.

In Gastrointestinal Tract Location of Escherichia coli O157:H7 in Ruminants (Grauke et al. 2002):

  in the lower GIT digesta, specifically the cecum, colon

It's about O157:H7, but I think the standard act a same.


glycogenesis, glycogenolysis and weight gain or loss I am under the impression (from dietary websites) that when excess serum glucose is stored as glycogen, body weight is increased and the reverse: when glycogen is converted to serum glucose, body weight is reduced.

I also understand that the glycosidic bond formation in glycogenesis is a condensation reaction, releasing water, whereas the rupturing of these bonds in glycogenolysis is a hydrolysis reaction absorbing water.

Please help me here: how does the body gain weight by releasing water and lose weight by absorbing water. What am I not understanding?

The answer to my question is that the glycogen molecule is extremely hydrophilic. For every gram of glycogen the molecule attracts 3 grams of water. When the glycogen is hydrolysed the attached water is excreted either directly in the liver or through cellular ATP processes.


Are there dangers to Teflon and aluminium cookware? I've been reading some articles on the internet about dangers of Teflon and aluminium to the body.

My family say I'm just exaggerating the situation, and maybe I am, though I'm not sure because not everything on the internet is true. They always tell me that if aluminium were dangerous then why would the government allow the use of aluminium bottles in drinks.

Are there strong references and facts to support dangers associated with aluminium or Teflon cookware? If aluminium or other chemicals enter the body from cookware, are they naturally eliminated, or do they remain in the body?

The US Department of Health and Human Services has a nice set of factsheets on aluminum. In brief, and to specifically answer your questions, they point out that:

Aluminum occurs naturally in air, water, soil, and plants.
The amounts of aluminum that we encounter in pots and pans are considered to be safe for healthy people. Cooking acidic foods in aluminum pots increases the amount ingested, but is still considered to be safe; and it still represents many times less aluminum than in over-the-counter antacids, which are also considered safe.
Much of the aluminum we ingest leaves ones body naturally through the digestive system (that is, feces), and is not taken up into the bloodstream. The small amount of aluminum that makes it to our bloodstream is mostly quickly eliminated in urine. Those with kindey problems may not process this bloodstream aluminum as quickly.

Nonstick pan coatings are a little more difficult, probably because they're so diverse. Cookware isn't even mentioned as a source on the factsheet for perflouroalkyls, the chemical which has been mentioned in connection with nonstick pan health issues. The US Environmental Protection Agency FAQ says:

  Consumer products made with perfluorochemicals include some non-stick cookware ... Consumer products made with fluoropolymers and fluorinated telomers, such as Teflon and other trademark products, are not PFOA. PFOA is used as a processing aid in the manufacture of fluoropolymers and can be also be produced by the breakdown of some fluorinated telomers [NB. I assume they mean overheating nonstick pans]. The information that EPA has available does not indicate that the routine use of consumer products poses a concern.


Cancer in cardiac cells We were recently taught that  cancer occurs only in those cells which undergo cell division so, cancer is not possible in cardiac cells and neurons.
But we know that till a certain age our heart grows in size so that means it goes under cell division. So doesn't that mean that cancer can also occur in heart cells?

As the other answer has already stated, there are cases of heart cancer. Just to expand on that answer further, according to this article, the rate of heart tumors is a mere 1.38 in 100,000 people per year and of that only around 10% are malignant (truly cancerous tumors) in nature. Just to put this into perspective of how low of a rate this is, the overall rate of cancer in the U.S. for both men and women combined is 352.2 per 100,000.[source]
Doing some rudimentary calculations, if the rate of malignant tumors is one tenth of 1.38 in 100,000, that means the rate of heart cancer is around 0.14 per 100,000! Just to add to how rare this is, the Mayo Clinic on average only sees around one case of heart cancer per year.[source]
Also, to clarify your statement about what types of cells can have cancer, it is not only dividing cells that can have cancer (even though the majority of cancer originates from cells undergoing a lot of cell division such as the skin and GI tract). While cell division by its nature causes a vast number of the mutations which would potentially lead to cancer, other environmental factors such as toxins and radiation could cause also cause similar mutations in cells that might not even be dividing.


Main methods used to predict functional annotations in GO Can someone provide me some information about the main method used to predict the inferred electronic annotations in Gene Ontology?

You can refer the IEA documentation maintained by GO consortium to get an idea about the automatically assigned evidence codes using IEA. Also please note that IEA is different from Computational Analysis Evidence Codes

ISS: Inferred from Sequence or Structural Similarity
ISO: Inferred from Sequence Orthology
ISA: Inferred from Sequence Alignment
ISM: Inferred from Sequence Model
IGC: Inferred from Genomic Context
IBA: Inferred from Biological aspect of Ancestor
IBD: Inferred from Biological aspect of Descendant
IKR: Inferred from Key Residues
IRD: Inferred from Rapid Divergence
RCA: inferred from Reviewed Computational Analysis


How does natural selection process escape from local optima? How does natural selection process escape from local optima towards global optimum in a fitness landscape during evolution?

From your profile, I see that you have some knowledge in computer science so I will try to use some terms from the field of machine learning!

Natural Selection

Natural Selection (NS) can only lead a population toward local optimum. In other words, NS is like a greedy algorithm. Mutations and genetic drift do not behave like a greedy algorithm.

Genetic drift

Genetic drift may allow to go toward the other direction than the heuristic of NS allowing eventually to reach another attractor. This concept is called shifting balance theory.

Mutations

Mutations can allow all sorts of jump! Mutations Causing large jumps are generally called large-effect mutations (see this section of the wikipedia article for more information).

Fitness landscape changes through time

Also note that the fitness landscape is not stable over time. The fitness landscape depends upon the environment the individuals experience. It would therefore be naive to assume that a specific population had to go through a specific fitness valley in the past just because the valley exists today.

Sexual reproduction and recombination

The fitness landscape analogy depicts the genotype - fitness relationship (some fitness landscape depict the phenotype - fitness relationship but I will ignore them here) for a given individual. One can place all individuals of a population over this landscape and may have some feeling of where the population position over the landscape is. However, this may be misleading.

The fitness landscape is highly multidimensional (one dimension for each amino acid and there are billions of them) and therefore through sexual reproduction and recombination, it is possible that an offspring finds itself in a totally different attractor than the rest of the population. As such, in presence of sexual reproduction and recombination, NS only could lead a jump from one attractor to another one (see Bergman and Feldman 1992). This effect is even more considerable in presence of epistasis.


Why do death cap mushrooms not warn of their poison? This has been puzzling me for a long time now. There is an evolutionary predilection for living things which have evolved strong defensive measures (that may not themselves be visible) to give distinct visual or audible warnings advertising these measures.
Wasps, hornets, snakes, and bees are all brightly coloured. Snakes may even have rattles to advertise their venom. These things by in large don't want to have to use their poison in a defensive capacity. Getting revenge on a predator who has mortally wounded you is a Pyrrhic victory.
These warnings are so potent that many animals without such measures will mimic these warnings in order to piggy pack on a general evolutionary bias towards an instinctive avoidance of anything that warns of being poisonous.
But take the death cap mushroom.

This innocuous fungus looks identical to completely harmless mushrooms. It has no foul smell. In fact, evidence shows that it actually has a pleasant taste! That picture above actually looks pretty tasty in my opinion.
This fungus has gone to the trouble of developing one of the most potent poisons in nature (humans have a seriously robust digestive systems by animal standards, and yet a single death cap can easily kill an adult human).
So why so secretive about its arsenal?
I know this same question about evolving poisons that are not well advertised could be applied to a large number of animals, insects, and particularly fungi, but I think the death cap is the most extreme example in both the lethality of the poison considered, and combined lack of advertising.

Most of this type of evolutionary question are generally worthless, IMHO. You can rationalize anything post hoc and then go away with the misapprehension that you have been involved in science.

To add a few of those possible post hoc explanations (which took longer to type  out than think up):

1) The poison is only accidentally a poison.  It serves some other function in the mushroom's metabolism.  There are numerous possible examples of this.  For instance, the stalks of rhubarb are edible, while the leaves are poison; potatos are edible unless they've turned green from exposure to sunlight...

2) The poison might not be directed at humans.  The mushroom might have some warning that would be obvious to other species, for instance a smell or markings visible in UV (such as many flowers have).  We have lots of examples of poisonous plants that we grow because they're attractive to us: datura, lily of the valley, foxglove, oleander, delphinium...

3) If I'm not mistaken, mushroom poisoning takes rather a long time to kill, which argues against it being a defense.  The poison might have evolved as an aid to reproduction.  Mushrooms are the fruiting body of the fungus.  If an animal eats it, it consumes the spores.  If it dies hours or days later, it has transported those spores to a distant location, and the corpse provides nutrition for the new fungi.

However…

Doesn’t the all-white toadstool look distinctive and memorable to you? It doesn’t look remotely like the field mushrooms or other edible mushrooms I would collect. What edible fungus would you confuse it with?


Dilution question about RNA I have a basic and probably silly question. I am isolating RNA with TRIzol. I have performed the basic steps and dissolved the pellet in 50 uL water. I ve measured the concentration and it was 3313 ng/uL (Around 165 ug total yield.). Now my next step is DNase treatment. It says 1 unit of enzyme for 1 ug of RNA in 10 ul reaction mix. I would like to dilute my RNA to 100 ug and use 100 units of enzyme in a 1000 uL reaction mix.

Is this logic true, and if it is how I am going to do the dilution?

Thanks!

If I understand correctly what you mean by "I would like to dilute my RNA to 100 ug":

Your RNA preparation is at 3.3 μg μl-1.

To add 100 μg to a reaction you need to add 100/3.3 = 30 μl

Then make the total volume up to 1000 μl with enzyme and buffer as appropriate.


What is the source of the fat in adipose tissue? I have heard the opinion that all of it comes from de novo lipogenesis of carbohydrates, but I'm skeptical. Is there evidence either way - either that dietary fat definitely gets stored in the adipose tissue, or that it never does, and all of it is from carbohydrate transmutation?

The proximal source of adipocyte lipids is mainly fatty acids from circulating lipoproteins (1) after hydrolysis by lipoprotein lipase (LPL).

LPL is activated by ApoC-II, which is present in hepatic-originating VLDL and IDL lipoprotein, but also chylomicron of direct dietary source. Insulin, secreted after meals, stimulates LPL production by adipocytes.

Thus the ultimate source of these lipids is both hepatic lipogenesis (from other substrates like glucids) and dietary fats.

Lipid transport in blood, for reference purpose (Michal G. Schomburg D., Biochemical Pathways, 2012)


Can all mammals swim? When I checked it seemed trivial to answer: yes, all mammals can swim. But research on the internet provided different information. I found:

people and primates cannot swim, but can be taught how to swim
giraffes can't swim
someone claimed elephants can't swim, but this video ad shows the reverse
porcupines nor rhinos can't swim
at least some bats can swim, but according to this source there's insufficient data.

Of each hit, I found other hits that claimed the reverse, sometimes with proof. Common sense tells me all mammals can swim, but is this true?

With respect to the giraffe claim, this article seems relevant:

D. M. Henderson, D. Naish, Predicting the buoyancy, equilibrium and potential swimming ability of giraffes by computational analysis, J Theoretical Biology 265 (2010) 151-159.

It cites several non-"random person on the internet" claims that giraffes cannot swim:

  It is generally thought that giraffes cannot swim, but relevant
  observations are few. Shortridge (1934) and Goodwin (1954) state that
  giraffes were poor waders and unable to swim. Crandall (1964)
  discussed a case where a captive giraffe escaped from a carrying
  crate, ran to the end of a jetty, and fell into the water. The animal
  reportedly sank without making any attempt to swim. MacClintock (1973,
  p. 54) stated ‘Giraffes cannot swim. Rivers are barriers they do not
  cross’. Wood (1982, p. 20) noted that ‘Because of its extraordinarily
  anatomical shape the giraffe is one of the very few mammals that
  cannot swim – even in an emergency! Deep rivers are an impassable
  barrier to them, and they will avoid large expanses of water like the
  plague’.

They then go on to show that a model giraffe could plausibly swim, writing: "For practical and ethical reasons we are unable to use live giraffes..."

They conclude:

  In summary, the results and speculations of this study show that it is
  not impossible that a giraffe could propel itself in water, but in
  terms of energy efficiency relative to that of the horse, it would
  appear that the costs of aquatic locomotion might be too high. It is
  reasonable to expect that giraffes would be hesitant to enter water
  knowing that they would be at a decided disadvantage compared to being
  on solid ground.


What controls the size of breasts? I am not a biology student, just a curious person. To be specific, I'm talking about female humans. I know that it might apply to other mammals.
What controls the size of breasts?
I have heard about progesterone hormone.

Is it just progesterone?

Are there any other factors?

I have seen a movie in which couple talks about breast size increases after sex. Is it true?

Can somebody give more info on this?

The known factors seem to be mainly oestrogen and genetic (although I haven't been able whatsoever to find detail on what genes):
Manning et al (1997): Breast asymmetry and phenotypic quality in women. Evolution and Human Behavior, 17 (2): 129–143.

Our data support the thesis that mammotropic hormones, particularly estrogen, are harmful because they suppress the immune system. Heavy women with high levels of body fat produce more estrogen and, therefore, bigger breasts. However, more estrogen leads to an increase in breast asymmetry. Women with “good genes” are able to produce symmetric breasts despite the presence of large quantities of estrogen. Large and symmetric breasts are therefore honest signals of high phenotypic quality in women.


Is there one centomere for the two chromatids in a dyad? I have no explanation for this. It is all I have to ask.

Thank you

Each chromatid has a centRomere. A chromosome is a pair of sister chromatids (general term)... also known as a dyad in meiosis. Tetrads are the precursors to separated dyads in meiosis. Having centromeres is super important for being able to pass down genetic information in eukaryotic cells. Prokaryotes and archaea have similar structures to physically keep track of their DNA.


Punnet Square for Genotype Probabilities I'm a computational physicist by trade, and today I was working with a student that is coding a simulation that requires the interactions of different genotypes to determine which phenotype will be expressed. This student drew a Punnent Square like so:

$
\begin{equation}
\begin{matrix}
& O & Y \\
\_ &\_ & \_ \\
Y& |YO& YY \\B &|BO & BY
\end{matrix}
\end{equation}
$

and then stated that each genotype should have a 25% probability of being expressed. I remember learning this as well in highschool bio, but since finishing my Bachelor's in Physics (with some focus on complex adaptive systems/chaos theory) I am a bit skeptical that biology really obeys the probabilities of the Punnet Square. Are there examples in biology where the probabilities of the Punnet Square are clearly broken?

Our germ cells are haploid, while our somatic cells are diploid. The diploid cells of a child result from the fusion of a paternal haploid germ cell and a maternal haploid germ cell. When these germ cells are generated during meiosis, the paired diploid chromosomes of each parent (which they in turn received one of from each parent) are randomly segregated such that for a given chromosomal pair there is an approximately equal chance of a given germ cell containing either member of the pair independent of the what other chromosomes it receives.

In the case of a single gene with a single copy on both the maternal and paternal chromosomes, the Punnet Square accurately estimates the probably of inheriting each possible genotype. (50% chance of getting one of two alleles from dad * 50% chance of getting one of two alleles from mom). In the case of multiple genes on different chromosomes, the 50% chance of any given allele still holds, as all the genes segregate independently. The accuracy of the Punnet Square fails when genes are sufficiently close to each other on the same chromosome. Genes distant from each other on the same chromosome still segregrate independently due to a high level of recombination events between chromosomes in meiosis I, but genes in close physical proximity no longer segregate independently. The closer two genes are physically the more they tend to co-segregate. This tendency is reported empirically as a "distance" in centiMorgans and is related to physical distance in base pairs (kB or mB) but is not completely proportional to physical distance due to the existence of recombination "hot spots."

It's important to note that is accurately predicts genotypic ratios, but not necessarily phenotype. Phenotypes can be less than 100% penetrant, can cause embryonic lethal, epistasis, etc. Such that the observed phenotypic ratio does not match the predicted ratio. (For example, if YY was known to be 100% embryonic lethality, live births -> observed phenotypes instead be expected at 1/3 of each of the remaining genotypes. If Y was instead phenotypically dominant (one copy of Y determines phenotype), then 75% of children would be expected to be phenotypically Y (genotypically, the Y phenotypic children would be expected to distribute evenly between YO, YY, BY).


Correct migration rate expression in infinite island model In Sewall Wright's infinite island model, where all demes exchange migrants each generation, I have seen the migration rate stated variously as $m$ or $\frac{m}{d - 1}$ (as in Matthew B. Hamilton's Population Genetics textbook, chapter 4, p. 132, figure 4.12), where d is the number of demes.

My question is, which expression for the migration rate is the correct one?

If it's the latter, then where does the "-1" come from?

Definition of $m$

There is no correct or wrong expression. It all depends what exactly you are interested in and what is the definition of m in a specific paper.

Def. 1

Some models assume that $m$ is the migration rate from a given population to another given population.

Def. 2

Some models assume that $m$ is the probability of migrating to any other population. In a two population case, this definition and the above are the same. In other case, the probability of migration to a given population is $\frac{m}{d-1}$

Def. 3

Some models assume a migration pool. With probability $m$ an individual is a migrant, goes to the migrant-pool and is then redistributed among all other populations (only works for island models). In such model, a migrant could be an individual that actually come back to the same population. So, the probability of really migrating is $\frac{m (d-1)}{d}$ and assuming equal migration rate among all populations, the probability to migrate to a given population is $\frac{m}{d-1}$.

Fst

If you're dealing with $F_{ST}$ in a finite island model, then you will have some $\frac{m d}{d-1}$ terms. I talk about it in this post but it is not complete, so you might want to read Slatkin (1991) and Charlesworth (1998)


What's the benefit of the average human body temperature? Why would the body choose a resting temperature of 36.1c to 37.2c? It seems a very inefficient mechanism of survival considering the typical ambient temperatures on Earth. If there is a benefit to needing to continuously do extra work, what is it?

What's the benefit of the average human body temperature?

It's a balance between preventing infection and not requiring excessive food intake. It is has also been claimed that this is the temperature at which the most essential enzymes are most reactive, without becoming damaged by excess temperature.

References:

"Mammalian Endothermy Optimally Restricts Fungi and Metabolic Costs", by Aviv Bergman and Arturo Casadevall, DOI: https://doi.org/10.1128/mBio.00212-10
"Fungal virulence, vertebrate endothermy, and dinosaur extinction: is there a connection?" (.PDF), by Arturo Casadevall, DOI: https://doi.org/10.1016/j.fgb.2004.11.008

  "The number of fungal species that can thrive and therefore infect an animal declines by 6 percent for every 1° C rise in temperature. This means that tens of thousands of fungal species infect reptiles, amphibians and other cold-blooded animals, but only a few hundred harm mammals.".

It is useful to refer to ectotherms (an organism in which internal physiological sources of heat are of negligible importance in controlling body temperature, which permits them to operate at very economical metabolic rates) as poikilotherms when applicable.

  "Poikilothermic animals include types of vertebrate animals, specifically some fish, amphibians, and reptiles, as well as a large number of invertebrate animals. The naked mole-rat is the only mammal that is currently thought to be poikilothermic.".

  "Poikilotherm animals must be able to function over a wider range of temperatures than homeotherms. The speed of most chemical reactions vary with temperature, and in order to function poikilotherms may have four to ten enzyme systems that operate at different temperatures for an important chemical reaction. As a result, poikilotherms often have larger, more complex genomes than homeotherms in the same ecological niche. Frogs are a notable example of this effect, though their complex development is also an important factor in their large genome.

  Because their metabolism is variable and generally below that of homeothermic animals, sustained high-energy activities like powered flight in large animals or maintaining a large brain is generally beyond poikilotherm animals. The metabolism of poikilotherms favors strategies such as sit-and-wait hunting over chasing prey for larger animals with high movement cost. As they do not use their metabolisms to heat or cool themselves, total energy requirement over time is low. For the same body weight, poikilotherms need only 5 to 10% of the energy of homeotherms.".

This update speaks to the theories on enzymes (solitary from metabolism), offered in other answers.

Articles and theories that are not discredited:

Enzyme assays by Hans Bisswanger:

That article is mostly concerned with the temperature used to conduct assays of enzymes.

  "The essential requirements for enzyme assays are described and frequently occurring errors and pitfalls as well as their avoidance are discussed. The main factors, which must be considered for assaying enzymes, are temperature, pH, ionic strength and the proper concentrations of the essential components like substrates and enzymes. Standardization of these parameters would be desirable, but the diversity of the features of different enzymes prevents unification of assay conditions. Nevertheless, many enzymes, especially those from mammalian sources, possess a pH optimum near the physiological pH of 7.5, and the body temperature of about 37 °C can serve as assay temperature, although because of experimental reasons frequently 25 °C is preferred. But in many cases the particular features of the individual enzyme dictate special assay conditions, which can deviate considerably from recommended conditions.".

  ...

  "Enzymes display their highest activity at their respective optimum conditions, deviations from the optimum cause a reduction of the activity, depending on the degree of the deviation. Moderate deviations produce only small activity decreases which can be tolerated (Figure 1), and so the physiological conditions prevailing in the cell may be taken as standards for at least of the mammalian enzymes. However, assay procedures are usually adapted directly to the features of the individual enzyme and not to obey general standards. Enzymes are sensitive substances present in small amounts and their activity in the cell can often be detected only at their optimum conditions.".

Royal Society of Chemistry - "Enzymes - Function and structure":

  "As the temperature rises, reacting molecules have more and more kinetic energy. This increases the chances of a successful collision and so the rate increases. There is a certain temperature at which an enzyme's catalytic activity is at its greatest (see graph). This optimal temperature is usually around human body temperature (37.5 °C) for the enzymes in human cells.

  Above this temperature the enzyme structure begins to break down (denature) since at higher temperatures intra- and intermolecular bonds are broken as the enzyme molecules gain even more kinetic energy.".

Note: Wikipedia: "Wilson's temperature syndrome":

  "The American Thyroid Association (ATA) describes Wilson's syndrome as at odds with established knowledge of thyroid function. The ATA described the diagnostic criteria for Wilson's syndrome as imprecise and non-specific, and raised concern that the proposed treatments were potentially harmful. Florida State Medical Board members described Wilson's syndrome as a "phony syndrome" and a scam during disciplinary action against Wilson."

  ...

  "The ATA stated in 2005 that a "thorough review of the biomedical literature has found no scientific evidence supporting the existence of 'Wilson's Temperature Syndrome'." The statement added that the mean temperature of normal persons in the AM on waking is 97.5 °F, not 98.5 °F, and that many of the symptoms described by Wilson are nonspecific and typical of depression, anxiety, and psychological and social stress. It also notes that a similar set of symptoms occurs in the alternative diagnoses of neurasthenia, chronic fatigue syndrome, fibromyalgia, multiple chemical sensitivity, chronic Epstein-Barr virus syndrome, and chronic candidiasis. Finally, the Association notes that chronic supplementation with triiodothyronine (T3) is particularly difficult and problematic, since various tissues set their own cellular levels of this hormone by making it individually from thyroxine, and supplementation of T3 may overwhelm this normal regulatory mechanism in some of these tissue.".

Reference: Wilson's Temperature Syndrome

"Metabolism Dependent on Enzymes"
"Enzyme Function Dependent On Temperature":

  "... when an enzyme-dependent chemical reaction is monitored for how well it takes place at various temperatures, the lower the temperature, the slower the chemical reaction. As the temperature is increased, the reaction rate will go faster with each increase until it reaches its optimum reaction rate. If the temperature is increased too much, the rate of reaction will diminish due to denaturing or change in shape of the enzyme.".

The treatment suggested by Wilson is what was discredited, the fact that enzyme reactions proceed differently at different temperatures is still supported. Reference to his article was included due to the partial overlap with established knowledge.


Identify this wild plant with brilliant scarlet red flowers Location is Virginia, USA

They seem to last all summer

It looks like some kind of Lobelia. A close up of the flower itself would be very helpful.

I believe it is a Cardinal Flower:

  This 1-6 ft. perennial has showy, red flowers in 8 in., terminal spikes. Each flower has three spreading lower petals and two upper petals, all united into a tube at the base. Erect leafy stems, often in clusters, with racemes of flowers resembling flaming red spires. The lower portion of the erect stem is lined with lance-shaped leaves.


Why is DNA double stranded and RNA single stranded? Why is DNA present as a double helix structure and RNA as a single helix? What causes the difference between them? What are the practical physiological differences between dsDNA and ssRNA? How are the key biophysicochemical features responsible for those differences? What is the role of these differences? Also, why is DNA preferred over RNA as the genetic material?

Though this is a basic question (a few google searches will provide all answers) and you have asked a lot of questions, I shall answer them one-by-one.

Why is RNA single stranded (and not double stranded like DNA)?

dsRNA is less stable than dsDNA.  See this: http://en.wikipedia.org/wiki/RNA#Structure. An important structural feature of RNA that distinguishes it from DNA is the presence of a hydroxyl group at the 2' position of the ribose sugar. The presence of this functional group causes the helix to adopt the A-form geometry rather than the B-form most commonly observed in DNA. This results in a very deep and narrow major groove and a shallow and wide minor groove. A second consequence of the presence of the 2'-hydroxyl group is that in conformationally flexible regions of an RNA molecule (that is, not involved in formation of a double helix), it can chemically attack the adjacent phosphodiester bond to cleave the backbone.
RNAses are very common.  Most critically, in biological systems, the presence of dsRNA is a signal of viruses and active transposable elements, so ssRNA is an easy way for the host cell to distinguish foreign elements.  Yes, that was an oversimplification and ignored functional dsRNA, but even then, dsRNA likely evolved from systems to foreign elements.1

Why is DNA double stranded (and not single stranded like RNA)?

Firstly, the 'information' part of DNA is the nitrogenous base, as opposed to the pentose sugar or the phosphate residues. In a single-stranded molecule, this important part would be exposed to the cellular environment, providing more opportunity for it to be mutated by the various chemicals there. In a double-stranded configuration, however, the two nitrogenous bases are locked within the complex, facing each other in the centre of the molecule. This organisation helps to safeguard them from local mutagens.

Secondly, having two complementary strands facing each other fundamentally means having two copies of the same thing placed right next to each other. This allows for proof-reading. George C. Williams summarised this beautifully in his pithy passage (from "The Pony Fish's Glow" (1997)) (recall that adenine [A] on one strand should always bind to a thymine [T] on the complementary strand, and visa versa; likewise cytosine [C] always binds to guanine [G], and vice versa i.e. Charagaff's rule).2

Source

What is the difference between DNA and RNA?

A complete table of differences can be found here (sadly I can't create a table in markdown) along with this image:

How are roles of DNA and RNA different?

RNA has several different functions that, though all interconnected, vary slightly depending on the type. There are three main types of RNA:

Messenger RNA (mRNA) transcribes genetic information from the DNA found in a cell's nucleus, and then carries this information to the cell's cytoplasm and ribosome.
Transfer RNA (tRNA) is found in a cell's cytoplasm and is closely related to mRNA as its helper. tRNA literally transfers amino acids, the core components of proteins, to the mRNA in a ribosome.
Ribosomal RNA (rRNA) is found in a cell's cytoplasm. In the ribosome, it takes mRNA and tRNA and translates the information they provide. From this information, it "learns" whether it should create, or synthesize, a polypeptide or protein.

DNA's genes are expressed, or manifested, through the proteins that its nucleotides produce with the help of RNA. Traits (phenotypes) come from which proteins are made and which are switched on or off. The information found in DNA determines which traits are to be created, activated, or deactivated, while the various forms of RNA do the work.3

EDIT- As you've asked another question in comments, I will add it here:

Why is DNA preferred over RNA as genetic material?

DNA offered several advantages over RNA so was chosen by natural selection to represent higher beings:

DNA was chemically more stable than RNA so it was possible to maintain greater length of DNA in comparison to RNA. RNA has hydroxyl group (OH) present on the 2’ carbon. This hydroxyl group invites hydrolysis reaction and so it was not possible to maintain long length RNA molecule. This hydroxyl group was absent in DNA leading to stability of DNA molecule.
DNA was more capable in handling self-repair during replication process due to the presence of Thymine instead of Uracil. It was due to the fact that often cytosine was changed into uracil due to the deamination. Now in case of RNA it was impossible for cell to know if uracil should be present there or not but in DNA since Uracil is not all present so it was quite easy to identify the error and rectify that.
DNA also offers more information security because of the double helical structure.4

A comparison of molecular structure of DNA and RNA from here

References:

https://www.quora.com/Why-is-RNA-single-stranded-in-general-and-not-double-stranded-like-DNA
http://medicguide.blogspot.in/2008/07/why-is-dna-double-stranded-but-rna.html
http://www.diffen.com/difference/DNA_vs_RNA
https://www.quora.com/Why-was-DNA-chosen-to-be-the-genetic-material-instead-of-RNA
http://www.atdbio.com/content/2/Molecular-weight-and-mass


Why do alpha-gal allergies only occur after a tick bite if alpha-gal is already present in red meat? I just read an NPR article about allergies to red meat being caused by tick bites. That stood out to me because I thought allergies are triggered by an initial exposure to some allergen. In this case, the allergen is alpha-gal, a disaccharide found in cell membranes of most mammals; humans and apes are a notable exception. The article explains that ticks might cause this allergy by transferring alpha-gal from other animals to us when they feed on our blood.

However, we also are exposed to alpha-gal every time we eat red meat. How are we protected from allergic reactions when we eat red meat but not when we eat peanuts? Why does that protection fail after alpha-gal is exposed to our bloodstream?

In order for the immune system to respond to an antigen, beyond recognition of that antigen, there needs to be a signal that there is something wrong. Co-stimulation can take a few different forms, but it requires the involvement of more than just one arm of the immune system, and generally helps prevent our immune system from what I like to call the Dr. Strangelove effect (a psychotic lone general can just decide that there is a problem and launch an attack). Here, costimulation might be from (or downstream of) the tick bite and other invaders associated with the tick bite, or from an allergy to peanuts. You can read about this in the first chapter of Sompayrac's How the Immune System Works, as well as the first chapter of Abbas Basic Immunology.


Are mediterranean sharks shyer than ocean sharks? I have been diving in the mediterranean for some time and have never seen a shark, heard of anyone seeing one or seen shark diving advertised. And still there are all kinds of sharks in the mediterranean. Why are they so hard to spot?

For comparison: There are a lot of accounts of people seeing sharks in for example the Maldives and other places.

Something like this would be unthinkable in the Mediterranean:
https://www.youtube.com/watch?v=Yg-dUPVzWiM

It really boils down to the species and the conditions. You are only able to cover a limited area and shallow depth and limited amount of time as a diver. Many species of shark are likely to know you are there before you know they are there and sharks can be shy and avoid divers. However certain shark spots can be popular feeding grounds, sleeping grounds, or mating areas. While I think there is a lot more historical pressure from fishing sharks in the Mediterranean, I don’t think there is anything innate about the sea there that makes all shark species there shy. I have heard of shark spots in Lebanon: http://www.nisd-online.com/article-101506-talesanddivesinlebanon.htm, though I do know the Red Sea offers a lot more in terms of shark encounters. There simply is a lot that goes into a shark encounter and we do not know nearly as much as we would like on their behavior. I’ve been on many dives in different parts of the world to see hammerheads in the wild and it can be a shot in the dark. It takes many years of local knowledge of the species’s behavior and conditions (season, tides, current, temperature, time of day, moon phases, undersea typography, etc). They are out there, but my best advice is to speak to fisherman and local divers, and also get creative in how you approach them (think about boat sounds, consider beach entries only, go in small groups, try early morning, try different seasons, etc.) Many scientists doing research on certain species in a locale find talking to fisherman to be a huge source of knowledge too.


Can a postsynaptic neuron 'shut itself off? I am an amateur interested in neuroscience and was curious whether there is a process by which a neuron or group of neurons would close their receptors and stop receiving signals from specific synapses for a temporary period?

An example would be the neurons that switch off/switch on based on our sleep cycle. Nerve-signaling chemicals called neurotransmitters control whether we are asleep or awake by acting on different groups of nerve cells, or neurons, in the brain. Neurons in the brainstem, which connects the brain with the spinal cord, produce neurotransmitters such as serotonin and norepinephrine that keep some parts of the brain active while we are awake. Other neurons at the base of the brain begin signaling when we fall asleep. These neurons appear to "switch off" the signals that keep us awake. Research also suggests that a chemical called adenosine builds up in our blood while we are awake and causes drowsiness. This chemical gradually breaks down while we sleep (reference and reference). Here is a study based on switch on/switch off of fear i mice (reference).

There are also artificial ways in which to shut down receptors like our sweet receptors (reference). There have also been studies done on other organisms where one particular study showed the switch on/switch off of olfactory receptors in cockroach antenna (reference).


Why does HIV chooses the Macrophage cells to infect first? Upon entering our body HIV directs the macrophage cells to manufacture more virus particles. It injects the Viral RNA into the Macrophages. With the help of the enzyme reverse transcriptase the Viral RNA converts into viral DNA that embeds into the DNA of macrophage cells. In this process the macrophages remain alive.

Just Curious-

Since Macrophage cells have phagocytic activity, why does HIV chooses them to be their Virus producing factory and not some other cell like RBCs which are apparently much more abundant and have no phagocytic activity at all.

In other words what facilitates the macrophages to be HIV's manufacturing plant?

Short answer

HIV infects macrophages because macrophages display the CD4 cell surface receptor needed for initial HIV attachment, and also display the co-receptors CCR5 and/or CXCR4 that are also needed for virus entry into the cell.

Cells that aren't good hosts for HIV don't have these receptors.

Addressing some confusion

You ask why HIV chooses macrophages as a virus producing factory. Be careful that you don't excessively anthropomorphise viruses - viruses 'choose' which host cell to infect in the same way that you 'choose' to feel pain when you stub your toe. It is a product of evolution, and not the result of a logical thought process by the HIV virus.

Other viruses happen to infect epithelial cells, or liver cells, or plant cells. HIV infects CD4+ cells. There is no 'best' option that viruses will somehow 'choose'. Anything that allows for successful reproduction and transmission is a viable option, and the rest is down to random mutations and evolution.

Red blood cells as virus factories?

Finally, you ask about red blood cells as a better host for viruses. In fact, red blood cells make very poor host cells for viruses, as they lack the cellular machinery required for DNA replication and protein production. It is this cellular machinery that is usually hijacked by viruses in order to replicate. Red blood cells lose their nucleus early in development, and it is only more complex organisms (such as the Plasmodium species that cause malaria) that can effectively hijack a red blood cell. These Plasmodium parasites have their own nucleus for protein production and DNA replication.


Why doesn't Sanger (fluorescent) DNA sequencing double count nucleotides? My understanding is that PCR is carried out until a fluorescent nucleotide halts replication. The segments of DNA are fed through the capillary tube based on size, sifting through the segments from smallest to largest; subsequently, the sequence is read from one end to the other.

I'm confused as to how we know that each nucleotide in the sequence has been accounted for, or if a nucleotide has been counted twice. If two fragments of the same size, ending with the same ddNTP, pass through the capillary tube at slightly different times, how do we know if that specific nucleotide hasn't been double-counted?

In chain-termination sequencing, a population of molecules is detected as opposed to a single one. The readout looks like this:

[ http://seqcore.brcf.med.umich.edu/doc/dnaseq/trouble/badseq.html ]

The peaks represent intensity of the four different fluorophores at the detector. Every fragment that is terminated at the same spot will have the same fluorophore and the same length. Because capillary gel electrophoresis separates molecules by size, these fragments will pass through at approximately the same time. "Approximately the same time" is why you see broad-ish and overlapping peaks on the readout as opposed to sharp and distinct lines.

Ideally, the readout will appear like the left half of the image, where there's minimal overlap between peaks. However, often you will see overlapping peaks, as in the right half of the image. The link above explains many reasons for why this occurs. Whether or not a peak is correctly assigned is determined by Phred scores, which is a statistical analysis of the shape and resolution of each peak.


B-cell and T-cell activation by parasites Parasitic infections lead to the production of parasite-specific IgE, but they also lead to the activation of nonspecific, polyclonal B-cells and T-cells. How do parasites trigger non-specific activation?

I've found a great article that says:

  Mitogens   and   superantigens   have   been   described   to
  explain the strategy used by microorganisms to avoid the
  host specifc immune responses and to ensure persistence.
  These  moieties  are  responsible  for  the  initiation  of  non-
  specifc  (polyclonal)  immune  responses.

Mitogens are chemicals (usually proteins) that promote mitosis. Superantigens (sAg) form a subclass of antigens and are capable of inducing massive polyclonal T-cell activation and cytokine release (Cytokines crucial role in immune system mediation). Their ability to inflict massive T-cell activation comes from the fact that they bind directly to MHC-II without any pre-processing, and stimulate T-cell activation.
Source: https://escholarship.org/uc/item/47g8w51m
Also there are B-cell sAgs that stimulate B-cells, and their activation.

These altogether (mitogens cytokines, sAgs) result in rapid expansion of B-cells and T-cells.

Also this paper might help to understand why parasites trigger polyclonal T and B-cell activation. Namely to avoid host specific immune system, dilute the pathogen specific anti-bodies. It is important to note that chronic infections could lead to several auto-immune diseases.


Stem cell and organ growing genitals I've been reading a lot about stem cell research and the work on growing artificial organs.

I assume, with sufficient advance in the technology, there is no theoretical reason it would not be possible to grow genital organs (gonads, uterus) in particular?

So my question is: is there any theoretical reason you could not use this process to grow the genital organs of the opposite sex of a stem cell donor?

So then, would an ovary grown from male stem cells potentially ovulate Y-gamete eggs?

No one knows if a uterus is capable of producing so-called "Y-eggs", because in persons affected by sex chromosome abnormalities (XXX and more, XXY, X, XYY, etc.), the presence of a functional Y generally produces a male phenotype, whether or not they are sterile or have natural levels of testosterone, because the Y contains the sex-determining gene SRY and other male developmental and fertility factors. In contrast, people with only X chromosomes (regardless of the number) are generally female-appearing, with at least some development of the associated organs and structures.

A second question is whether a male-derived stem cell could be coaxed, hormonally and otherwise, to become a uterus in the first place. An X is already present, so all the purely genetic (though not necessarily epigenetic) instructions are there, but, as far as I know, the question of whether a Y would interfere with the development process has not been answered in humans.


Question: Annotation search in scientific literature In a scientific paper I have been studying ("Predicting Novel Human Gene Ontology Annotations Using Semantic Analys" S.Draghici et al., 2010), I have read that authors checked the accuracy of their annotation predictions by searching on available literature the scientific evidence of their discoveries.

So, for instance, if they predicted an annotation X, they would search for scientific papers that prove that the predicted annotation is correct.

I think I could use the same method for my annotation prediction experiments, but how to do it? How to search evidence of a certain annotation by browsing literature?

Should I just visit PubMed website and use annotation id as keyword for search? And which source (EntrezGene, etc) id should I use?

Well here's my take.

Too bad there is no open access to this article.

I see that they only had statistics for the top 50 annotations, which implies a fairly manual process - you are going to have to read a bunch of articles or abstracts to decide directly whether the software is right.

In this case, the authors are using a weighted latent semantic indexing method, which have started with a bunch of articles for each gene.  In this case they would need to only look over the data they put into their training.

That might not answer your question though.  If you wanted to search through the literature to confirm annotations generated by a different method...you could create a semi automated process perhaps like this:

Do a rough search from NCBI in an automated fashion (I use biopython) and then read every article for validation of the Gene Ontology result.

Its possible you could search for the gene and the GO term if to get a more focused result, load them into a database or just create a set of files with the data.  I would build a little website that would let me scan through the abstracts with links to the complete articles (pubmed supplies DOI numbers) and just check 'yea' or 'nay' on whether confirmation happened.

There's other potential options on finding articles for search.  the Genbank record for the gene often has a few references in it. One might use pubmed's referencing feature, where you can start at these confirmed articles that describes the gene in question and use pubmed to show articles that have referenced that first article.  I'm not sure if this is accessible by API, but you can build an article graph by crawling the bibliographic references.

For anything that was neither directly contradicted nor confirmed you would have to go back to google and look until you found something.  Clearly there are genes for which you will find no reference at all, and you will have to avoid these for confirmation.

I'm not sure if they checked for any biases here. If something like interpro2go which generates GO mappings from protein domains was used to generate the annotations, you would want to take care that you weren't just rediscovering the references which helped generate the annotations in the first place.


Are there any viruses that integrate their DNA into organellar DNA? It is known that many viruses (e.g. retroviridae) integrate in the nuclear genome of their host as part of their cycle. However, I'd like to know if integration can happen in organellar DNA (cpDNA and mtDNA) as well.

I've found a paper proposing that some chloroplast genes have a viral origin; however, the virus would have been present into the ancestral alpha-proteobacterium that later became the chloroplast, so no direct chloroplast infection is involved.

There is also this almost identical question on ResearchGate, but frankly the answers there are not satisfactory.

I'm only aware of one paper that claims to show regular viral integration into mitochondrial DNA, and even there they suggest it might be a host defense rather than a viral life cycle thing:

Interestingly, 69.4% (50/72) of HBV integration sites were observed in human mitochondrial DNA (mtDNA) (Supplementary Table 2). ... However, 32% of HBV integration sites in mtDNA (16/50) were in the displacement loop (D-loop) region, which is known as the major control site for mtDNA expression as it contains the origin of replication for the heavy DNA strand and the major promoters of transcription (Figure 1B). Of note, we repeatedly detected mtDNA integration events through the same micro-homology site in independent mice, indicating the hotspot for HBV integration in mtDNA, which is probably related to replication or transcription. ...
We found that HBV integrations were mediated through MMEJ, which is known as an alternative DNA double-strand break (DSB) repair system and reported as a principal mediator during mitochondrial DNA lesions. This suggests that early-phase HBV integration occurred in mtDNA. Damage in mtDNA is known to induce autophagy and was removed in C. elegans, therefore it is possible that integration of HBV DNA into mtDNA might be a defensive mechanism to protect the nucleus from HBV integration.

--Characterization of HBV integration patterns and timing in liver cancer and HBV-infected livers
I would like to see this replicated and extended before I spent too much time wondering about functions and mechanisms.


Is there a type of amnesia that separately affects long-term memory? Is there a medical condition that affects the long term memory, but leaves the short-term and working memories totally or fairly intact?

If I understand your question correctly, what you are describing is retrograde amnesia.  This is further subdivided into pure, focal and isolated.

From the site:

  Typically, episodic memory is more severely affected than semantic memory, so that the patient may remember words and general knowledge (such as who their country’s leader is, how everyday objects work, colours, etc) but not specific events in their lives. Procedural memories (memory of skills, habits and how to perform everyday fucntions) are typically not affected at all.


Epinephrine vs. Adrenaline Both names are widely used, with what appears to me as a slight prevalence of “epinephrine” in scientific literature and an overwhelming prevalence of “adrenaline” in popular media.

Are there any well-documented and/or well-motivated guidelines for the usage of these terms?

Apparently I asked too soon. Summarizing my recent findings, I conclude that adrenaline is the better term.

To be more explicit, here is why:

The US National Library of Medicine recommends “epinephrine”, this is however mainly due to historical reasons (adrenaline used to be a trademark name in the USA).
This quite comprehensive paper on the issue presents a series of arguments for the use of “adrenaline”. These include: Better compatibility with other languages (where epinephrine is not at all in use); Better integration with other biological terms (adrenergic receptors, adrenal gland, adrenectomy, etc.); Better historical accuracy (epinephrine used to be the name for a neurochemically inactive crude extract from the adrenal glands).

I find the arguments of the referenced publication convincing, though I would recomend you read them in full.


Creating expression template from PCR: What annealing temperature to use? I am creating a transcription template for expression in PURExpress and was confused about the annealing temperature to use.

I have two primers with the T7 promoter and an RBS on the forward primer and a termination sequence on the reverse primer.  The melting temperature of these primers are 84.4 and 83.8 degrees C.  The melting temperature of the regions that are complementary to the gene of interest I want to amplify by PCR are both about 65 degrees C.

What annealing temperature should I use a h?  Since at the beginning of the PCR reaction I will have mostly template that will have the complementary sequences of the primers binding to the GOI and not the 5' and 3' extensions.

It seems the answer, which may be context specific, is to use an annealing temperature about 5 degrees below the entire oligo melting temperature.  I did not get any bands at lower temperatures.


Increase rate of change in coding regions? If a sequence is under selection will it acquire  more changes over time because of faster fixation than if changes were neutral? Is this true or am I missing something?

Generally speaking, there are sequences that are under purifying selection (where new mutations are often deleterious) and there are sequences that are neutral. Sequences under constant positive selection do not really exist. So, when you ask

  If a sequence is under selection will it acquire more changes over time because of faster fixation than if changes were neutral?

No! If a sequence is under selection, then it is under purifying selection. As such the rate of fixation will be lower than for a neutral sequence.

If you have a sequence, where most mutations are beneficial, then it the sequence would fix new mutations at a higher rate then a neutral sequence. However such sequence don't really exist! If it were to exist, then mutations would quickly fix such that new mutations would then be deleterious again.

Of course, a single beneficial mutation has a higher chance of fixation than a neutral mutation. Also, when a mutation is under selection (whether purifying or not), the expected change in heterozygosity in the population is higher than if the mutation is neutral (the expected change in allele frequency is equal to the additive genetic variance for fitness at this locus). But those are not details you are asking about.


Identification of a purple flower What is this purple flower? Picture taken from a garden in India.

It closely looks like Tibouchina urvilleana* or any other Tibouchina species. You can have a look here.

[Source:Wikimedia common]

  Tibouchina urvilleana is a species of flowering plant in the family Melastomataceae, native to Brazil. Growing to 3–6 m (10–20 ft) tall by 2–3 m (7–10 ft) wide, it is a sprawling evergreen shrub with longitudinally veined, dark green hairy leaves. Clusters of brilliant purple flowers up to 10 cm (4 in) in diameter, with black stamens, are borne throughout summer and autumn.[Source]

*Credits to @RHA for suggesting the right species.


If the xylem of a woody plant is composed of dead tissue, how does sapwood become heartwood? If the xylem of a tree is composed entirely of dead tissue, then that means the sapwood is dead. If so, how does it transform into heartwood, and what starts the process?

I'm no expert, but I liked this question and did a quick literature search:

Xylem cells are certainly dead at maturity, and it is these cells that make up the majority of what we call wood. However, wood also contains other tissue types, some of which have live cells at maturity. From what I can glean here and here, it is ray parenchyma tissue that is responsible for many of the changes that take place during the transition from sapwood to heartwood. Ray parenchyma is formed at the vascular cambium, along with xylem, during stem secondary growth (wood formation). Ray parenchyma cells remain alive for years after the xylem cells in the sapwood die. Their functions are transporting nutrients radially in the stem, and storage of carbohydrates.

As the stem grows in diameter, there is a zone of transition from sapwood to heartwood where the ray parenchyma tissue begins to die. Before it dies, the cells undergo some metabolic changes and begin to synthesize secondary phenolic compounds (many different kinds) from stored starch or sugars. Then, as ray parenchyma cells die, they dump these phenolics into the surrounding xylem tissue, and the accumulation of these durable, decay-resistant compounds in the xylem leads to the formation of heartwood. In many hardwood trees this parenchyma death and phenolic accumulation is preceded by vessel-plugging, in which the ray parenchyma cells form balloon-like growths that block the flow of water through the xylem. So, once sapwood changes to heartwood there should be no living cells left, and the water transport capacity of its xylem is gone or greatly diminished.

There appears to be quite a bit of variability between species in when heartwood formation occurs and what triggers it. From what I could see in my brief literature search, it is all under fairly complex genetic and hormonal control that remains an area of active research. I would suggest (and speculate a bit) that the trigger has something to do with maintaining an optimum amount of sapwood as the tree grows in leaf area (which increases demand for water transport) and height (which increases demand for support, or stem diameter).


Do the mother's genes determine the sons' (heredity) intelligence more than the father's? It is a general belief that a person's intelligence is determined by both nature and nurture.

I can find a study by Turner 1996 ( in fact, this is the motivation of this question), which makes the claim that since several genes which determine intelligence appear to be located on the X chromosome, the one men inherit from their mothers, and since a man only has one X chromosome inherited from his mother, so that's why mom's intelligence is very important to her sons, even more so than the father's!

Thus, my question is, do the mother's genes determine the sons' inherited intelligence more than the father's, as claimed by the above paper? In other words, a man inherits less intelligence from his father than from his mother? Note that I don't discount the possibility that the father could have helped to raise his son's intelligence by actively nurturing him in the correct way, just that as far as the "intellect genes" ( if there are such things) are concerned, the father plays less role than the mom.

A similar question is asked at Skeptic.SE, but it is geared more towards the contribution of mom's genes against all factors that account for son's intelligence, nurture and nature. My question is focused exclusively on the contribution of mom's genes vs. dad's.

Any new research on this front?

You might want to take a look on the wikipedia site for x-linked recessive inheritance. The article by Turner mentions that out of 325 known recessively inherited genes associated with mental retardation, 17 are positioned on the x-chromosome. In case you are a male and have one of these seventeen recessive genes on your x-chromosome causing you in some way to be less intelligent, you must have inherited that gene from your mother. In those cases it is more like you inherit "stupidity" genes from your mother, who might be an unaffected carrier of the stupidity gene due to the fact that she has two X-chromosomes and the gene causing mental retardation is only present in one of those x-chromosomes.

There might of course also be recessive genes on the X-chromosome causing males, who has only one X-chromosome, to be smarter but genes that are not causing disease might not be so interesting to investigate from a medical point of view.

According to wikipedia there are 499 x-linked genes and the total number of "vaguely defined traits" are 983.

I would say that yes, as a man you inherit more genes from your mother than from you father affecting your intelligence due to the fact that some genes on your x-chromosome affect your intelligence. Whatever the 499 x-linked genes do, you could say that traits affected by those genes to a greater extent are determined by your mothers genes than by your fathers, if you are a male.

Technically you would of course also have to take the genes on the y-chromosome, which are much fewer, into account.

If we approximate that the human male genome has a total of 20000 protein coding genes, the x-chromosome has 800 protein coding genes and the y-chromosome has 60 protein coding genes a male gets on average (19940/(19940+19200))*100 = approximately 50.945 percent of his protein coding genes from his mother. Now for a highly polygenic trait depending on genes homogenously distributed on all chromosomes one would naively expect that 50.945 percent of the genes contributing to that trait is inherited from his mother.


Why is our voice deeper in the morning? For most (if not all) people, their voice sounds a lot deeper when they've just woken, compared to how they sound during the day. This effect can easily last for a few hours, like for me today. What are the biological reasons for this? I've heard that it has something to do with relaxation of your muscles during sleep, but I'm not sure how that is supposed to work, and there might be other factors at work.

I'm surprised there hasn't been any answer or comments but yes, this is a fairly well known phenomena. It's quite possible that not everyone finds this to be true for them or possible they've never even noticed it. If a person doesn't need to talk for the first 15 minutes to hour, they might not realise their voice is deeper and/or raspier first thing in the morning.

Speech pathologists, voice teachers and professional singers are certainly aware of this. There's been no solid research on why that I know of. After all who's going to fund research into something that's mainly a curiosity with no medical repercussions or profits to be made? Still, there are various thoughts on why this occurs (outside of acid reflux irritating the vocal cords).

During sleep while we're in a horizontal position, a certain amount of fluid collects in our upper body (read from the neck up), so our vocal cords will swell and thicken slightly. It's why our eyes look more puffy first thing when we arise. During the night, we're not using our vocal cords either but while breathing, air is still passing over them. So while the tissues swell a little, their outer membrane dries a little. To counter the drying effect, the body secretes more mucous as a protective coat. This effect is much worse in people who are mouth breathers.

Another possible reason is what voice teachers and singers think happens, too. Vocal cords, being muscles, need to stretch and contract to vary the voice's pitch. Unused through the night, they're nit as limber and can't stretch as well as later. Vocal cords stretch to reach higher pitches. If that idea sounds far-fetched, just remember opera singers and other professional singers need to limber up before performing. They practice hours each day but before a performance, they need their voice to be at its best. Hence they'll practice singing notes up and down the scale.

Supposedly, drinking a cup of lukewarm water first thing in the morning helps, and tea or coffee is supposed to dry out the throat even more. I never drink coffee but, personally, I've found that first hot cup of tea in the morning doesn't just help my voice return to normal but wakes me up.

I've never heard of this effect lasting for a couple of hours though I haven't gone around quizzing people. :) So try either the lukewarm water or a hot drink and see if it makes a difference. You can also try singing or just talking aloud to limber your cords in the morning.

Edited June 14/17
Links (but not scientific studies) where others have noted this phenomena

Why do people's voices sound deeper in the morning? I gave greater credence to the first answer since it comes from an opera singer.

Raspy Voice In The Morning?

And from Music SE Why is my voice lower pitched when I get up in the morning


Do "scars" in humans replace all the skin layers or only some layers? When someone has a cut or surgical incision that results in a "scar", is the scar tissue replacing all 3 layers of the skin (epidermis, dermis, hypodermis)? Or only the first one or two of them?

This depends on how deep was the initial wound, and how that wound healed. There are mainly two ways a wound could heal, either by primary intention (like in surgically closed wounds), or by secondary intention (like in wound left to scar up with the edges not closed properly).

In very well closed wounds that involves all layers of skin, such as primary intention healing following plastic surgery on previously healthy skin, the skin would regenerate all the layers after a long process that could last for 2 years or longer and involves constant life long remodelling of the remaining scar.

In wounds healed by secondary intention, such as following a third degree burn without treatment with skin grafts, there is extensive scaring (mainly consistent of collagen which could be thought of as a filler and adhesive that allows the epithelial skin layer only to grow over it, without renewing the deeper layers). In such cases the scar is large, adherent to underlying tissue, and has only a thin overlying layer of epithelial skin cells. This scar might also be insensate (numb) as a result of superficial nerve injury due to the initial wound.

Most scars are somewhere on the spectrum between the two extremes mentioned above. A badly sutured surgical wound, or a surgical wound that gets infected later, might still heal by secondary intention causing extensive scaring that doesn't replace all the skin layers. A good plastic surgeon might later remove that scar and allow the wound to heal by primary intension to improve the outcome.

If you would like to expand on how wounds heal, here are a couple of links to start you off:

http://teachmesurgery.com/skills/wounds/wound-healing/
https://emedicine.medscape.com/article/1298129-overview


trp operon repressor Does trp repressor form a tetramer or a dimer before it binds to its corepressor tryptophan?
I've been reading BIOS Molecular biology it says that it is a dimer

  The repressor is a dimer of two subunits that have structural similarity to the CAP protein and lac repressor.

but according to wikipedia it is tetramer. What is correct?

Revised answer summary

My original answer provided evidence that the trp repressor is a dimer, and that conclusion stands, especially as regards its functional form. I still regard the statement in Wikipedia that it is a tetramer as incorrect, although I now see how it might have arisen. It seems to be a misinterpretation of results in vitro that show an equilibrium can exist between dimer and tetramer (not tetramer only). I have expanded on this in an additional section.

A functional dimer

The functional form of the is certainly a dimer, as originally reported by Schievitz et al. (1985). The summary of this paper includes the statement:

  “The crystal structure of the Escherichia coli trp repressor has been solved to atomic resolution. The dimeric protein has a remarkable subunit interface in which five of each subunit's six helices are interlinked.”

It was crystallized in combination with the operator DNA, and the structure deposited in the Protein Database (PDB) as 1TRO. I reproduce an image from the PDB entry below. Many other DNA-binding proteins also have dimeric structures.

A dimer–tetramer equilibrium observed in solution

The statement in Wikipedia probably arises from a report by Fernando and Royer (1992) — subsequently confirmed — that in solution there is an equilibrium between the dimer and higher oligomers (the tetramer predominating). Tryptophan was found to shift the equilibrium to the dimer. The authors claim that this has physiological relevance, although this still seems a moot point.


How do researchers map root systems of plants? For example, here is a picture of the root systems for some prairie grasses:

(Click image for higher-resolution PDF) from: http://www.conservationresearchinstitute.org/educational-offerings.html

How is it possible to follow one root thread 15 feet down? Especially when they are so densely packed in the top foot of soil that you couldn't dig at all without destroying roots.

You originally posted this question on the Garden and Landscaping Section - that's where I'm from, and though it was moved here instead, I'll answer it anyway:

That image you've shown isn't like a photograph, its an impression of what the roots are like. Usual method of working out root patterns on plants is to remove what's known as a monolith, or a block of soil where the plant is - the soil is then either carefully removed by hand, in the manner that archaeologists use, or air blasted, or soaked off in water to reveal as much of the roots as possible. For trees or plants with very large roots, newer methods include geophysical surveying by machine, or electric resistance surveying. Even this doesn't reveal everything - many roots may penetrate too far down, or run along cracks in rocks beneath the soil. The root length and distribution pattern vary according to local conditions, so its hard to be definite about where the roots of any particular plant are in a particular position in the landscape.

Reference and further reading:

Plant Physiological Ecology (ISBN 978-94-009-2221-1; Google books link)

Especially, check the Introduction on page No.367


Do humans have skin cells that trigger oxytocin release in the brain? I was reading an article by Montgomery on the therapeutic effect of pets (Boston Globe, January 12, 2015), and I found this quote:

  All animals appear to have cells directly under the skin that activate oxytocin in the brain. So gentle touch — from grooming your
  horse’s coat to making love with your spouse — is a powerful trigger.
  But so is simply thinking about someone you love, whether it’s a
  person or a pet. And in fact, a small study published this fall at
  Massachusetts General Hospital found that MRI scans of women’s brains
  lit up in the same areas when shown pictures of their pets as when
  shown pictures of their children.

Do humans have oxytocin triggering skin cells or formations under the skin? If so, are there higher concentrations of these cells in certain areas of the body? In the human erogenous zones, like neck, lips, etc?

Short answer
Oxytocin release has been associated with the cutaneous low-threshold (CT) afferent fibers in hairy skin.

Background
Oxytocin is released from the paraventricular nucleus in the brain in response to low intensity stimulation of the skin, such as touch, stroking and warm temperatures.

In a recent review Uvnäs-Moberg et al. (2015) report that the specific sensory nerve type mediating oxytocin release in the brain is unknown. Although myelinated somatosensory fibers mediating the discriminative sense of touch may be involved, a more likely candidate mediating affective touch are the unmyelinated low-threshold mechanosensory nerves, called C low-threshold mechanoreceptors (CLTMs) in animals or C-tactile afferents (CTs) in humans. Their terminal morphology (i.e., the skin receptor they connect to) is currently unknown. The fibers have been characterized mainly through  electrophysiological and electron microscopy research (McGlone at al., 2014).

The association of CT fibers with affective touch stems mainly from the finding that their activation patterns with various stroking velocities correlates with subjective pleasantness ratings. Specifically, the relationship between brush-stroking velocity and firing rate was distinctly different between CT and myelinated afferents. CTs showed an inverted U-shaped relationship,
whereas mean firing rates increased monotonically with brushing velocity in all myelinated afferents (McGlone at al., 2014).

However, CT fibers have only been identified in hairy skin in mammals, and the fibers mediating affective touch through glabrous skin (including the fingertips, palms and lips) are unknown (McGlone at al., 2014).

References
- McGlone et al., Neuron (2014); 82: 737-55
- Uvnäs-Moberg et al., Front Neurosci (2015); 5(1529): 1-16


How old does a baby have to be before it can retain memories? For most people (my earliest memories are of perhaps when I was 2 or so) their earliest memories would be when they were over a year old.

How old does the average baby have to be before it can retain memories?
Are there any preconditions that need to be fulfilled?

Surely an important question. But there are different kinds of memory (classified mainly as declarative and procedural) which you don't specify exactly in your question. Wikipedia and Scholarpedia list here many known facts. I will give you some short hints and links for introduction and overview instead of pasting that stuff here.

You are probably referring to autobiographical or episodic memory, that is memorizing consciously particular events within one's own life within a context. And for this type of memory researchers agree that self-awareness seems to be a necessary precondition. The existence of this cognitive ability can be checked by the mirror test. Human infants pass this test normally around a age of 18 months (also some animals). The cognitive self develops between 21 and 24 months and marks the end of infantile amnesia.


Diabetes-diabetes comorbidity Is it possible to have both type-1 (insulin-dependent) and type-2 (non-insulin-dependent) diabetes mellitus? That is, to have both insulin resistance and zero (or negligible) insulin production? If not, why not? And if so, then how common is this (among humans with each type of diabetes)? Any information on why the comorbidity may be high or low is also most welcome.

Yes you could think of an individual as having both(1).  A good place to start looking at "newer" diabetes other than the classic 1 and 2 is latent autoimmune diabetes (LADA).  Though, I don't know if one would say you had no insulin production.  It would seem as though patients exhibit some characteristics of both types(2), and indeed there maybe a continuum possible(3) between ether "pure" type on each extreme.

(1) The type 2 diabetes-associated variant in TCF7L2 is associated with latent autoimmune diabetes in adult Europeans and the gene effect is modified by obesity: a meta-analysis and an individual study. Diabetologia. 2012 Mar;55(3):689-93. doi: 10.1007/s00125-011-2378-z. Epub 2011 Nov 23.

(2) Latent autoimmune diabetes (LADA) is perched between type 1 and type 2: evidence from adults in one region of Spain. Diabetes/Metabolism Research and Reviews 2013; 1520-7560.

(3) Latent autoimmune diabetes in adults: evidences for diabetes spectrum?.Chin Med J 2013;126:783-788


When might an inhibitor of bacterial transformation be useful? I am part of a project elucidating some structures that are required for bacterial transformation. We have the opportunity to screen inhibitors of the system to stop it from functioning. I am not a microbiologist and have never worked with transformation, and this research process would be time and resource intensive. I am weighing up the pros and cons, however am struggling with how the inhibitors could be practically applied.

How useful would stopping transformation be? My thoughts so far boil down to:

Could it enhance controls by allowing two separate strains to grow on the same plate without any genetic conference?

Could it be applied to stop contamination of genetic information from otherwise insignificant contaminants?

Are there any other problems that transformation is causing in laboratory experiments?

In the research lab? I thought about it for a while and found no usage. But it could be interesting for clinical applications to prevent bacteria spreading their resistance genes (which are usually organized on extra chromosomal plasmids) and thus preventing multi-resistant bacteria.


What is the function of the human eye white? If you have a look at the eyes of most animals, you never see the white part unless the eyes are averted. In contrast, humans always have the whites visible because the iris is quite small. The only explanation I found so far is that the evolution made it this way because we are very social animals and we express a lot by eyes movements. I wonder if there is any other explanation?

Short answer
The relative large surface area of the white sclera in humans has been linked to an enhanced ability to detect eye gaze.

Background
The white of the eye is caused by the sclera. Human eyes indeed have the highest relative amount of visibly exposed white sclera. The amount of visible sclera provides information about the orientation of the eyeball. Specifically, the iris-to-sclera ratio is an important cue for eye gaze perception (Schulze et al., 2013).

Eye gaze is important. Most mammals generally interpret direct gaze as threatening, or as a sign of dominance. Humans, in contrast, tend to associate mutual gaze with positive interest, love and attraction. A preference for direct gaze seems to be present at a very early age. Infants as young as 2 days old prefer to look at faces that gazed directly at them, than to faces with averted gaze. Yet, humans sometimes find eye contact uncomfortable, for example if a stranger keeps staring at them (Schulze et al., 2013).

The ability to detect gaze has been established in many primate species, other than humans. Gaze detection may have evolved because direct gaze can signal that a predator is attending, making its detection an important tool for survival. Many animal species respond to the presence of staring eyes with displays of fear and submission, indicating that such stimuli act as warning signal. In humans, prolonged eye contact can also be perceived as an aggressive approach signal, as it leads to increases in galvanic skin response (Frischen et al., 2007).

The cooperative eye hypothesis assumes that the large scleral surface in humans developed especially for gaze detection (Tomasello et al., 2007). The authors base this conclusion on the fact that human infants mainly followed gaze, while several species of great apes (including gorillas and bonobos, but not macaques) mainly followed head movements.

However, from my humble opinion, concluding that humans developed a large relative surface of white sclera for communication purposes is kind of far-stretched. For one thing, macaques also have quite a large white scleral surface (Fig. 1.) and macaques share a dedicated neural circuit with humans that involves the superior temporal sulcus (STS). The STS is thought to process biological motion, including gaze. The STS projects to the amygdala, a structure of the limbic system that implicated in the processing of the emotional content of stimuli, including facial expressions and gaze detection. It links this information to emotional responses in the observer. There are also connections between STS and the intraparietal sulcus, an area that is associated with spatial processing and shifts of attention. Via these connections, information about eye-gaze direction could project to spatial attention systems to initiate orienting of attention in the corresponding direction, as in joint attention. Indeed, passive viewing of a face with averted gaze elicits a stronger response in the IPS than viewing a face with direct gaze (Frischen et al., 2007).

Fig. 1. Macaque. Source: Fine Art America

Personally, from these data I think the brain in humans and primates like the macaques adapted to process the information available from the eyes. It can be true, however, that brain circuits and eye structures developed/evolved in parallel to ultimately result in a large white scleral surface and a dedicated neural circuit to process its information.

References
- Frischen et al., Psychol Bull (2007); 133(4): 694–724
- Schulze et al., Front Hum Neurosci (2013); 7: 872
- Tomasello et al., J Human Evol (2007); 52 314-20

Further reading
- Frans de Waal


"The rhesus macaque is pretty much the closest thing we have to humans" -- why? Vincent Munster (researcher at Oxford) states (in the context of testing vaccines for COVID-19):

  The rhesus macaque is pretty much the closest thing we have to humans

I thought chimpanzees and bonobos were the two living species most closely related to humans? Why don't we try the vaccines on them instead? Why is the rhesus macaque a better candidate?

Short answer:

Chimpanzees are indeed closer, but perhaps...too close. Almost all invasive research on non-human great apes has halted for some time over ethical concerns.

Rhesus macaques are the main non-human primate still used in research (some others are also used, like marmosets). "Pretty much the closest" is in reference to which species are available to scientists as a model organism; I assume the researcher quoted included "pretty much" as a bit of a hedge, acknowledging that chimpanzees are closest while not being available for vaccine research. Even then, many countries have limited research using all primates and do not use macaques anymore, either.

Longer answer:

The primates include great apes like gorillas, orangutans, and our closest non-human relatives: chimpanzees. They also include more distant relatives, like Old-world and New-world monkeys, and even more distant lemurs.

Many humans (including influential organizations) have decided that chimpanzees and other apes are too closely related to humans to be eligible for certain types of research for ethical reasons. It has been deemed more ethical to use human subjects, who can consent to participation in studies, or to use other model animals. Apes are also difficult as model organisms: they develop slowly, grow large, and have long life spans with few offspring; all these factors make them expensive research subjects. There is no one biological fact for this distinction between apes and other monkeys, besides their closer relationship to us and the perception that they have more advanced intellectual faculties. Further discussion is outside the scope of this answer.

Old-world monkeys, including rhesus macaques, are the next-closest grouping of primates to the human lineage. Macaque monkeys live and breed fairly well in captivity, and are used in research when other model organisms like mice and rats are unsuitable (like when an aspect of their biology is not sufficiently similar to humans).

Rodents can also be models for vaccine research, but their distance from humans and differing response to certain pathogens may make them less useful for measuring efficacy. Therefore, close relatives like rhesus macaques have been used in past vaccine research.

There is no perfect model organism; even humans aren't always great models for other humans, when they vary by age, sex, pre-existing conditions, etc. There is a balance in risk and ethics in choosing model organisms for research: simpler animals like mice and rats are typically used at earlier stages of research. Primates are used when rodent models don't correlate well enough with humans or when there is a large risk to human trials.

Some references:

https://en.wikipedia.org/wiki/Animal_testing_on_non-human_primates

https://www.nih.gov/about-nih/who-we-are/nih-director/statements/nih-will-no-longer-support-biomedical-research-chimpanzees

https://www.nature.com/subjects/rhesus-macaque

https://www.sciencemag.org/news/2018/11/record-number-monkeys-being-used-us-research

Nath, B. M., Schumann, K. E., & Boyer, J. D. (2000). The chimpanzee and other non-human-primate models in HIV-1 vaccine research. Trends in microbiology, 8(9), 426-431.