What is the biological potential for vision of wavelengths outside the human visual range? Humans eyes have evolved to perceive light only between approximately 350-700nm, because that form of light is most common to our lifes. Other animals can perceive lights with slightly different fequencies. Can eyes theoretically evolve in a way that they can observe all light as we know it today? If not what would approximately be the maximum amount of frequencies that can be perceived?

There are some limits on what light can be detected biologically based on physics and chemistry. Although there are animals that can sense more UV or more infrared than humans, they are still subject to these limitations.

How Vision Works

The way most types of vision operate is by using photons to cause a conformational change in an opsin protein by influencing a chemical bond in a sensitive molecule (a chromophore, for example retinal, which changes from 11-cis to all-trans) bound to the opsin. To sense a particular wavelength of light using this mechanism, it is necessary that the energy of the light is sufficient to cause this chemical change in the opsin-chromophore, without being enough energy to destroy the molecule entirely by breaking a bond.

Sensing low-energy (long wavelength) light

Longer wavelength light ('infrared') is also known as heat. Detecting "heat" photons is difficult because they don't have much energy. Therefore, you need a molecule that is very sensitive. It turns out that the opsin-based vision strategies use chromophores that are too stable to sense long wavelength light.

Some snakes have particular sensitivity to infrared, for example the pit viper. However, these animals do not "see" infrared using their eyes: they have another specialized organ called the pit organ. The pit organ uses receptors that are much more like the heat receptors in your skin than the photoreceptors in your eye, but the pit organ uses a pinhole camera effect to organize the incoming light onto a very sensitive heat-sensitive membrane.

Humans of course are able to sense infrared, too, but the same way: through the skin rather than the eyes, and at low resolution. However, if you stand outside in the sun and close your eyes, you can probably still "see" the direction of the sun: one side of your body will feel warmer than the other! In a way, this is like a form of low-resolution "vision" if you want to define that term very broadly. The snake's infrared sensitivity is more like this sensation than eyesight.

When you get to very long wavelengths, for example radio waves, the wavelength is too long and too low-energy to even be relevant at a molecular level: these forms of light will travel right through cells, and individual photons don't carry enough energy to influence molecules in ways that can be sensed by biology.

Sensing high-energy (short wavelength) light

Very short wavelengths of light have the opposite problem: too much energy. Ionizing radiation (from the upper ultraviolet range and shorter) has enough energy to actually free electrons and create ions. This type of radiation damages biological molecules, including DNA, so organisms have a lot of good reasons to avoid these types of radiation. Exposure to short-wavelength radiation can also cause bleaching (permanent destruction) of photosensitive molecules and potentially damaging heating of tissue surrounding pigments, in addition to direct effects on other molecules in the cells.

Insects and other organisms that can see into the UV range see mostly in the near-UV range, >300nm, not too far from our own vision range (roughly corresponding to "UVA"). However, it isn't true that humans can't see these wavelengths due to some lack of sensitivity of our photoreceptors: instead, UV light is (at least partly) blocked by the cornea and lens, presumably to protect the retina from damage!

Humans and other organisms do have some sensitivity to damaging UV wavelengths, just not through vision. Instead, humans and other organisms sense UV based on the damage done within cells, which recruits repair mechanisms and apoptosis to prevent damage from leading to cancer.

Summary:

The chemical processes behind vision determine the range of potential wavelengths that can be sensed. Animals on earth are able to sample from this entire range. Mechanisms to sense wavelengths outside that range would require wholly different approaches, and maybe even a unique biochemistry. The mechanisms would have to be so different that we probably wouldn't refer to those mechanisms as "vision" (for example, even the infrared sensitivity of the pit viper isn't really though of as vision) but we would come up with a new term, such as "radio sensitivity" or "radiation sensitivity" just like we have different names for "hearing" relatively high-frequency pressure waves with the ears but we have "vibration sensitivity" for low-frequency pressure waves felt through the skin.


What species of bird inspired Nebraska's nickname Bug-Eating State? Nebraska's early nicknames include Bug-eating State, inspired by a bird. One reference describes it as the "“bull bats (Caprimulgus europaeus).” However, that's the Latin name of the European nightjar.

I'm therefore assuming Nebraska's nickname was a reference to a native nightjar species - but which one? Of course, it could have referred to multiple species, or all of them.

I just wondered if anyone might know if this nickname referred to a particular species. If that can't be answered, it would be interesting to know if there's a species that's a likely candidate. For example, is there a particular nightjar that was especially widespread or common in Nebraska in the late 19th century?

Though this question feels a little more like history than biology, since I was able to easily & quickly find information that answers this question, I will provide a response anyway.

  What species of bird inspired Nebraska's nickname Bug-Eating State?

After a bit of research, it appears that no species of bird contributed to this nickname. Instead, Homo sapiens are the culprits! =P

According to the Official Nebraska Government Website:

  This bug-eater business is said to have originated during the potato-bug and grasshopper times. An eastern man came out here to visit his relatives. On his return they asked him, of course, how things were in Nebraska? It was our worst time, our one year of a double plague, so he answered, 'Oh, everything is gone up there. The grasshoppers have eaten the grain up, the potato-bugs ate the 'taters all up, and now the inhabitants are eating the bugs to keep alive.' Some newspaper man heard it and published it as a good joke, and it stuck to us for a good while.

..

  At the very first meeting of the [Territorial] Pioneers [Association] in May, 1892, a member protested against the nickname, or totem name as I call it, of Nebraskans, namely, 'bug-eaters.' The 'Sons and Daughters of Nebraska,' composed of those born in the state, was organized at the same time, and they were on the street with ribbons and badges of their order, which had printed on them a big bug and the legend, 'Bug-Eaters.' Of course they did not think how it looked or sounded, but did it merely as a joke. A committee was appointed at the time to suggest a more euphonious and appropriate name, but nothing was really done about the matter until our October meeting this year when the name of 'TREE PLANTERS' was suggested and adopted at once, as emblematic, a pleasant sounding name and most appropriate, for Nebraska has planted more trees since she was named and settled than any other state in the Union.

..

  By all means, then, give us the 'Tree Planters,' which is an honor, a glory, a fact and a pleasant reminiscence of the great change that has come to our prairie country in the short time since its first settlement. Help the Pioneers to fix this name in the public mind, and say good-bye to the Bug-eaters forever. -- Jno. A. MacMurphy, Secy. T.P.A., 1921 Farnam St., Omaha, Neb.

Nebraska now carries the official nickname "The Cornhusker State", and has done so since 1945. More information about the history of Nebraska's nicknames can be found here and here.


What is the difference between naive and adjusted p-values in a GWAS study? What is the difference between a naive p-value and an adjusted p-value in the results of a GWAS study? See from this paper:

  After Bonferroni adjustment, a single gene, DCTN4 (encoding dynactin 4) on chromosome 5q33.1, was significantly associated with time to chronic P. aeruginosa infection (naïve P = 2.2 × 10−6; adjusted P = 0.025; Supplementary Fig. 1).

There’s an XKCD comic which explains the problem. Unfortunately, that comic is too big to post here. Briefly, a p-value of 0.1 says (roughly) that there’s a 10% chance (0.1) of the observed result being as extreme1 as it is simply due to chance (sampling variation from a population), assuming the null hypothesis is true.

Often, 5% is more or less arbitrarily chosen as “cut-off”: results with p-values below that (which occur by chance 1 time out of 20) are called significant – results above are insignificant.

However, this directly implies that when doing multiple studies, say 20, there’s a very high chance of getting a “significant” result by pure chance, without there being a real effect.

GWAS studies essentially perform experiments on many (hundreds or thousands) of factors simultaneously. Therefore, reporting the pure p-values would be very misleading since there would be a lot of spurious results with “significant” p-values. The probability of getting one or more spurious hits is called the familywise error rate (FWER).

The FWER can be reduced by adjusting the p values, for instance by performing the Bonferroni correction. The resulting p-values are quite a bit higher, which reflects the reduced certainty that the result is due to chance, i.e. the reduced significance.

It doesn’t generally make sense to report the unadjusted p-value. It was probably reported here because correcting for FWER is quite conservative (i.e. it trades a low false-positive rate for an increased false-negative rate) and the authors feared that the adjusted p-value looked less impressive than it should. This involves a fair bit of interpretation.

1 extreme = different from the expected result under the null hypothesis


Do gibbons have a monogamous sexuality? the question is already in the title. If possible, it might be extended to:
Have animal taxa (mammal) who tend to live in a family structure have a monogamous sexuality? Or are there cases of these taxa, where the sexual partner is not the social one.

Regarding gibbons, yes. According to National Geographic:

  Gibbons are monogamous and live in family groups consisting of an adult pair and their young offspring.

There isn't a generalized answer for "family living", although specific family types are indicative of relationship type. Nuclear families (parents and children) tend to be monogamous, families with multiple males and one female tend to be polyandrous, and families with one male and multiple females tend to be polygynous. See this page on primate social structure for more information.


What's the name of this insect? Here's a picture:

That's pretty much it, besides that it was found in Vienna, Austria.

Edit: Thanks to Magne Flåten; it's called Hausmutter in German.

This is probably a large yellow underwing not finished pumping up its wings: https://en.wikipedia.org/wiki/Large_yellow_underwing


Cell cycle selection Is it possible to select from colonies only cells which are at a certain stage in the cell cycle? E.g. if I was trying to analyse expression of a number of genes during different stages of the cell cycle.

I could imagine that if this is possible, the selection mechanism might target cyclins, or use an artificial gene cassette controlled by them.

So for example, a method may attach some gene to a certain cyclin which protects against a substance that otherwise destroys the cell. We could then use that substance to destroy all cells which were not in the cell cycle stage that we want to look at, wash away their nucleic acids, and then extract the mRNA from remaining cells to analyse expression levels at this particular stage in the cell cycle. If we repeat that for the different stages, we should be able to get a nice picture of what is expressed when. Does any method like this exist or is commonly used?

Depending on the stage of cell-cycle you are interested in, people often use the size/morphology of the cell as an indicator. Then you select cells with a cell sorter.

Another option is to specifically tag some cellular molecule that can give an indication as to the relevant stage and then sort the cells based on the tag. This does not necessarily have to be cyclins - for example if you are only interested in S/G2 you could tag the DNA or maybe histones.


How do we know the human species arose in Africa? I have heard (from multiple sources) that the current scientific opinion is that the human species arose in Africa. What are the reasons for this opinion? If possible, simple and non-technical explanations (as far as possible) would be appreciated.

There are two big prongs of the out of Africa theory or whichever name you wish to call it.

Prong the first: fossil evidence. There are lots of different kinds of protohuman fossils. Homo erectus/ergaster are found all across Europe, Asia, and into Indonesia from about 1.5 million years or so until about 70 thousand years ago, where they stop showing up. Up until 125 thousand years ago anatomically modern humans were only found in Africa. About 70 thousand years ago they start showing up in the Middle East, and then they spread out roughly following these paths. The fossil record shows not-humans or almost-humans (Homo erectus mostly) for millions of years, then humans show up at a certain point and then there's loads of human fossils. This point gets more recent as you get further from East Africa.

Prong the second: genetic diversity. Starting with this paper (not sure if this is behind a paywall but the details are not important anyway) human mitochondrial DNA was compared using restriction enzyme mapping. This kind of mapping is super crude (roughly analogous to grinding pottery into a fine dust and grouping the dusts by color) and the original study was pretty limited by the computers available at the time. Nonetheless, they showed that the most genetically diverse geographical group was Africa, and furthermore that any two people from outside Africa are likely more closely related to each other than any two people inside Africa. Genetic diversity goes down the further away from East Africa you get, matching what you'd expect if humans hadn't been living there long. There have only been (very roughly) 60 generations since humans colonized New Zealand. All Maori people, therefore, are at most 58th cousins. All indigenous Australians are at most 1998th cousins. All Africans are at most 8000th cousins.

More recently we've done proper sequencing on the mitochondrial DNA (actually knowing whats written there) and that's allowed much more precise estimation of this sort of thing, and estimation of the timeframes involved. The genetic evidence backs up the fossil record, by and large. (There are a few interesting examples where interbreeding with Neanderthals and maybe Denisovans can be detected, and that the settlement of the middle east by modern humans about 125 thousand years ago failed. They left no descendants.)

Fun side consideration (warning, extra science, proceed with caution): all humans inherit their mitochondria from their mother, and all males inherit their Y-chromosomes from their father. This lets us trace matrilineal lines with a relatively high degree of accuracy, since mitochondria reproduce asexually. To clarify: your matrilineal line is your mother, and her mother, and so on. Your paternal grandmother is not part of your matrilineal line, nor are your aunts or sisters. These lines are statistically guaranteed to eventually converge on a single woman whose mitochondrial descendants now live in all of us. The reasons for this are complicated. There are actually lots of these women, since she inherited her mitochondria from her mother, ad infinitum (well, not infinitum. Ad failed-endocytosis-of-an-alpha-proteobacterium-leading-to-mitochondria doesn't roll off the tongue though). Science has tight estimates on the most recent mitochondrial ancestor, or "Mitochondrial Eve". To be clear: there were loads of other women alive at the time, and we inherit a lot of their non-mitochondrial DNA. Over millennia all those other women had fewer daughters, and their matrilineal lines died out. She lived about 200 thousand years ago, plus minus 20 thousand years. As a mathematical guarantee we'll never find her body or have a really tight estimate on how long ago she lived, but she's genetically guaranteed to exist. The same principle applies to patrilineal inheritance, but the estimates for the most recent ancestor of all Y-chromosomes are a little looser (200-300 thousand years ago). See here for a more detailed handling of Eve and what's going on there.

In sum: old fossils only in Africa, everyone outside Africa is only 2800th cousins with each other or less, but intra-African relatedness is less than half that (more than twice as far away genetically).


What's a good reference for choosing histological staining chemicals? It's often difficult to find the appropriate or best stain to use when I want to examine a new type of tissue. I think that's partly because many histological techniques were developed a long time ago, so the papers don't turn up in Google Scholar. Is there a standard reference which links tissues, cell types or states and their corresponding best stain?

I'm mostly interested in a reference text or website covering plant histology, but general references are welcome too.

If you want to go way back, google books has Methods in Plant Histology (Chamberlin, 1905) with a PDF. It details stains and the tissues they are used for and even has a section titled "Selection of a Stain."


What is the name of this biting bug? I just was bitten by a bug!!! It is 3mm long and has large pincers. Here is a photo:

I live in Colorado. Any help identifying it would be great.

It's a larva of a green lacewing (Family Chrysopidae). Yes, they can bite hard but you're not its intended victim and they're not only harmless but beneficial as they're aggressive predators of aphids and other soft bodied plant pests. I can't be specific to what species of lacewing as they look fairly similar.

Another larva that looks very similar to yours.

Source from BugGuide.net

What the adult looks like (remember,they're an entire insect family so there are differences but not to most people).

Source also from BugGuide.net


What is trans-complementation? Is trans-complementation a complementation of transgenes?

The crystal structure reveals a trans-complementation mechanism whereby an incomplete immunoglobulin-like domain assimilates an isoform-specific myomesin interdomain sequence.
https://www.ncbi.nlm.nih.gov/pubmed/27989621

The term complementation refers to the recover of a phenotype or characteristic ("or function of a protein") that was altered due to mutations. The complementation can be a cis, a mutation in the same gene that restores function, or trans mutation on a secondary gene that restore the function.

An example from wikipedia:

  For a simple example of a complementation test, suppose a geneticist is interested in studying two strains of white-eyed flies of the species Drosophila melanogaster, more commonly known as the common fruit fly. In this species, wild type flies have red eyes and eye color is known to be related to two genes, A and B. Each one of these genes has two alleles, a dominant one that codes for a working protein (A and B respectively) and a recessive one that codes for a malfunctioning protein (a and b respectively). Since both proteins are necessary for the synthesis of red pigmentation in the eyes, if a given fly is homozygous for either a or b, it will have white eyes.
  Knowing this, the geneticist may perform a complementation test on two separately obtained strains of pure-breeding white-eyed flies. The test is performed by crossing two flies, one from each strain. If the resulting progeny have red eyes, the two strains are said to complement; if the progeny have white eyes, they do not.
  If the strains complement, we imagine that one strain must have a genotype aa BB and the other AA bb, which when crossed yield the genotype AaBb. In other words, each strain is homozygous for a different deficiency that produces the same phenotype. If the strains do not complement, they both must have genotypes aa BB, AA bb, or aa bb. In other words, they are both homozygous for the same deficiency, which obviously will produce the same phenotype.


Is it possible that a set of functionally related proteins in a pathway fulfill different functions? Could it be that a given pathway of enzymes (or proteins in general) may fulfill different purposes in a cell by for shifting partners? Say protein A activates B, B activates C and C has a specific action X (e.g. X = phosphorylation of protein D). Now do pathways exist where, e.g., A can activate C directly resulting in action Y (e.g. dephosphorylation of protein D)?

At this time I am in need of real-world examples of this scenario, but I can't find any. Can anyone help?

If Y can be seen as the inverse or absence of X function, it sounds to me like an incoherent type 3 feed-forward loop, where
A activates B
B activates C
A inhibits/reverses C

example from literature, E.coli: fnr as A, and arcA as B, cydAB as C
source: http://www.pnas.org/content/100/21/11980.long


Why does human chromosome 19 have the second highest number of protein-coding genes? While chromosome 19 only is the 19th largest autosomal chromosome, it contains 1440 protein-coding genes, and thus has the second highest number of protein-coding genes of any human chromosome.

For comparison: If one would naively assume the same density of protein-coding genes as on chr1, which has the highest absolute number of protein coding genes (2109), the anticipation for chr19 would be ~540 protein-coding genes.

The x-axis of this graph highlights the increased density of protein-coding genes on chromosome 19;

This Nature paper from 2004, by Jane Grimwood et al. goes at least a long way towards giving an answer to the question of the OP. In short: there were inordinately many duplications, especially during an event 30-40 million years ago, as well as during a much more recent event. These duplications are, uncharacteristically, predominantly intra-chromosomal rather than inter-chromosomal. Also, chromosome 19 contains a lot of immunoglobin-like paralogues: a type of gene for which it is clearly evolutionarily adaptive to undergo rapid duplication followed by random mutation, as they play a role in adapting to potential antigens.


Interaction of charged triphosphates with the ATP binding region in proteins DNA-histone interactions involve positively charged amino acid side chains groups neutralizing the negatively charged phosphate of the sugar-phosphate backbone. Is the same true for ATP binding sites on proteins?
In most models I’ve seen, it looks like the base, adenine, is involved in the binding. But the triphosphate seems like it would bind specifically to positively charged side-chains. I Googled a bit, but I couldn’t really find any models depicting this. Does anyone know whether this is so?

Summary
Many proteins that bind the nucleotide triphosphates ATP and GTP have an evolutionary conserved motif — the P-loop — that binds the phosphate portion of the molecule. This has the sequence, GXXXXGKS/T. Although the conserved basic lysine (K) is interacts with two of the positively charged phosphate moieties, other interactions involve Mg2+ ions (with which NTPs are always complexed) and polar, rather than charged, amino acid residues and the polypeptide backbone.
Detailed Illustration
Although the question asks about ATP, I have chosen the GTP-binding protein H-ras p21 as an illustration because the paper by Pai et al. describing it gives full details of the interactions of the phosphates, which are essentially the same for ATP and GTP. (Many other papers tend to show only ribbon diagrams of the protein.) Note also that the crystal structure was, of necessity, of a complex with the GTP analogue, GppNp. (GppNp is not rapidly hydrolysed, unlike GTP itself.)
In this case the evolutionary conserved P-loop that binds the phosphate has the sequence:
Gly Ala Gly Gly Val Gly Lys Ser

 10  11  12  13  14  15  16  17

A three-dimensional representation of the phosphate-binding region is shown below. The left-hand frame shows the P-loop and residues Thr35 and Asp57 without the nucleotide. The right-hand frame is the same but with GppNp and a magnesium ion included, and only the conserved residues of the P-loop labelled.

[Own work based on Fig.6 of the paper by Pai et al. using Jmol software and Protein Data Bank file 5p21.pdb.]
A two-dimensional schematic of the interactions is shown below. The side-chain interactions (and those from the magnesium ion) are shown as red dotted lines, whereas those from the backbone are shown in black. The conserved residues of the P-loop are indicated by blue text.

[Simplified redrawing of part of Fig.5 of the paper by Pai et al., excluding water interactions and interatomic distances.]
Reflections
Although positively-charged basic amino acid side-chains are involved in neutralizing the negative charges of nucleic acids and nucleotide phosphates, they are not the sole means of doing so, and in the case of the NTPs they are not the main means. Magnesium ions and polar residues (including the protein backbone δ+ve NH groups) can play an important role. To my mind this reflects two things. First, that life is dynamic; so weaker interactions are often favoured in enzymes because they can be easily broken as well as made. (NDP must be released from the enzyme after hydrolysis.) Second, and more speculative, the P-loop is thought to be very ancient as it is found in a wide variety of conserved NTP-binding proteins. A specific backbone conformation has been identified that facilitates this interaction. It could have arisen before all 20(ish) proteins specified by the genetic code had arisen, when the protein backbone could have played a greater role in interacting with small molecules. (This has also been suggested for backbone NH groups binding δ+ve sulphur in iron–sulphur clusters.)


Immunity during pregnancy I have learnt that our immune system distinguishes self from non-self by using MHC. So a mother during pregnancy should also develop antibodies against the fetus as it is also a genetically different individual. Answering by saying that antibodies won't cross the placental barrier seems wrong as there is so much research going on this thing that such a simple explanation wouldn't suffice.
Why doesn't the mother reject the baby?

Awesome question! The immune system detects the presence of non-self using MHC and T cells and the lack of self using NK cells. The placenta first of all doesn't display MHC so T cells can't detect it, and expresses NK inhibitory receptors which stop NK cells killing it. Furthermore, the immune system isn't able to get to the foetus so it isn't able to activate against these antigens nor produce the antibodies which require T cells to be activated first, which then activate B cells. This is because the placenta is a syncitium, thus no spaces between cells for immune cells to slip through (a mechanism used by viruses). The placenta also secretes Neurokinin B, this makes it hard for the immune system to see the baby, and is a mechanism used by parasites. There are T reg cells which act to supress an immune response.


Rice left in water for several months - what biological reactions or growths would occur? In an attempt to make a hair care product, uncooked white basmati rice was left in an air-tight container half filled with tap water for several months.

When opening the container, the smell was extremely foul and disturbing, one of the most revolting things I have ever smelt.  It was worse than the smell you would usually associate with yeast, alcohol, or mold.  This horrid smell immediately spread to the entire property and took many hours of fan extraction to remove.  It was worse than the smell of sewage.

I rinsed the container used and cleaned it in the dishwasher several times at 75'c.  After several dishwasher cycles, the disgusting smell remains.  It makes me wonder what kind of biological or chemical product has been created that even a dishwasher cannot neutralise or sterilise at high temperatures?  Is this a safe substance?  This is especially concerning as this recipe exists on several hair care forums; is it widespread misinformation caused through malice?

I believe this is a valid scientific question about microbial life so on that basis I would not expect it to be down voted.

The substance looked like water with rice or rice starches dissolved in it; it was murky with a whitish colour.  There was no air bubbles which could be visually observed, although the murky texture could have been caused by micro-bubbles. The smell was very strange, unlike anything I have smelled before.  The closest description I could give is that of sewage, yet it is more disgusting than the smell of sewage if that is relatable at all.

It is likely a volatile organic compound (VOC) that is released as a by-product of microbial metabolism, although microbes can also produce some inorganic compounds, such as hydrogen sulfide (rotten egg smell). It could be any of a number of compounds, depending on the microbial species and the environmental conditions. The only relevant paper I could find based on a cursory search was by Yanqiang et al. (2013) on volatile compounds released from the anaerobic digestion of food waste in general; based on the results, the odor likely consists of a complex mixture of gases, and may be especially rich in aromatic compounds. Whether it could have any negative health effects is challenging to prove, but you would likely want to avoid exposure.

I presume that your container is made of plastic or at least contains a silicone ring. You can remove odors from metal or glass by washing them, but porous substances like plastics, rubber and the like will absorb volatile compounds, rendering them largely inaccessible to solvents such as water, and will release them slowly over time, which you can perceive via olfaction as you have noticed. If you want to eliminate the odor faster, you will need to accelerate this outgassing process. The way this is usually done is by baking in an oven (optimally in a vacuum, although this is not necessary). The rate of outgassing grows exponentially with the temperature, so you should use the maximum temperature that the material in question can withstand.


How does symbiogenesis explain reproduction of organelles along with the cell? Symbiogenesis is an evolutionary theory that says that prokaryotes eventually evolved into eukaryotes (having multiple organelles and better structure) by forming symbiotic relationships with other bacteria that have been absorbed, or have entered the cell in an initially parasitic way.

My question is that when the individual bacteria have become organelles, what happens when the cell reproduces? The bacteria were individual entities with their own reproduction mechanisms before they became organelles. Do they still divide in their own way inside a cell (and are subsequently present in both halves of the cell when it is dividing itself), or does their division somehow get incorporated into the cell's own DNA?

I'm not sure about all organelles but mitochondria and chloroplasts are commonly used examples of independent devision in eukaryotic cells. They have independent DNA that forms separate mitotic spindles during division. Similar mechanisms likely existed for other organelles originally but the genetic material may have eventually been combined with the nuclear DNA for simplicity. This is a very simplified explanation but I think addresses the basic question.


What makes DNA helical? Why isn't DNA like RNA; why isn't RNA like DNA, that is, helical? Why are RNA chains straight?

The helix shape of DNA molecule is a consequence of its secondary structure. This refers to the bases contained in the molecule which pair, thus determining tertiary structure [1].
Basepairing also occurs in RNA, so it can form a double helix. In fact, RNA is composed of short helices packed together [2]. Base pairs maintain DNA's helical structure no matter the nucleotide sequence [3].
A nucleic acid strand is composed of nucleotides joined together by covalent bonds between the sugar of one nucleotide and the phosphate of the next. Adenine pairs with thymine and cytosine pairs with guanine by hydrogen bonds and form the double-stranded structure [3]. Because covalent bonds are stronger than hydrogen bonds, the double helical structure of DNA is easily broken by heat [4], but the nucleotides remain bonded together.
Here is the tRNA molecule (you can see it has short helices):
"TRNA-Phe yeast 1ehz" by Yikrazuul - Own work. Licensed under CC BY-SA 3.0 via Wikimedia Commons.
Here is the DNA structure:
(source: wikimedia.org)"ADN animation" by brian0918™ - Own work. Licensed under Public domain via Wikimedia Commons.

References:

Wikipedia contributors, "Nucleic acid double helix," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Nucleic_acid_double_helix&oldid=609435163 (accessed June 26, 2014).

Wikipedia contributors, "RNA," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=RNA&oldid=612056511 (accessed June 26, 2014).

Wikipedia contributors, "DNA," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=DNA&oldid=611891356 (accessed June 26, 2014).

Wikipedia contributors, "Nucleic acid thermodynamics," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Nucleic_acid_thermodynamics&oldid=606379256 (accessed June 26, 2014).


Why do eyes water in response to particular emotions? It is common for people to experience very moving situations (sad movies, etc) and have a physical reaction to it (such as crying). I am curious about how emotions can physically lead to the act of crying. Why/how does this happen? What is the mechanism?

When we are sad, our emotions are in an overdrive and the parasympathetic nervous system triggers lacrimation i.e. tears, and we cry.


The Water hyacinth and its ability to absorb pollutants from the water What genes makes the water Hyacinth able to absorb pollutants from the water it lives in? (2) can this gene be successfully harvested? And how?

Genes don't necessarily work in isolation (most don't). An ability to absorb pollutants would likely be a combination of many genes.

Also, what constitutes a "water pollutant" is very broad - you could be talking about pesticides, heavy metals, fertiliser, organic waste... If water Hyacinth absorbs all of these, it could just be the result of absorbing more water than other plants (with pollutants accumulating in the plants). Who knows - you should state your source of information.

In terms of how to figure out what gene(s) are responsible, you could consider a radioactive tracer to tag the specific compound (or even element) that you consider Hyacinth to absorb better than other plants. This might give you some idea of how it's doing what it's doing. For example, if you think it's absorbing a compound, you can tag that compound with a radioactive tracer, see where it's being accumulated (even it's path), and from there figure out what's happening.

The fastest path to figuring out which gene(s) are responsible from there would be to build up a list of all the genes you think might be involved in this path and create an array of cloned plants with those genes removed. If you remove the correct gene(s) from the equation, the plant will have less or no proclivity for absorbing the type of pollutants in question.


What is the antagonist of epinephrine? Norepinephrine and epinephrine have similar stimulant properties on the nervous system and the body. I was wondering which hormone is the antagonist of epinephrine?

You should understand that it is not the neurotransmitter that is responsible for an effect; it is the neural network that causes an effect and the neurotransmitter is just a mediator.

In CNS, glutamate is generally used in excitatory synapses whereas GABA is chiefly used in inhibitory synapses. Similarly, in peripheral nervous system epinephrine and acetylcholine are used in excitatory synapses whereas glycine is used in inhibitory synapses. Some neurotransmitters always cause excitation in the post-synaptic cell (for example glutamate), however, they can also cause activation of inhibitory neurons and thereby cause inactivation, indirectly. Also, the post-synaptic effect depends on the type of receptor expressed by the post synaptic cell and not the neurotransmitter per-se. For example, α-adrenergic receptors cause smooth muscle contraction whereas the β2- receptors cause smooth muscle relaxation [1]. Similarly, there are both inhibitory and excitatory dopamine receptors [2].

The two divisions of the autonomic nervous system — the sympathetic and parasympathetic systems act in a complementary manner. The former uses epinephrine and norepinephrine whereas the latter uses acetylcholine.


What's the difference between a free chromosome fragment and an extrachromosomal array? This is reference to a review on C. elegans mosaic analysis by Yochem and Herman, in which the authors make a distinction between free chromosome fragments and extrachromosomal arrays.

For the former, they reference Herman 1984.
For the latter, they reference Lackner et al 1994 and Miller et al 1996, but these are studies that use extrachromosomal arrays, not papers defining them as a technique, per se.

I am curious to know what the distinction is - I am under the impression that extrachromosomal arrays are fragments with many copies of the gene of interest + a marker.

I asked my professor, and the answer appears to be differences in both the generation and the final product.

Free chromosome fragments are created through irradiation/other damage of the germline in one animal.  Through a series of crosses, it is possible to introduce individual fragments (containing a duplication of your gene of interest, as well as a marker) into a mutant background.  The extrachromosomal fragment will be lost during mitosis at various points in development, and in a mosaic analysis, you can look for the loss of your marker (and therefore the loss of the wildtype allele), and see if yfg product is required in certain cell types for a wildtype phenotype.

Extrachromosomal arrays are created by cloning, and you typically have many copies of both the gene and marker.  It's the same principle as free chromosomal fragments in terms of mosaic analysis, but it's very powerful, as you can easily clone individual genes (versus irradiating and hoping to discover yfg on a fragment) and markers (and now you can use non-endogenous markers like GFP).

Even though extrachromosomal arrays are comparatively easier to generate, the problem is that you end up with many copies of the gene, which leads to non-endogenous dosage levels. Even if this doesn't cause a completely different mutant phenotype in the cells, it is possible that enough of these proteins could segregate at mitosis into the daughter cells, such that even if the fragment is lost, you could still have your gene product around in the daughter cells (if your marker protein didn't also segregate like this, you might draw erroneous conclusions about the necessity of yfg product in those particular cells).


What does lymph actually look like? I have scoured Google and a number of my anatomy textbooks for a picture of lymph. However, I cannot find any such photo (or video) showing its actual appearance.
Can someone provide a reputable image or source where a photograph of lymph can be seen?
What I do know:

Tortora & Derrickson (14th) A&P textbook mentions it consists of a "clear liquid extracellular matrix that is similar to blood plasma but with much less protein."

A photo purporting to be lymph does exist on Wikipedia, but lacking any further corroboration leads me to remain uncertain of the photo's authenticity.

Context:
I'm preparing a lecture for my 100 level college A&P course, and I was hoping to include a photo for my students to see and compare.
NOTE: I am hoping for a photo of lymph that is not classified as lipid-containing Chyle, for which I can find photos. However, a comparison photo would be ok :)

This seems to be one of rare actual photos of lymph online (suggested in the comment above):

Image: Lymph (source: IJCRI - Case Reports Journal)

This particular lymph (or "lymph fluid" or "lymphatic fluid") was aspirated from a "lymphocele", which is an abnormal collection of lymph in the body (appearing outside of the normal lymphatic system).

While a lymphocele is not normal, the lymph in it, such as in this photo, looks quite normal: it is a clear (translucent) and yellowish liquid.

  The lymphatic (lim-FAT-ik) system is a network of tubes that collects
  lymph (LIMF). This clear, pale yellow fluid drains out of blood
  vessels all over the body. (KidsHealth.org)

The froth is from proteins as they normally appear in the lymph.

The image of lymph in Wikipedia is not a clear lymph, but obviously a chyle (a milky fluid containing the lymph and chylomicrons due to thoracic duct injury).


How's idiotype different from paratope? What I understand of these two terms is that:

Paratope is a portion of antibody that recognises and binds to specific antigen.

Idiotype is an antigenic determinant of antibody formed of CDRs that have specificity for a particular epitope. Some authors call the antibodies recognising a particular epitope an idiotype.

Well the CDRs, they actually form the paratope so is it right to say the CDR that acts as an paratope also forms the idiotypic determinant/ idiotype ?

I have read that the unique amino acid sequence of the VH and VL domains of a given antibody can function not only as an antigen-binding site but also as a set of antigenic determinants. the idiotypic determinants are generated by the confomation of the heavy- and light-chain variable region. Each individual antigenic determinant of the variable region is referred to as an idiotope. In some cases an idiotope may be the actual antigen-binding site (The paratope), and in some cases an idiotope may comprise variable region sequences OUTSIDE of the antigen-binding site. Therefore, each antibody will present multiple idiotopes, and the sum of the individual idiotopes is called the IDIOTYPE of the antibody.

I hope that had been helpful


Recessiveness of allele for protection of organism Heterozygous organisms profit from pairs of gene alleles. Harmful alleles when being recessive can be carried without any harm for the organism. Only when two harmful recessive alleles form a gene the negative effect is produced. As described in wiki article on allele:

  A number of genetic disorders are caused when an individual inherits two recessive alleles for a single-gene trait. Recessive genetic disorders include Albinism, Cystic Fibrosis, Galactosemia, Phenylketonuria (PKU), and Tay-Sachs Disease. Other disorders are also due to recessive alleles, but because the gene locus is located on the X chromosome, so that males have only one copy (that is, they are hemizygous), they are more frequent in males than in females. Examples include red-green color blindness and Fragile X syndrome.

But some illnesses are carried by dominant alleles (from the same article):

  Other disorders, such as Huntington disease, occur when an individual inherits only one dominant allele.

My questions are:

How does harm from alleles correlate with their recessiveness? Generally speaking, do harmful alleles tend to be more recessive?
How does benefits from alleles correlate with their dominance? Generally speaking, do "beneficial" alleles tend to be more dominant?

Instead of dividing mutations into two classes, dominant vs. recessive, consider categorizing them into classes based on how the mutation affects the gene--or the gene product.  This yields loss-of-function (lf) alleles, that reduce the activity of the gene, or its product, and gain-of-function (gf) alleles that act as if they somehow increase the activity of the gene, or its product.

The logic underlying this classification was described in this classic reference: Muller, H. J. 1932. Further studies on the nature and causes of gene mutations. Proceedings of the 6th International Congress of Genetics, pp. 213–255.  Since this was before DNA had been shown to be the genetic material his arguments are based solely on the phenotype of animals carrying various combinations of chromosomes.  In particular he relies on genetic duplications and deficiencies (or deletions).  In this nomenclature + indicates a chromosome carrying a wild-type (wt) allele of the gene, and m indicates a chromosome carrying a mutant allele of the gene.  So if an +/m animal appears Wild-Type then that allele is recessive.  Similarly, if an +/m animal has a Mutant phenotype then the allele is dominant.

There are two types of lf alleles:

a hypomorph is a partial reduction in function and retains some residual gene function (e.g., a weak missense mutation, or a temperature-sensitive (ts) mutation. A hypomorph is recessive to a wt allele.
an amorph is what we would call a true genetic and molecular null allele, a complete knockout of the gene, where there is no measurable function left (e.g., a nonsense mutation early in the protein coding region, or a small deletion that only removes a single gene).  Amorphs are normally recessive to a wt allele (but see below for an exception)

There are three types of gf alleles:

a hypermorph that elevates the level of the wt gene function (e.g., a promoter mutation that removes a negative regulatory site, leading to increased expression). Hypermorphs are dominant.
an antimorph, or so-called dominant-negative (dn) allele that produces a mutant gene product that somehow interferes with the wt gene product (think poison product as one model). Antimorphs are always dominant over wt.
a neomorph, an allele the results in a completely new gene function (e.g., if a glycolytic enzyme acquired sequence-specific DNA-binding activity, perhaps from a gene fusion event(?)). Neomorphic alleles are extremely rare and almost always dominant over wt.

So we have a straightforward mapping of lf alleles to recessive phenotypes, and gf alleles to dominant phenotypes.  However there is an important exception to this simple scheme for genes that are dose-sensitive, or haploinsufficient. These are dominant lf alleles. For example, when halving the level of the gene product causes a mutant phenotype: +/null. Some well-known examples from the developmental genetics of model organisms are the Ubx gene, and the Notch gene from D. melanogaster.

Further discussion of these terms can also be found in Wikipedia


Why does weight loss lower blood pressure? I have read that weight loss is an effective lifestyle modification for people with hypertension, and systolic pressure may be reduced by up to 1-2 mmHg for every 1kg of weight lost.

What is the physiological reason for weight loss reducing blood pressure or weight gain increasing it?  Please provide a physiologically detailed response rather than simply saying that more weight means the body must work harder to pump blood.  I understand this but I want to know the mechanisms of how the body detects the increased weight and adjusts the blood pressure accordingly.  Thanks!

Weight gain increases blood pressure, the reason for this process is due to the effect of hormone called Leptin.

Leptin is made by fat and circulates in the bloodstream to reach the brain, where it acts as a signal for energy reserves, adjusting both energy expenditure and the sensation of hunger – hence it is sometimes referred to as the ‘satiety hormone’.
The group showed that some obese people who were lacking the hormone leptin because of a genetic disorder had low blood pressure despite being very heavy. This was also the case for people lacking the gene for the leptin receptor in the brain, meaning that the brain was unable to respond to the hormone.
Reference

The team lead by Professor Michael Cowley, Monash University, Australia, in collaboration with Professor Sadaf Farooqi, from the University of Cambridge, UK suggests that the leptin signalling is necessary for obesity-induced increased blood pressure. The clinical studies in severely obese humans showed that these observations are relevant to humans.

Professor Cowley said: “High blood pressure is a well-known consequence of obesity. Our study explains the mechanism behind this link, showing that leptin, a hormone secreted by fat, increases blood pressure.”
Professor Farooqi, from the Wellcome Trust-Medical Research Council Institute of Metabolic Science added: “We now know that leptin regulates both our weight and our blood pressure through its action on the brain. Targeting this action could offer a useful way of helping people fight obesity and associated problems such as high blood pressure and heart disease.”
Reference

It is thought that Leptin's only task is to activate the sympathetic nervous system connected to the brown fat and there by directly burns energy. But it is also behind the activation of sympathetic nervous system of heart and kidney, thereby increase the blood pressure.

Genetic and drug experiments in mice, they have pinpointed an area in the mouse brain that increases blood pressure when it is exposed to high leptin levels.
This region is called the dorsomedial hypothalamus, and is thought to be involved in controlling energy consumption. Their findings show that high levels in leptin do indeed boost blood pressure, via this brain region.

Reference
http://ndt.oxfordjournals.org/content/15/8/1115.full.pdf+html


What type of epithelium are the pancreatic Islets of Langerhans? The human pancreas contains exocrine acinus cells (simple cuboidal epithelium) and Islets of Langerhans. Despite looking online I cannot identify what type of epithelium the Islets of Langerhans conform to (e.g., cuboidal, columnar, squamous). I'm confident it is not squamous due to the shape of the cells, but the distinction between cuboidal and columnar seems equivocal here.

I think the image you've attached lacks clarity. If you see the image below, you could say that the epithelium is cuboidal with central rounded nucleus.

Unlike the oval nuclei of columnar epithelium, rounded nucleus suggests that they are cuboidal in shape.
The image is from https://webpath.med.utah.edu/HISTHTML/NORMAL/NORM010.html


Cellular respiration in carnivorous animals What is the equation for cellular respiration in carnivores as they don’t consume carbohydrates to break down into glucose in the following manner:

Glucose + oxygen -> water + CO2 +energy.

Do they (mammalian carnivores) primarily use ketones to produce energy without using glucose?

Does this mean that glucose is not the only energy source for humans/other animals?

Am I wrong in thinking that every source (protein, fats or carbohydrates) need to be convert into glucose for energy.

Your guess is correct: glucose is not the sole source of energy in the cell!

While cellular respiration is the classic mechanism for energy production (in the form of ATP) in the cell, there's another process that's equally important and a little less well-known: beta oxidation. Beta oxidation is how fats and other lipids in the cell can be broken down to produce energy. In this process, the last two carbons in the long chain are sliced off and transferred to Acetyl-CoA, which can then be used in the citric acid cycle to produce ATP.

Here's the equation describing it:

$$C_{n}acyl-CoA+FAD+NAD^{+}+H_{2}O+CoA -> C_{n-2}acyl-CoA+FADH_{2}+NADH+H^++acetylCoA$$

And here's a good diagram from the Wikipedia page that summarizes it:

Courtesy of Cruithne9 on Wikipedia [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)]

This process is why fats actually have a higher energy density than sugars: 9 Cal/g, as opposed to sugar's 4. It's also why organisms tend to use fats as energy storage - while sugar and cellular respiration is great for immediate energy, fats are stable and energy dense so it's an evolutionarily favored idea to use them for long-term storage.

You're also quite correct that animals don't tend to have a lot of free sugars and carbohydrates, unlike plants. Instead, we've converted those carbs into the fat molecules via the reverse process, fatty acid synthesis. So, carnivores largely get their energy from beta oxidation and the metabolism of fats, rather than glucose.


Survivorship Curves: Type II curve mortality rate is not constant? In graphs of survivorship curves, I'm seeing that the Type II curves are straight lines, and the supplementary text says that the mortality rate is constant (i.e. the slope of the line is constant). However, it's also clearly stated that the y-axis is a logarithmic scale, which means that the original Type II curve is exponential:
$$\ln y=-rx+b$$
$$y=Ae^{-rx}$$

This implies that the real mortality rate is not constant, but changes as $$y'=-Ar(e^{-rx})$$
How are we defining the word rate, anyway?

$r$ is the individual mortality rate per time step. Survivorship curves (plotted on a log scale) show the proportion of individuals surviving with time, and with a Type II curve a constant proportion is dying at each time step (constant mortality with age, $r$). When the model is expressed as $y$ you are looking at the number of individuals surviving to a time step, which is an negative exponential for Type II, since a smaller and smaller proportion of the population remains at each time step. Therefore $y'$ is the change (slope) in the number of individuals surviving over time. This can be seen as a rate, but it is not the mortality rate of individuals, and it is not accurate to describe it as the "..real mortality rate..".

For an introduction to survivorship curves you can also look at "Survivorship Curves" from Nature Education


Can low temperatures induce a withdrawal reflex? I read in "Essentials of Pathophysiology: Concepts of Altered Health States
By Carol Porth" that

  "The thermal pain receptors are stimulated only by extremes of temperature such as "freezing cold" below 5°C and "burning hot" above 45°C."

Also in "The Journal of Neuroscience, April 7, 2010 • 30(14):4933– 4942 • 4933" it states:

  "In lightly anesthetized rats, hindpaw cooling with ethyl chloride, but not acetone, was sufficiently noxious to evoke withdrawal reflexes"

We know, 'burning-hot'-receptors induce a withdrawal reflex when we touch a very hot object, say hot frying pan.

But does this mean if we touch a very cold object (temperatures below 5°C), the 'freezing-cold'-receptors would induce a withdrawal reflex in humans?

The withdrawal reflex is a nociceptive flexor reflex and is a spinal reflex intended to protect the body from damaging stimuli.

In other words, activation of heat receptors is not the trigger of the withdrawal reflex, it is the activation of pain receptors at high, tissue-damaging temperatures.

Extreme cold is also damaging and causes skin lesions akin to heat-induced burn wounds. Again, at a certain tipping point extremeley low temperatures become damaging, and cause frost bites (Sachs et al., 2015). At this point tissue damage will activate pain receptors and these cause the withdrawal reflex to be initiated.

Reference
- Sachs et al., Dtsch Arztebl Intv; 112(44): 741–7


Grafting vegetables onto fruit-bearing trees There are multi-fruit trees with as many as 40 different fruit, but would it be possible to graft a vegetable onto a tree?

Or maybe something in between, like grafting onto an apple tree a fruits in the botanical sense, but one of those often eaten as savory food, similar to vegetables: tomato, squash, avocado?

For grafting to "take", the the two plants' vasculatures have to be organized similarly. This is not possible for two such differently organized stems as a pepper and an apple.

This is a cross section of a young woody stem (such as an apple, though this example is a tilia):

This is a cross section of an herbaceous stem (such as a pepper):

You can see there is dissimilarity in organization. Furthermore, herbaceous plant stems die back in the winter.

Even if possible, grafting an herbaceous (non-woody) stem onto a woody stem (e.g. apple) would not confer any advantage for the green pepper, a tender annual, and would be disadvantageous to the woody stemmed tree (pruning for no reason, when the branch would otherwise have produced apples, and the leaves performed their useful functions.


Relative roles of ATP and NADPH in anabolic and other processes Chemistry isn’t my strong point, but I’m trying to understand why NADPH is said to be the main agent necessary for anabolic reactions, and if NADPH is used for anabolic reactions what is ATP used for? Movement?

An example of what I'm wondering: When skin cells are exposed to sunlight, to synthesize melanin is the free energy of ATP hydrolysis sufficient? For example by catabolizing some protein in the cell and using the amino acids to synthesize melanin? Or is NADPH always necessary?

I have not been able to find an explanation on-line that addresses this, so suggestions of a suitable book would be appreciated.

Preamble

I don’t know where you read the statement “NADPH is... the main agent necessary for anabolic reactions”, but  out of context it is very misleading, and it is difficult to envisage circumstances in which it would be helpful for students of metabolism.

Put simply, NAPH is only used in anabolic pathways which involve chemical reduction.

You ask for a suitable book, but the book I’m going to quote from (Berg et al., Biochemistry) would overwhelm you (and any other student — it is grossly overweight). However an old edition is available on-line, and by citing specific sections you can read what is relevant (and spare me breaking up my answer with pirated diagrams).

ATP and NADPH: energetic similarities and differences

ATP and NADPH can both be regarded as ‘energy-rich’ in the sense that they can undergo reactions that have a high negative change in Gibbs Free Energy (which is what determines whether a reaction proceeds) and that this can be linked to certain other reactions with a positive free-energy change — including, but not exclusively, those in biosynthesis — to drive an overall reaction. (Incidentally both these compounds are synthesized in reactions powered by solar energy during photosynthesis.) However the nature of this linkage or coupling to other reactions differs between NADPH and ATP, and this difference determines the roles that they can play.

The oxidation of NADPH to NADP+ has a standard redox potential of +0.32V , which is an effective a negative standard free-energy change, but it can only occur in conjunction with another redox ‘half-reaction’ with a redox potential that will result in an overall negative free-energy change. Berg et al., section 18.2.1, presents a calculation to show how NADH (essentially similar to NADPH in this respect) can reduce pyruvate to lactate. The key point is that this overall reaction is a chemical reduction, so that the ‘energy’ of NADPH is only of use in reductive synthesis.

The ‘energy’ of ATP (more properly its group transfer potential) is in fact the negative free energy of the hydrolysis of ATP to ADP (and orthophosphate), or to AMP (and pyrophosphate). If an enzyme can couple this reaction to another with positive free energy of hydrolysis then it can drive the second reaction. This important point is dealt with in Berg et al. section 14.1.3 and it is also worth reading the preceding section. ATP is not a reducing agent so is not limited to oxido-reduction reactions. (The hydrolysis of ATP can also be used to provide e.g. mechanical or electrical or light energy, which is why Berg et al refer to it in section 14.1.2 as “…the Universal Currency of Free Energy in Biological Systems”.)  In synthetic processes ATP (or other nucleotide triphosphates derived from it) is often used in reactions forming bonds (C–C, peptide, glycosidic, phophodiester). In some of these cases the hydrolysis of the ATP is used to generate an activated form of the basic component, which allows it to form the bond in a subsequent reaction.

Example of a synthetic pathway using both NADPH and ATP

In Fatty acid synthesis NADPH is used for two reduction reactions — ketone to alcohol, unsaturated C=C to saturated C–C bond — whereas ATP hydrolysis is coupled to the formation of the C–C bond of the condensing unit, malonyl CoA. This is shown in Figure 22.22 of Berg et al..

Example of synthetic pathways using ATP but not NADPH

The synthesis of the peptide bonds of proteins requires condensation of the carboxylic acid group of one amino acid with the amino group of another. This is not a reductive process and NADPH is not involved. ATP hydrolysis ‘activates’ each amino acid by attaching it to the ribose of a transfer-RNA in a bond that has a high enough free energy of hydrolysis to ‘drive’ peptide bond formation to the growing polypeptide chain at the peptidyl transferase centre of the ribosome.

Melanin synthesis?

This is an area in which I am profoundly ignorant, but from Googling it would appear that the first phase of melanin synthesis is the conversion of tyrosine to DOPA and then to indoles. These reactions are oxidative (using molecular oxygen) rather than reductive, so do not use NADPH, and the bond formation is cyclization to form the pyrole ring. This seems to proceed without ATP — presumably it is energetically favourable overall. There is a Wikipedia entry for the key tyrosinase oxidation reaction.

I suppose the anabolic phase is the polymerization of the aromatic units to form the crosslinked polymeric structure of melanin. This appears to be poorly understood, but there is certainly no indication that NADPH is involved, and it would appear to depend on chemical features of the environment of the melanosome, rather than on ATP. (There is a recent short review in this area by VJ Hearing).

You mention the role of sunlight in this process. Although sunlight in itself can provide the energy for one stage of the synthesis of Vitamin D in the skin, this is a ring-splitting step. A direct role in the polymerization of melanin doesn’t seem to be suggested.


Is it ok if I define Genes this way in Biology? Genes are found in chromosomes and their job is to show us the traits of someone (height/hair color)

I do know that alleles specify the height of the person (Tall/Short) and their hair color(blue/green), etc. So is it correct to define Genes this way in my exam?

The term gene has been defined (by Wilhelm Johannsen) much before we even knew about the structure of DNA (by Watson and Crick). As such, a gene is typically a vaguely defined functional unit in the genome that codes for a gene product (typically a protein). Have a look at the wikipedia entry for more info.
For a given gene, you might have different variants. Such variant is called an allele. Let's consider a given phenotype such as eye color for example. There would be a gene that we could call "EyeColor" and there could have different alleles at this gene that we could call "BlueEyes", "BrownEyes", "GreenEyes", ...
Of course, in reality it is rarely that easy. A given phenotype is often the result of the interaction of alleles at several genes. Also, the environment (type of food, temperature and many other things) affect a lot the phenotype of an individual.
From your comments, it is made clear that you do not understand the interplay of the different factors that affect variance for a phenotype in a population, you have to understand the concept of heritability. You might want to read Why is a heritability coefficient not an index of how “genetic” something is?.

Genes are found in chromosomes

This sounds like a chromosome is a box containing genes which is misleading. In this regard, I like the folded shirt analogy by @terdon below in the comments.

and their job

In science, always avoid the concept of purpose, of goal, of intention. Things just happen.

is to show us

As if genes wanted to please humans. Sounds very wrong.

the traits of someone (height/hair color)

Genetic variance in population does affect phenotypic variance in the population indeed.
Answer to comment

just want a clarification on why genes are found in chromosomes isn't clear?

No, it was not clear and it still is a bit unclear (but I'll give some info below that will hopefully help). The easier for you is probably to have a look at an intro course to molecular genetics such as this one by Khan Academy for example

DNA is found in chromosomes, and large strings of DNA are genes so why?

DNA is a big molecule which contain the genetic information. It looks like that

To be more accurate the genetic information is held in the sequence of base pairs (base pairs shown on the figure). In eukaryotes (animals, plants, fungi and others but not bacteria, archea or viruses) there are several big molecules of DNA and each one is organized into a chromosome. Here is a drawing to help you visualize that

If you screen through a human genome, you will realize that the vast majority of the sequences of base pairs are not within genes. There are many other sequences such as regulatory sequences, repetitive sequences and other things. Note, also that within a gene (but again the term gene is typically poorly defined) not everything will end up coding for a protein. Only about 1.5% of the human genome directly code for a protein.
Giving you a complete answer would require writing way too much. It is much simpler to seek for further information on such introductory questions in a introductory course to molecular genetics (as the khan academy course I recommended earlier).


How and why do skin tags develop? WebMD writes:

  Skin tags are small, soft pieces of skin that stick out on a thin stem. They most often appear on the neck, armpits, upper trunk, and body folds. The cause of skin tags is not known.

Do we really know nothing about why they appear? Is there research that suggest hypotheses of the causes of skin tags?
It seems to me a pretty well established phenomena for it to be without good research.

Given that skin tags are considered benign, it doesn't surprise me to find very little published research focusing on them. It's unlikely that much grant money exists to answer questions about them.

That said, though, I found a handful of groups that have done some work on them. It seems that they all noticed a statistical relationship between the occurrence of skin tags, obesity and metabolic syndrome. These are the papers describing their research efforts so far:

http://onlinelibrary.wiley.com/doi/10.1111/j.1468-3083.2011.04401.x/epdf

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4740583/

http://www.ncbi.nlm.nih.gov/pubmed/21860156

None of the groups suggest a mechanistic explanation for the occurrence of skin tags, which makes me think that this remains a very open question. However, they all notice a correlation between skin tags and elevated leptin levels.

Leptin is best known as a hunger/satiety regulating hormone. However, it functions through the activation of the JAK/STAT pathway, which in turn activates a number of genes involved in cell survival and in turning off apoptosis, or programmed cell death.

This image comes from this paper in Nature, which, unfortunately, is behind a paywall.

So, my guess based on these data is that increased levels of leptin activate proliferative pathways in cells, leading to the occurrence of skin tags. That this proliferation results in benign cell growth probably has to do with competing tumor-suppressor and related pathways, which I can reasonably assume to be active and functioning, where outright cancer is not present.

What I wonder now, but can't find any information on, is whether skin tags are the only visible evidence of differential cell proliferation, or whether there are other instances within the body. That is, if the leptin-to-skin-tag hypothesis holds, is there something special about skin cells in that response, or are they just the only visible signs of it?


Plasma cells and memory cells What decides whether an activated B cell will get converted to plasma cell or memory B cell? Is it necessary that out of a mitotic division one will convert to memory B cell and the other to plasma cell?

A summary of what we know so far includes that for B cells to become plasma cells they need BLIMP-1. For memory cells CD40 engaging with CD40L on B cells is required. CD40 is expressed on Th cells and thus they are also necessary for memory cell development. Problem is though, it's really damn confusing after that. It really isn't known but if you're interested in this stuff consider reading this review which talks about memory cell differentiation and this which discusses plasma cell differentiation.

The image below helps (taken from this review)

PC = Plasma Cell, MBC = Memory B cell


Do individual neurons communicate with the origin of thoughts? When mapping the different neural pathways in the brain, often pictures such as these are drawn:

Or similar versions. Clearly these sketches draw the neural pathways as being a two-sided connection, as can be judged from the double arrows. I was wondering, how such bidirectional pathways work. Specifically, I am interested to know whether individual neurons constitute such a bidirectional pathway between different parts of the brain, or if the bidirectional pathway can be thought of as a 'circuit': a pathway of neurons that eventually comes back to a certain part of the brain.

This question is especially interesting in light of abstract thoughts. Let's make some extremely generalising (and ludicrous) assumptions and assume that our conscious thoughts are governed by our hippocampus only. That is, we assume that thinking about a matter without input from sensory neurons causes the hippocampus to fire an action potential into some specific cluster of neurons (somewhere in the brain). E.g. we assume that thinking about the letter 'A' causes the hippocampus to fire an action potential into the cluster of neurons that represents the letter 'A'. Let's also assume that the memory we have regarding the letter 'A' must be returned to the hippocampus, in order to continue our thought process. For example, I might want to recite the alphabet in my head. Starting with the letter 'A', I then continue to the letter 'B', which arises in my conscious thoughts as a result of the firing of the cluster of neurons that contain information regarding the letter 'B'.

So if we assume the circuit, conscious thoughts $\rightarrow$ cluster of information fires $\rightarrow$ conscious thoughts to exist, then how would its feedback most likely work?

Let's take the example where we think of the letter 'A' and want to think of the letter 'B'. I have sketched two different theories about how the communication between these two clusters of information and the 'governing body of thoughts' (which I assumed to be the hippocampus), might be:

The difference is the following: in the second theory, all individual neurons are expected to be able to communicate directly to the hippocampus. Whereas in the first theory, the feedback to the hippocampus arises only when we have reached our destination: the letter 'B'. Clearly, if we assume that a specific thought process is able to self-induce action potentials (of course, this is highly debatable), at least one of the two theories must be partially true. For which one exists evidence?

My first intuition would be to say that the first theory is more likely, but this is ambiguous under Dale's principle: why would only some cells be connected to the hippocampus? On the other hand, I found it hard to believe that every individual neuron is directly connected to the hippocampus.

So now that I have explained my thought process, my question can be formulated as follows:

  How are clusters of neurons that are involved in abstract thoughts bidirectionally connected to the thought-governing-body (whichever actual part(s) of the brain this is)? Can we say that just a single neuron in the cluster provides the feedback to the thought-governing-body, or is every individual neuron that is involved in conscious thought potentially capable of a feedback loop?

Disclaimer: Yes, I'm not up-to-date to all the latest advances in neuroscience. Yes, I'm aware that my question might be ambiguous with respect to all the different types of neurons, connections and theory about neuronal networks and micronetworks. My question, however, is concerning the likelihood of the theories I presented. For which one do we have evidence. Are both wrong? If so, in what way? Are both right? If so, when does their difference play a role? etc.

To give a simple answer to the first part, the feedback generally happens in circuits of at least two neurons. A synapse is generally one way, transmitting information from the presynaptic neuron's axon to the postsynaptic neuron's dendrite. I'm sure there's caveats and exceptions because biology always has that, but that's the norm. A simple feedback loop might look like this: A excites B which excites C. C inhibits A as negative feedback.

The second question relies pretty heavily on the assumption that conscious thought originates from a particular part of the brain, or that one neuron is dedicated to one concept. This doesn't seem to be true. Things like memory and thought appear to be distributed, emergent properties of several circuits and areas. They might be organized or integrated by a particular part of the brain but it's not the same as having one central executive looking at all the inputs deciding what you think.

Think of it like a person working on an Excel spreadsheet. There's all the code for the OS, the software, the formulas in the spreadsheet. Those are all important parts of the process but the user doesn't need to see any of that. All they need to see is the end products of each process, and then they can figure out what to do with those products. So circuits and neurons can be involved in lower processing without connecting directly to the area that organizes and integrates information. Also, because higher level processes like thought are so distributed, there's likely to be multiple centers organizing/integrating information and all giving feedback to each other. Does that make sense?

Side note: I think you might be misunderstanding Dale's principle. When it says that neurons have the same chemical action at every synapse, that means they release the same neurotransmitter(s) but that doesn't mean they have to be connected the same way or that the neurotransmitter release has the same results. For example, say a neuron releases the excitatory neurotransmitter glutamate. If it synapses on another neuron that releases glutamate, that will promote excitation. But if it synapses on an inhibitory neuron that releases GABA, then exciting that neuron will actually result in inhibition.


How did scientists establish the reactions that occur in metabolism? How did scientists establish that macromolecules like proteins, carbohydrates and lipids are synthesized from other molecules with intermediate products by living cells. Did they observe this under microscope. I want to know this because I am studying bioenergetics and while studying photosynthesis and cellular respiration I have doubt that whether this all stuff is correct or not. I hope that you will help me to clear this doubt.

In addition to biochemical methods, a lot of this was figured out using radioactive tracers. Cells would be fed a radioactive substrate and as they convert the substrate to other molecules through metabolic reactions, the radioactivity can be detected in the products and intermediates.

Calvin's 1940s-50s experiments to establish carbon flow during photosynthesis (i.e. the Calvin-Benson Cycle) using $^{14}CO_2$ remain some of the most elegant work along these lines. You can actually read some of his reports here, though maybe someone else has a good link to a less technical overview.

Similar methods are still used today, though stable isotopes instead of radioactive ones are more commonly used.


How did the endoplasmic reticulum come to be? Organelles are sub-cellular compartments in cells. However prokaryotes don't use organelles to organise their intracellular space.

Evolutionarily, there is evidence that mitochondria and chloroplasts are ancestors of symbiotic prokaryotes. This theory is called the endosymbiotic theory.

I've tried to find an evolutionary story that explains other organelles, specifically the endoplasmic reticulum. There is plenty of literature about biogenesis of these organelles, but nothing about the history of their evolution. I don't think I have found the right area of literature. What did organelles originate from? I'm happy just to know a few keywords or a citation to look it up myself.

Found the following on wikipedia. Seems pretty self explanatory:

  The Golgi, ER, and lysosomes are likely to have evolved as a result of
  the plasma membrane going through invagination. An increase in the
  overall volume of a cell would require the plasma membrane to fold in
  order to maintain a constant surface area to volume ratio. These folds
  may have led to the specialization of internal membranes to maintain
  communication with the environment. In the first stages of eukaryotic
  cell life, the membranes may have been interconnected and attached to
  the plasma membrane. Later on, as their functions diverged, the
  membranes may have become separate structures


How credible is the Remenko's two-component color vision theory? I've come across an article (in Russian), which describes a nonlinear two-component color vision theory made in 1975 by S. Remenko. The article heavily criticizes trichromatic theory as very imperfect. There's a whole page related to the criticism. Some of the citations there refer to Feynman's lectures vol. I ch. 35, where also some doubts are expressed. See e.g. the part by Feynman:

  Using the three different kinds of color blindness, the three pigment response curves have finally been determined, and are shown in Fig. 35–8. Finally? Perhaps. There is a question as to whether the three-pigment idea is right, whether color blindness results from lack of one pigment, and even whether the color-mix data on color blindness are right. Different workers get different results. This field is still very much under development.

But the only English-language place I've found mentioning Remenko's two-component theory was the book "Computer Systems for Healthcare and Medicine" by Piotr Bilski and Francesca Guerriero, where the first name also looks suspiciously Russian.

So I'm somewhat skeptic about credibility of all this Remenko's theory and the criticism of the trichromatic theory. But having not much expertise in color vision theories, I thus prefer to ask the experts: is the theory by Remenko actually credible? Is it even known outside of Russian-speaking world? Has it been falsified? Is trichromatic theory really flawed in any significant way so that a replacement theory would be required (are Feynman's remarks out of date?)?

That era produced a lot of very questionable science from Russia; there is no good reason to doubt the three-component color vision theory, and it's also the basis of all RGB TVs and computer monitors. However, I can't read Russian so I don't have any idea what this two-component theory is.

Typical humans have three cone cells, which is the biological origin of having three components for color vision. Colorblind individuals who lack one of the three cones have color discrimination issues consistent with the three component model. I am not aware of any credible research that questions this.

The lack of further study into the theory you refer to probably puts it into the category of "not even wrong" - based on such flawed reasoning or premises that it isn't worth disputing.

Nathans, J., Merbs, S. L., Sung, C. H., Weitz, C. J., & Wang, Y. (1992). Molecular genetics of human visual pigments. Annual review of genetics, 26(1), 403-424.


Is marriage with half-cousin's daughter more risky than marriage with others? I want to know is marriage with half-cousin's girl more risky than marriage with a non-family girl?

Also I like to know if her parent are cousins(but from mother side), does it add more risk to this marriage or not?

The medical term here is consanguinity, or a consanguineous union. The risks of consanguinity are well studied, and based on the principle that children born to parents with shared genes are more likely to be homozygous for recessive alleles. Population level measurements of specific risks for, e.g., fetal loss, major birth defects, or other problems vary depending on the population studied. Many of these studies look at first cousins, where typical numbers are between a 1-5% greater risk for major birth defects and 4-5% greater risk for late miscarriage or death of a child before age 10. The data on earlier fetal or embryonic loss isn't conclusive.  You can read more about this in the review I linked to at the end of this answer. The specific risk for a specific individual isn't on topic here, since it is a personal medical question. If you are looking for an answer to that question, I'd suggest scheduling a visit with a medical geneticist.

Your diagram depicts marriage between half first cousins once removed, with an expected shared percentage of genes of 3.125%, equivalent to second cousins, which fits the definition of consanguinity generally used in the medical literature and allows application of studies that use that definition. The fact that one of the potential parents in this marriage was also the product of a consanguineous union may increase the risk.

Consanguinity is an important risk factor for many birth defects and other diseases (see Cecil Medicine Chapter 41 and this review)


How come only a handful of animals can do photosynthesis? As far as I understand, all the energy that living beings rely on comes from the sun. It's processed by plants in photosynthesis. These plants are consumed by herbivores, which in turn are consumed by carnivores. Energy trickles down that way, with photosynthesis being the crucial basis for all the other layers.
A couple of days ago I was wondering, how come animals don't do photosynthesis? This story talks about a few exotic animals that can do photosynthesis, but they seem to be an edge case.
It seems like there's a rule of thumb: Iff a creature can do photosynthesis, it can't move. Why is this so? Wouldn't it be beneficial for a herbivore-like mammal to be able to create sugars directly from sunlight? They wouldn't have to graze at all, just find water and sunlight. It's possible they'd have an easier time avoiding predators and expanding into more territory.
Can you think of a good reason why such creatures never became mainstream?

It is all about energy.
It is estimated to take 5000 square meters of plants to feed the average person in the developed world, while the same source gives the lowest possible for a human under ideal conditions at 700 square meters.  In comparison, the average person covers less than 1 square meter.  While there is a lot of waste (animals are able to eat only a few percent of the energy the plant produces), the total energy available from photosynthesis is still orders of magnitude smaller than daily requirements for a typical animal.
Even in the case of the slug you linked (which you would expect would need about as little energy as possible for a mobile animal), it seems they obtain little or none of their actual energy from photosynthesis.
Hence you see photosynthesis restricted to life that has extraordinarily low energy requirements, which typically means being stationary (or moving very, very slowly as in the case some plants).  As soon as you adapt to a mobile, higher energy niche, you need access to a lot more energy than photosynthesis can provide.


Difference between Cary-Blair and Amies transport media for Staphylococcus and Streptococcus? I normally use Amies medium, but I today heard that Cary-Blair is also possible.

When should you use Cary-Blair medium?

This site (no connection) states (my emphasis):

  Unlike Cary-Blair Medium, which is almost exclusively associated with enteric transport, both Stuart and Amies Medium have been widely used for the transportation of a diverse range of clinical swab samples from sites including the eye, ear, nose, throat, skin, genital tract and wounds.


Do different microscopes and attached cameras differ in crop factor between each other? I analyzed a bunch of microphotographs recently and used "% of image area" to describe the area of structures (chorionic villi, had to show their density in placenta). However my professor suggested I should have used mm2. There is no problem in conversion, but I suspect different microscopes may have different areas of field of view for the same scale. Thus the conversion will make the results just more difficult to interpret.

So does the absolute area of microphotographs of the same scale and size differ between microscopes/cameras? Or is it somehow standartized?

Thus the conversion will make the results just more difficult to interpret.

I'm not personally familiar with this specific measurement, but in general, unless there is a specific convention in how to report a measurement, an absolute measurement should make the results easier to interpret, not more difficult (vs. % of image area). From a quick search, it seems like absolute measures of area, volume, and density are typically used when reporting chorionic villi measurements, so there isn't a convention to do it another way.


Why do we sweat after drinking water and running? Why do we sweat after running?
Also we sweat sometime after drinking lots of water. Why it is so?
Can someone please enlighten me in this regard?

Exercise, such as running, increases muscle activity.  This increases the energy demand of these tissues, which increases the rate of cellular respiration.  Respiration releases heat as a by-product, therefore the body is hotter during and after exercise.

Sweating is a homoeostatic mechanism to keep core body temperature constant. It is a response to lower the body temperature. When the body becomes too hot, sweat is released onto the surface of the skin.  The water from the sweat then takes some of the excess heat energy from the body and uses it to evaporate.  Because water has a relatively large specific heat capacity a lot of heat can be carried away by this method.


Are all cone cells connected directly to the brain? Coming from a computing science background, I noticed that cameras have orders of magnitude fewer wires than pixels. For example, the Raspberry Pi Camera v2 has 8 megapixels, but only 10 wires connecting it to the board. In human-made systems, it is preferred to time-multiplex pixels over few wires or, even better, already compress or encode image information on the camera.

I was wondering if the human optical system features something similar. Does the eye compress, encode or time-multiplex the image "pixels" it captures before sending the information to the brain? Or is each cone cell ("pixel") connected directly to the brain?

(In case the latter: Wow! The optical nerve must have a huge bandwidth.)

Are all cone cells connected directly to the brain?

No.  Cones connect to ganglial cells.

Let's explore the numbers.  Our eyes contain about 6 million cone cells, 90 million rods, and comparative handfuls of additional photosensitive cells (ipRGC's) that don't play a role in vision.

The optic nerve is a bundle of roughly 1 million fibers (perhaps up to about 1.7 million).  So by just running the numbers, it doesn't fit.

I was wondering if the human optical system features something similar.   Does the eye compress, encode or time-multiplex the image "pixels" it captures before sending the information to the brain?

Let's focus on photopic vision (color vision, which happens when lighting conditions are sufficient).

Our perception of color starts not with the cones, but with ganglial cells in the retina.  This is different than how an RGB camera works; our brains don't process color in terms of "pure cone signals".  Instead, color is processed in three channels; a "red-green" channel that measures the difference between L cones and M cones;  a "yellow-blue" channel that adds input of L and M cones and subtracts out contributions from S, and a "brightness" channel that computes the sum of all cones.  This is referred to as opponent processes.  Maybe we can call this encoding.

In addition to this, there are ganglial cells in our retina that contribute to edge detection.  These cells work similarly to ganglial cells that perform difference measurements for opponent processes, only they connect to the same cone types.  Since ganglial cells connect locally, if there's a large difference between stimulation of two cones next to each other, it's an indication that there's an image of an edge of something projected onto that spot.  If we can't distinguish individual cones, but these things can distinguish edges which to us are the more interesting property, maybe we can call this lossy compression.

Outside of this, a huge amount of our brain is devoted to visual perception.  There are some really strange quirks about our eyes; most popular is the existence of the blind spot.  Additionally, our 90 million rods are squeezed more into peripheral vision, leading to fuzzier imaging in photopic conditions the farther away we are from the fovea.  Furthermore, chromatic aberration can be quite a pain, but L and M cone sensitivities are very close to each other.  So where absolute sharpness matters, we have less S cones around; in fact, in our foveola, there's nothing but L and M cones.  Our brain makes up for this, by stimulating us to move our eyes constantly and rapidly (saccades).  As we do so, the visual cortex goes into overdrive, filling in that blind spot, crisping up that periphery a bit, painting in an illusory blue in our center vision, etc.  Though this involves "moving the camera around", we could maybe call this a sophisticated, high level form of time multiplexing.

Much of this information is available from wikipedia articles, though you might need to know what to look for; so here's a starting guide:

Cone_cell for cone cell counts
Fovea_centralis for cone density in center in vision, with picture
Optic_nerve for count of optic nerve bundle fibers
Opponent_process for opponent process theory
Receptive_field contains discussion of edge detection


Why doesn't the avocado turn brown when it is kept with its seed? Why doesn't the avocado turn brown when its kept with its seed?
What does the seed release that slows down the oxidation process?

This is actually only partly true: When you cut the avocado in half, only the part where the seed really sits stays green, while the surrounding cut area gets brown over time.

Avocados turn brown because of an enzyme called polyphenol oxidase, which oxidizes the green contents of the avocado upon contact with oxygen. The seed blocks the access to oxygen, thats why it helps here (but only where it makes close contact). See this and this links.

There are two ways of preventing the browning of cut avocados (besides avoiding oxygen contact): Use either lemon juice, which inhibits the enzyme (by chelating the metal ion from its active center) or keep it cooled to slow down the procession rate of the enzyme (which will only work for some time).


Dyes to bind to double stranded DNA? Are there any commercially available fluorescent dyes that will bind only to double stranded DNA (not RNA, single stranded DNA etc.) for studying in vitro using confocal microscopy?

Most of the dyes used for visualization bind with a much higher affinity to dsDNA. This would be SybrGreen, EtBr (although this will bind RNA as well).
There is a pretty comprehensive website from Life Technologies about Nucleic acid stains that is worth a look.

There is as well a publication on this topic: "DNA Staining for Fluorescence and Laser Confocal Microscopy"


Human genetic diversity in Africa in comparison with the rest of the world Background

The claim ...

  Most of the genetic diversity in humans is in Africa

... is quite common. On Biology.SE, it is easy to find posts that make this claim. Consider for example:

Do humans have enough biological differences to be grouped into races or subspecies?
How do we know the human species arose in Africa?
What is the correct classification of population groups of homo sapiens?

Question

Is the claim true?
What fraction of the total genetic diversity is present in Africa?

I understand that the term genetic diversity is often used in a vague sense. Please make sure to explain what statistics has been considered in the study you would refer to when giving estimates of what fraction of the genetic diversity is found in Africa. Note that I am not asking "why is it true?" but only "is it true"?

Here is a tree based on mitochondrial DNA variations in human populations.

van Oven M, Kayser M.  Hum Mutat. 2009 Feb;30(2):E386-94.
Updated comprehensive phylogenetic tree of global human mitochondrial DNA variation.

Looking at genetic distance between populations via mitochondria DNA, all nonafricans are descended from a founder in one mtDNA group (L3).  All the other L groups are African populations: L0 is the San people, L1 is Mbenga pygmies, L5 is Mbuti pygmies, and the others are other African groups.

If one considers each L haplogroup to represent genetic variation then 5/6 (83%) of human genetic variation is from African populations.

From a different source looking at genetics differently   A map of human genome variation from population scale sequencing Nature. 2010 Oct 28; 467(7319): 1061–1073

  Populations with African ancestry contributed the largest number of
  variants and contained the highest fraction of novel variants,
  reflecting the greater diversity in African populations. For example,
  63% of novel SNPs in the low coverage project and 76% in the exon
  project were discovered in the African populations, compared to 20%
  and 33% in the European ancestry populations for the exon and low
  coverage projects respectively.


Are human males and females more genetically different than members of other species? I'm looking at this Ted talk about a Saudi Arabia woman who dared to drive a car in the last few years. This reminds me that until the last century or so, women (all over the world?) enjoyed less rights and might've been pigeonholed into roles predetermined by society. Those roles might've encouraged certain traits, and discouraged others. Those who did not conform might've been punished, like the woman in the talk above received death threats and was jailed.

This sounds to me like selective pressure, did it really exist, and did it have any effect on the genetics/traits of modern women?

This makes me interested in the question - compared to other species, are men and women more genetically different because of selective pressure put on women to conform to male-dominated world for thousands of years before 19th century?

I'm not sure I buy your premise: firstly, the degree and form of male-female differentiation in social roles has varied widely across time and culture in human history so I doubt it forms a uniform evolutionary driver such as you describe. Secondly, the degree of male-female differentiation appears to me to be much greater in species such as gorillas, lions and peacocks than it does in humans so I'm not convinced that humans would stand out on this front as a species we'd expect to have greater genetic differences.

Even so, the only genetic difference between male and female humans is the Y-chromosome. The X appears in both males and females and doesn't have exclusively female lineage so it can't acquire separate genes for male and female. The Y chromosome contains very few genes so its not capable of manifesting a major genetic gap and because there is no recombination in the Y chromosome it is not a fertile ground for new genes anyway.

So males and females have essentially the same genes. However, this isn't the whole story because how, when and whether genes are expressed is about as important as what genes are encoded anyway. It is these differences that enable big differences between the sexes not actual coding differences.


Would salt cause a pistachio nut not to be able to germinate? If I buy a bag of pistachio nuts that have been hand picked off the tree when ripe, then salted in a (light) saltwater solution, then vacuum-sealed, and stored in a refrigerator, then will they germinate if I take them out and soak them in a moistened towel laying out in the sun?

This article https://wikifarmer.com/how-to-grow-pistachio-tree-from-nut/

says unsalted.  Lots more on that site about growing them.