In what "space" does egg mature in Kiwi? This huge egg here, is it sort of tethered to the ovary, filling up the coelomic cavity, and then exiting out of the infundibulum, or, where is it in the bird exactly? What "space" does it occupy?

In birds, eggs mature post-fertilization in the magnum and "shell gland", sometimes called a uterus.

I can't find anything to suggest a kiwi is any different, despite their large egg size. An exception is that kiwi have two functional ovaries (yet the join in one functional oviduct and the rest of the reproductive system is only present once) (Ballard & Cheek, 2016). Given this source mentions this specific difference, it seems unlikely they would have omitted any other important differences.

This course page may be useful for bird reproductive anatomy more generally: http://people.eku.edu/ritchisong/avianreproduction.html

Ballard, B., & Cheek, R. (Eds.). (2016). Exotic animal medicine for the veterinary technician. John Wiley & Sons.


Is there a biological term for an activity period that is determined by temparature In general we refer to the activity period of organisms in terms of the period of the day that they are active.  Diurnal, crepuscular, nocturnal, matutinal, and vespertine, for example.

There are certain desert animals whose activity patterns seem to match a temperature range more than they do the day/night pattern.  Is there a term for this type of activity pattern?

I doubt there is such term.

Note that diurnal and seasonal are likely pretty well correlated with the temperature cycle. The temperature cycle is, I would presume, mainly affected by the daily and seasonal cycle.

You can talk about a behaviour that is dependent upon the temperature which fluctuates daily and seasonally. Looking for specific keywords on Google Scholar, it appears that most authors go through short phrasing of the kind to express this concept.


Why did humans lose their fur? The little amount of body hair humans have don't seem to be of much use for keeping warm.
Our Simian cousins on the other hand sport thick furs.

At which point during the species evolution and why did humans lose their fur?

This is an interesting question, and there are a number hypotheses available to explain this phenomenon. The short answer (as far as I can say after my literature search) is that we don't know the answer for sure. The long version follows below.

The main problem with all these hypotheses is that though they may have a valid point, a definitive hypothesis hasn't been demonstrated yet. All these hypotheses are listed in the first reference, with a ton of additional references in the paper. I will summarize the different hypotheses only briefly here; for details please read the paper. The second reference is also interesting.

The point when this process started was after the last common ancestor of chimpanzee and humans when our two lines diverged. Chimpanzees are our closest relatives and still have hair coats, so this process must have started afterwards. Analyses of MC1R mutations (which affect pigmentation) suggest that human have been hairless for at least 1.2 million years. See reference 3 for details on this.

Aquatic ape hypothesis (also known as aquatic ape theory): This hypothesis states that modern humans spent some time semi-aquatic. In this lifestyle fur does not insulate very well and this led to an evolutionary disadvantage.

Cooling hypothesis: This hypothesis states that the modern humans lost their hair when they left the forests and started to live on the savannah. There they got too warm with their fur and finally lost it. This hypothesis sounds logical at first thought, but has a few problems. Naked humans have two problems: during the day they collect quite some heat via their skin, which requires them to have a cooling system (we sweat to cool us), and during cold nights we need a lot of internal energy to keep our temperature stable. Insulation however works both ways (not only keeps the warmth in, but also can keep heat out), and indeed some savannah monkeys have denser fur than their relatives in the forest. The cooling system will also lead to water loss and potential dehydration.

Hunting hypothesis: This hypothesis states that humans started becoming carnivores and therefore had the need to run for extended periods of time to hunt for meat. This leads to thermal overload; without a fur they can release this heat much faster to avoid overheating.

Bipedality hypothesis: This hypothesis assumes that modern humans, walking on two feet, have a lower direct influx of solar radiation. This lowers the chance for overheating.

Allometry hypothesis: Allometry states that species which get bigger during evolution, do not have all their organs getting bigger at the same rate. The hypothesis states that humans got bigger, the number of hairs stayed the same, and finally got lost.

Clothing hypothesis: One of the more illogical hypotheses, this assumes that hair loss wasn't critical for humans as they managed to make themselves clothes.

Vestiary hypothesis: A mix of the cooling and the clothing hypothesis: Here it is assumed that hair loss is beneficial due to more cooling and that the negative effects of too much loss of heat were counteracted by the invention of artificial insulation.

Neoteny hypothesis: Neoteny denotes the retention of of juvenile physical characteristics in adults. Humans are characterized as retarded in development (compared to the apes) and mature more slowly. Additionally, it is assumed that some characteristics (here loss of hair) of juvenile or fetal apes are maintained.

Carrion-eating hypothesis: Another strange hypothesis, this assumes that man as a messy eater (like vultures and condors, which have naked necks) have an advantage of being hairless.

Sex-related hypothesis: This hypothesis assumes that hairless skin is more sensitive to stimuli like touch, temperature and pain. This would allow more sensitive social contacts, especially between man and woman, but also between woman and child. Pubic hair is not explained by this hypothesis.

Adaptation-against-ectoparasites hypothesis: Here it is assumed that naked humans are less prone to harbour ticks, fleas and other parasites which hide and live within fur. Apes have great social rituals of removing these within their group.

References:

Evolution of nakedness in Homo sapiens
The Hairless Mutation Hypothesis Explains Not Only the Origin of
Humanization from the Human/Ape Common Ancestor but also Immature
Baby Delivery
Genetic variation at the MC1R locus and the time since loss of human
body hair.


Does muscle get bigger by increase in size of individual cells or increase in number? Somewhere in the back of my mind, I have the claim that a muscle never increases its amount of cells but, if the muscle gets bigger, it's simply because individual cells get bigger.

The book Anatomy Trains on page 36 cites "Changes in sarcomere length and physiological properties in immobilized muscle by  Williams et al" when it makes the claim :

  Stretched, a muscle will attempt to recoil back to its
  resting length before giving up and adding more cells
  and sarcomeres to bridge the gap.

Is that true? Do muscles increase the number of their cells in that way?

The "back of your mind" is correct: "if the muscle gets bigger, it's simply because individual cells get bigger."

Growth of muscle can occur in three ways:

by an increase in muscle cell numbers
by an increase in muscle fiber diameter
by an increase in fiber length.

However, growth in cell numbers is limited to the prenatal and immediately postnatal period, with the animals and man being born with or soon reaching their full complement of muscle cells.

  [G]rowth occurs by either hypertrophy of the existing muscle fibers by adding additional myofibrils to increase the muscle mass or by adding new sarcomeres to the ends of the existing muscle fibers to increase their length. Both of these mechanisms occur during the growth process. Growth in the girth of the muscle fibers... may be stimulated by development of stress creating an unequal pressure with splitting at the Z-band and development of additional SR and T-tubule systems. This adds to the diameter or girth of myofibers without any hyperplasia. The growth in length occurs at either end of the fibers and results in addition of new sarcomeres. In both cases, new myofibrillar protein must be synthesized and deposited in the muscle cells.

Adding or removing sarcomeres and myofibrils is determined by exercise, that is, the degree of force a muscle can generate which is in turn dependent on the degree of overlap of the thick and thin filaments. Thus, the amount of tension would control the number of in-series sarcomeres and the number of myofibrils in a single muscle fiber.

Nutrition is also known to play an important role in muscle growth, but growth (that is, increase in girth) cannot occur without exercise.

The exact roles of GF and IGF-I are not completely clear.

Muscle size does not increase by the addition of new muscle cells:

  The results show that the increase in muscle cross-sectional area from childhood to adult age is caused by an increase in mean fiber size. This is accompanied by a functional development of the fiber population: the proportion of type 2 fibers increases significantly from the age of 5 (approx. 35%) to the age of 20 (approx. 50%), which, in the absence of any discernible effect on the total number of fibers, is most likely caused by a transformation of type 1 to type 2 fibers.

Activation of satellite cells, a claim made by body builders, is mis-represented by them. The satellite cells seem only to aid severely damaged muscle cells to heal, not to increase in number.

Muscle growth and exercise
Muscle hypertrophy
Growth and development of human muscle: A quantitative morphological study of whole vastus lateralis from childhood to adult age
Regulation of muscle mass by growth hormone and IGF-I


Forest Fires and Horsetails In our school textbook, it is written that sometime forest fires can occur due to rubbing of two horsetails. In the image that I searched online, the plant itself looks thin and rod like with leaflike structures arising from nodes. But many other plants have similar structure. So it might not be its morphology.

What special thing about horsetail starts the fire? Why don't other plants show same thing?

I didn't believe this was a real thing, and I'm still very skeptical, but it is something that's claimed to happen!

  Their stems & leaves have a siliceous epidermis, so if rubbing b/n 2 horsetails occurs, a forest fire may be produced

--The Bottled Ocean of Biology, by Nisarg Desai, 2017

Why don't other plants show same thing? Another plant, bamboo, is supposed to do the same thing:

  How these fires originate is uncertain ... it has been suggested that a probable cause is the rubbing together of the silica-coated bamboo stems as they sway in the breeze.

--Burma, by R. Talbot Kelly (2004)

The same claim about bamboo is made in an Indian Government document on forest fire management.

What special thing about horsetail starts the fire? Apparently the claim is that it's the silica in the stems of the plant that is the important factor, and that horsetail and bamboo are both unusual in that regard. This does seem to be true:

  ... in general, ferns, gymnosperms and angiosperms accumulated less Si in their shoots than non-vascular plant species and horsetails.

--Phylogenetic Variation in the Silicon Composition of Plants

Bamboo isn't mentioned in that article, but the presence of silicon in bamboo is supported elsewhere:

  One of the advantages of bamboo over wood is that bamboo contains some silicon in both inner surface (pith-ring) and outer surface (rind) of the bamboo culm.

--Calcium phosphate formation induced on silica in bamboo

As I say I remain very skeptical. There's no evidence shown that this has actually happened. Is it telling that all these claims come from the same general region (India and Burma)? My guess is that this is an old wives' tale that's been written down and uncritically accepted, but if someone has actually seen this happen I'd be happy to be proven wrong, because the idea of plants sparking out flames in the wind is a pretty cool one.

Edit to add a link claiming that bamboo-on-bamboo generates sparks due to the silicates:

  The method consists of striking sparks out of  the culm of Schizostachyum bamboo with flint, broken pottery, china or even another piece of bamboo. The sparks that occur by striking the Schizostachyum bamboo are presumably generated by the high silica content in this genus of bamboo.

--Bamboo Strike-A-Light, by Tom Lourens, Ash Kivilaakso and Ed Read (My emphasis)

Edit to add that the overall concept of plants starting their own fires has been seriously looked at; the author is skeptical:

  Individual plant traits (such as leaf moisture content, retention of dead branches and foliage, oil rich foliage) are known to affect the flammability of plants but there is no evidence these characters evolved specifically to self-immolate, although some of these traits may have been secondarily modified to increase the propensity to burn. ... It is more parsimonious to conclude plants have evolved mechanisms to tolerate, but not promote, landscape fire.

--Have plants evolved to self-immolate?

Notably, in his list of factors potentially allowing self-immolation, he does not list silica, and horsetail isn't mentioned at all.


Does a plant have to have leaves to produce fruit? Is it possible that a plant can still produce fruit, even though it may not have leaves? Are there any plant species that can produce fruit without leaves?

In short: yes, a plant have to have leaves to produce a fruit. Both from the evolutionary viewpoint as from the anatomical viewpoint.

All the fruit producing plants belong to a group we call Anthophyta (or Magnoliophyta), meaning in greek "plants with flowers". These fruit producing plants are all descendant from ancestors that have leaves, specifically what we call megaphyll ("big leaves").

Even Anthophyta that apparently stopped producing leaves, as cactuses, still have them. According to Mauseth (Botany: An Introduction to Plant Biology):

  Although all flowering plants possess leaves, stems and roots, these parts have been modified so extensively in some species that they may not be recognizable without careful study. For example, cacti are often described as leafless, but they actually have small green leaves between 100 and 1000 micrometers long.

More important, spines are highly modified leaves (and that's the difference between spines and thorns). In a cactus, these highly modified leaves come from a structure called areole, that also produces another highly modified leaf: the flower.

Now to the anatomical part: flowers are specialised leaves:

http://www.ncbi.nlm.nih.gov/pubmed/11440721
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1677-04202005000400001
http://dx.doi.org/10.1016/S0960-9822(01)00024-0
http://www.ijdb.ehu.es/web/paper/052020pr

...and the list continues. According to Lodish, "Molecular Cell Biology" (http://www.ncbi.nlm.nih.gov/books/NBK21561/):

  Genetic studies have shown that normal flower development requires three classes of floral organ – identity genes. In plants with mutations in all three classes, concentric whorls of leaf-like structures replace the floral organs, indicating that these structures are modified leaves. (emphasis mine)

And according to Durner, "Principles of Horticultural Physiology":

  Flowers are modified leaves. Upon exposure to specific environmental signals such as daylength or temperature or at a specific point of plant development, shoot meristems start to form flowers rather than leaves. (emphasis mine)

And from a paper published in Nature, 2001 (http://www.nature.com/nature/journal/v409/n6819/full/409469a0.html):

  Goethe was right when he proposed that flowers are modified leaves. It seems
  that four genes involved in plant development must be expressed together to
  turn leaves into floral organs. (emphasis mine)

Flowers have several parts, and one of them is the ovary, which will turn into the fruit after (but not necessarily) the fecundation. Thus, in conclusion, fruits are a modified part of a flower, and flowers are specialised leaves.

It's worth mentioning that all fruit plants have leaves, but of course not all plants with leaves have fruits.


Experiments in vitro vs those with dead organisms and fixated tissue Does the term in vitro necessarily imply that the organism/organs/cells of study are  dead?

If not, is there an alternative latin term to refer to studies of dead biological matter ? (e.g. in Connectomics where the tissue is biologically dead, and has been fixated and sectioned with a microtome)

Does the term in vitro necessarily imply that the organism/organs/cells of study are dead?

No, in vitro studies are often carried out with living cells - just think of in vitro fertilisation. The nearest I can come up with for what you want is histology, but I think even this encompasses studies of living cells and tissues.


What is background binding? I'm reading a journal article about mitochondrial protein import and it mentions that one of the mutant proteins tested showed background binding with another protein. What the heck is background binding?

Background binding in this case would be the extent to which two proteins associate together by chance.

A hypothetical example: you may have a mitochondrial protein import complex.  Usually cases there is a specific peptide sequence the import complex binds to , but proteins without an import peptide sequence will occasionally be bound to the import complex.  This is called the background binding for the protein complex.  The experimentalists might have measured this by cutting the import peptide sequence off a mitochondrial protein for instance.

Any candidate would have to bind to the complex more than the background case to be considered a target for mitochondrial import.


Embryo development terms I'm trying to couple the following terms:
cytoplasmic determinants, induction, positional information, hox genes, pattern information, morphogenisis, determination and differentiation.

I hope someone can explain me the connection between these terms,

thankyou,

When in doubt go back to definitions I say (as I am now).

cytoplasmic determinants: regulatory molecules located in specific distributions around egg cytoplasm

Induction: process by which the presence of one tissue influences the development of others

positional information, signals cells about its relative position to other cells.
hox genes

Differentiation: the process of a cell becoming a specialized type of cell through regulated gene expression

Determination: process by which portions of the genome are selected for expression in different embryonic cells

Pattern formation (aka morphogenesis) → events that determine the spatial organization of an embryo

Hox genes establish anterior posterior axis and regulate gene expression.

I would change,
cytoplasmic determinants → differentiation via determination → pattern formation (rather than information)
morphogen lead to pattern information (since these are the signals)
hox genes → morphogens → pattern information → pattern formation


Do cows produce milk excessively? Do cows produce more milk than it is required for their calves? It seems like cows are able to provide milk all the time (all year around). Is it so? Or do they, like other mammals, produce milk only in ammounts requeired by their offspring?

The average domesticated dairy cow produces far more milk than would be required to feed their calf. All cows, wild and domesticated, will only lactate in the period between their calf's birth and weaning. Milk is calf-food, and when there's no calf, there's no evolutionary advantage in producing milk.

On dairy farms, cows are milked twice daily, from spring (when they give birth) until late autumn. This mechanical milking 'fools' the cow into continuing to lactate. When a cow has stopped lactating, they will only start again after giving birth. This means that you can't just start milking a cow and expect to get milk.

Generally farmers milk their cows from spring (birth) until late autumn. The reason for stopping in autumn is simply because the grass grows much slower in winter, so there isn't enough food to support lactating cows. However, it is entirely possible to milk longer than a year; I know of farmers who milk their cows continuously for two years. These farmers will have to purchase a lot of supplimental food (like hay or silage) during winter. The advantage of milking for longer than one season is that the cows do not have to give birth every spring, but instead only every second spring.

I believe (but can't guarantee) that in winter, most milk purchased in a shop comes from the opposite hemisphere. I do know that here in New Zealand, we export a lot of milk to northern-hemisphere countries.

If you were to suddenly stop milking a cow, they might get sick but generally they will survive. It's still something to avoid!
Although if the calf is left with their mother then the cow would be relieved.

I do not have an 'official' source for these facts. However, I grew up on a dairy farm, so this was my life.


What biological constraints are there on how large a spider can grow? Spiders fascinate me, but what intrigues me the most is just how big some spiders can get, which leads me to my question. What biological constraints (if any) would limit how large a spider could grow, given ample food and no predators?

The standard view on this is that the size of terrestrial arthropods like insects and spiders  is limited by the atmospheric concentration of oxygen. This is because they rely upon diffusuion of oxygen into the 'blood' or haemolymph via a system of tubes called trachea that open on to the body surface at the spiracles. As the body grows larger the proportion that has to be taken up by the trachea gets larger. Consistent with this is the presence of fossil giant dragonflies, Meganeura dating from the Carboniferous era when oxygen levels were at an all time high. However you will find that if you go to the Wikipedia page for Meganeura that this idea has been disputed, so the answer may be that no-one really knows.

In relation to alternative explanations; a recent paper by Clapham & Karr (2012) compares fossil insect wing lengths and oxygen concentrations to study the historical drivers of evolution of body size. They conclude that oxygen seems to be the main driver until the end of the Jurassic, but after that biotic interactions (such as bird predation) could be more important.


Hardy-Weinberg Equilibrium Question I have four questions concerning H-W Equilibrium:

(i) In a population of mice, the presence of black spots is the result of a homozygous recessive condition. If the frequency of the allele for this condition is 0.15, what is the approximate percentage of heterozygous genotypes in this mouse population? (Assume that the population is in Hardy-Weinberg equilibrium.)

I thought this implies that $q=.15$, $p=.85$ and thus the percentage of heterozygous genotypes is $2pq = .255$. Online answers seem to yield a ubiquitous $.72$.

(ii) In a population of giraffes, dark brown spots are the result of a homozygous recessive condition. If the frequency of the allele for this condition is 0.10, what percentage of the individuals in the next generation would be expected to be homozygous dominant?

Is this simply $(1-q)^2 = .81$?

(iii)   In a population of monkeys, the allele that causes long hair at the tip of the tail (H) is dominant, while the allele that causes short hair at the tip of the tail (h) is recessive. If 67% of the monkeys have long hair at the tip of their tails, what is the frequency of the dominant allele?

I worked this as $p^2 + 2pq = .67$, so $q^2 = .33$, so $p = 1-\sqrt{q} = .4255$. Again, this seems to come up on the internet as incorrect.

Moreover, in the below picture:

It seems to me that the answer should be $(1-G)^2 = (1-.45)^2$, but this does not appear as an answer.

Any help appreciated.

In a population of mice, the presence of black spots is the result of a homozygous recessive condition. If the frequency of the allele for this condition is 0.15, what is the approximate percentage of heterozygous genotypes in this mouse population? (Assume that the population is in Hardy-Weinberg equilibrium.)

We know the frequency of the allele (0.15) and we're looking for the frequency of the heterozygotes. $2\cdot 0.15(1-0.15) = 0.255$.

  (ii) In a population of giraffes, dark brown spots are the result of a homozygous recessive condition. If the frequency of the allele for this condition is 0.10, what percentage of the individuals in the next generation would be expected to be homozygous dominant?

Yes, you are right it is 0.81

  (iii) In a population of monkeys, the allele that causes long hair at the tip of the tail (H) is dominant, while the allele that causes short hair at the tip of the tail (h) is recessive. If 67% of the monkeys have long hair at the tip of their tails, what is the frequency of the dominant allele?

Although the notation is wrong ($p=1-\sqrt{q}$), the result is correct.

  [last question]

As both genotypes GG and Gg are grey, we know that $p^2 + 2pq ≈ 0.45$ (Rather looks 0.48 from the figure though), where $p$ is the frequency of the G allele. From that you can calculate $p$ and $q$ and therefore calculate the frequency of the double homozygous gg


Will dead cells in culture media have any significant impact on Live cells during incubation? I am generating stable cell lines and have something like 25+ culture flasks to take care of. Ideally I can let dead cells sit in the media with the live adherent without rushing to change media constantly - Will this affect growth of live cells - I don't want to hinder them as they are already sitting in high[] Hygromycin

I'm not sure if this is linked to the actual dead cells, but I've found that not changing the media on plates while trying to generate lines from primary cultures can lead to contamination. Again, I haven't determined if this is because there are dead cells available for contaminants to derive nutrients from, or if it's just because changing media removes contaminants before they can grow too much. You might want to keep that in mind, though. I've found that changing media every 3 days is good enough.

Also, it depends on what you want to use your lines for. If you're hoping to study cell signaling or polarization (like if these are immune cells), it may be a problem, as the dead material will activate immune cells, and alter their signaling patterns. This has less to do with your worry about overall growth and more about you developing a good model for whatever you're doing.

To be fair, these signaling shifts can modulate proliferation in culture, but that's really going to vary from cell type to cell type. Sorry for being a bit vague! It's just that all cells are different- I happen to work with immune cells that are fairly finicky. There are other types that are a lot more robust, however, like fibroblasts, that you could probably spit on and they'd be fine.

If changing the media every 3 days really is too cumbersome, you could try splitting off small subcultures and doing a mini-experiment to see if changing the media vs not impacts confluence after a week or so? That would tell you how flexible your cells are when it comes to this.

Edit: Here are some publications that discuss the effects of dead cells in culture and differences between cell types. I also recommend that if you're using a cell line, looking up information via the ATCC website and reading their datasheet and some of the top references they site that likely describe how the line was isolated and best practices for culture.

"Inhibitory effects of persistent apoptotic cells on monoclonal antibody production in vitro" - a good example of how a lack of dead cell removal in vitro can impact cell function/phenotype and highlights the differences between different cell types.
"Cell death in mammalian cell culture: molecular mechanisms and cell line engineering strategies" - a good review that touches on the actual molecular mechanisms to which I was alluding. I particularly recommend reading the section "Induction of cell death in mammalian cell cultures", as it summarizes and links to several primary resources that show how increases in cell death can affect things like productively, growth, and cell number. It also does a good job of touching on the different kinds of cell death, which is important to understand but may be a bit too in-the-weeds for the original question.
"Links between metabolism and apoptosis in mammalian cells: Applications for anti-apoptosis engineering" - similarly good as the previous source, but looks at it through a more metabolic lense, which I think is helpful when considering the realities of cell culture.


Why do most plants reflect green and others other colors? I have read that chlorophyll absorbs red and blue.

  As shown in detail in the absorption spectra, chlorophyll absorbs light in the red (long wavelength) and the blue (short wavelength) regions of the visible light spectrum. Green light is not absorbed but reflected, making the plant appear green. Chlorophyll is found in the chloroplasts of plants.

It did not mention what the difference in chlorophyll between a red leafed plant and a green plant?

Does chlorophyll only come in green?
 So what in chlorophyll determines if other colors than green are reflected in plants that are naturally red? If chlorophyll needed can only be green would not the color green and the red from a " pigment" look brown?

Japanese Blood Grass

Blue Selaginella

Solenostemon scutellarioides

Tl;dr : Some plants reflect green while others don't simply because some plants are green while others are not.

Plants contain chlorophyll, but are not 100% made of it. Parts of the plant that contain a high amount of chlorophyll will look green, (Leaves, stem) while other parts that contain less chlorophyll and contain more of other pigments will look different. The flower looks red because it contains a lot more red pigment than any other pigments. The fruit looks yellow because it contains a lot more yellow than other pigments.
Carotene(orange) and Xanthophylls(yellow) are examples for pigments which absorb all colors except orange and yellow respectively, they reflect these colors. so it appears to be orange or yellow.

"Chlorophyll absorbs red and blue" is just another way of saying chlorophyll is green in colour.


Are polyploidal organisms parasatized by selfish genes? And if not, why not? Certain prokaryotes are polyploids. For example, Thermus thermophilus has about five copies of its genome (http://jb.asm.org/content/192/20/5499.full). One extreme polyploid, Epulopiscium fishelsoni, has tens of thousands of copies of its genome (http://www.pnas.org/content/105/18/6730.full). (Some eukaryotes are polyploid as well.)

As each copy replicates separately it would seem likely that spontaneous mutations would arise and over time, and such an organism would become a hybrid of many distinct genomes coexisting in a single cell.  This seems like an ideal place for selfish copies to arise (though perhaps no more so than any other organism - I think I've read that even prokaryotes are prone to plasmid parasites).

So, does this happen?  If not, why not? Is there some copy-checking mechanism (some extremeophiles seem to have a DNA-repair mechanism) or some mechanism that inhibits reproduction by genomes that are (somehow) determined to not be contributing to the overall metabolism of the cell?

In short, being haploid or polyploid should not protect you from Selfish Genetic Elements (SGES).

Almost all eukaryotes are polyploid. Plants are the oft-cited example. Wheat, I believe, is hexaploid for example. Polyploid bacteria are the exceptions typically (if we consider ploidy to be of the whole genome). However, even in truly haploid bacteria, the genome in any given cell is usually actively being replicated, so some of the genes are actually present more than once.

Regardless, replication and repair is an enormously well controlled and regulated process: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1479556/

SGEs can take many forms depending on your definition and are ubiquitous in nature as far as we can tell. Plasmids which harbour addiction factors, insertion elements, transposons, prophages etc are all technically SGEs. See here for a review:
https://www.ncbi.nlm.nih.gov/pubmed/21227262

I can't find any literature on SGEs in polyploidy directly, but it is well documented that bacteria harbour a considerable amount of selfish DNA - it seems likely that this will be the same if not worse in polyploidy. Plasmid detection is a difficult computational and experimental process (http://bioinformatics.oxfordjournals.org/content/early/2016/11/18/bioinformatics.btw651.full) but one of the hallmarks of plasmid sequences are typically addiction factors (a gene that the host cell must maintain in order to survive - usually an anti-toxin to neutralise a toxin present on a different DNA molecule) as well as phage genes.

To address a couple of things specifically:

  As each copy replicates separately it would seem likely that spontaneous mutations would arise and over time

This is somewhat true, there is always minor variation in a population (else evolution wouldnt work!). Sometimes you'll find this is also the case in a single cell - but less often. All cells we have found so far have DNA replication and repair mechanisms - https://en.wikipedia.org/wiki/DNA_repair. The frequency of mutation in the genome is not directly linked to the amount of selfish elements though, making your second point contentious:

  This seems like an ideal place for selfish copies to arise

I agree with the premise of polyploidy probably inviting more SGEs (thinking specifically of IS elements and transposons here really), but not because of mutation - rather, just because there are more DNA molecules and sites present for those elements to incorporate into.


Why do cats meow but lions and tigers roar? So as far as I know the cat animals are related to each other by evolution. (Please correct me on this if I am wrong?)

How come the big cats; lions, tigers et.c. roar but smaller cats like house cats meow?

Has the evolution of meowing contra roaring been backtracked?

Is it possible to tell from the anatomy of a cat and a lion what differences cause the meowing and the roaring? Is there some peculiarities in the design of their voice boxes which cause the differences in sounds?

They have different vocal cords, differently-shaped pharynx. I would imagine that is all that explains the difference in sound. As to mewing versus roaring, the vocalizations you reference are not applied to similar sithations.  I wonder if there are videos of baby lions mewing or making similar sounds to get their monther's attention?


Correct/complete representation of RTPCR statistics In papers reporting a relative quantification of gene expression by RTPCR, I often see a bar chart with mean ± standard error or deviation, with the deviation belonging to biological replicates. This ignores all the previous layers of technical replicates. In the regular $2^{\Delta(\Delta Ct)}$ estimation with 3 reactions per primer/template, we have the standard deviation (SD) from each technical replicate, then the SD from normalization, end finally the SD from quantification. If the end results are fold changes, add one more layer to this. I'm not even including normalization with the geometric mean of 3 housekeeping genes (the better method)  How can I  correctly calculate / depict the statistical variations in this case?

I think you can follow this method:

Test the statistical significance of a single experiment by comparing technical replicates (lets say Tests: T1, T2, T3 and Controls: C1, C2, C3). This will tell you if the instrument can reliably detect difference or not. Note that you should compare the relative expression (i.e. wrt your reference gene) and not the CT values. The ΔΔCt method is fine but you should note that it is not necessarily a power of 2; 2 denotes perfect PCR efficiency. See these posts:

Real time PCR normalization algorithm
Real time PCR standard curve

If the difference is found significant in all technical replicates then test the difference between biological replicates by using the means of the technical replicates in each experiment; for example mean of T1, T2 and T3 in biological replicate-a ($\bar{T_a}$) used as the sample value for that replicate. You can proceed with t-test for computing statistical significance which will tell you if the difference in expression is because of a random cellular behaviour or not. You can also do an ANOVA to compare the variance between technical replicates (within an experiment) and biological replicates (mean of the technical replicates between experiments). ANOVA lets you know some aspects of reproducibility of a measurement technique.
Fold changes (FC) are a problematic issue because many biologists seem to mess up with the interpretation of the data. First of all a t-test cannot be applied to FC directly (especially if FC is calculated pairwise for each replicate). Now all you have is a single random variable i.e fold change that you cannot statistically compare with anything. Fold changes are not really bad but I would recommend that a t-test be done between the control and the test samples and if the difference is found statistically relevant then report the FC. I personally know many people who do the other way round and set variance of the control sample as zero (because pairwise FC would be = 1 in all cases): This is a blunder.


What does "cell type composition" mean? I am reading an article about detection of differential methylation. They use the term "cell type composition" in the following context:

"Researchers need to carefully design studies that associate phenotypes with DNA methylation. Some aspects, such as cell type composition, cannot be readily controlled by design; patients and therefore individual DNA samples simply differ in their cell type composition." (Robinson, MD., 2014)

I would like to know to what "cell type composition" refers?

Does it refer to the composition of a specific cell-type in terms of its methylation pattern (or can it refer to something more general outside this context)? It makes sense to me that different cell-types should have different methylation patterns, that's why there are different cell-types in the first place. But is it that even within one specific cell-type, the composition of methylation pattern is different across different individuals?

The problem is that for most sequencing operations you nowadays still need more than one cell - even though this will change soon.

Accordingly, you have to sample cells from a tissue which often, if not usually, contains more than one cell type, see e.g. this picture from a lung tissue from the Wikipedia article on tissues linked above:

It is not always easy to pick cells of one type only (think of trying it with blood, which is a tissue as well). So what you then get is a mixture of different cell types which probably differ in methylation patterns.

  Does it refer to the composition of a specific cell-type in terms of its methylation pattern (or can it refer to something more general outside this context)?

No, it means that you have cells of different types within your sample.

  It makes sense to me that different cell-types should have different methylation patterns, that's why there are different cell-types in the first place.

At least one of the reasons, there are more, e.g. other modifications and mutations.

  But is it that even within one specific cell-type, the composition of methylation pattern is different across different individuals?

That is a different problem and may also be true. But this is not what your quotation, as I understand it, refers to. They refer to the problem that you might sample the same tissue across patients but still get a different composition of cells from different types due to sampling error.


Why does NAD+ become reduced if it gains a hydrogen proton? I've heard that $\ce{NAD^+}$ gains a Hydrogen proton during glycolysis and the Krebs cycle and becomes reduced to $\ce{NADH}$. However, isn't reduction when a molecule receives an electron?

Maybe I've been misinformed? Does $\ce{NADH}$ gain a Hydrogen electron, not a proton?

You are correct that reduction is simply a gain of electrons. This results in a decrease in oxidation number.

You know that NAD+ is reduced by this process because it starts off with a positive charge (+1) and ends up with a neutral charge (0).

The reducing agent that is donating the electrons is the hydrogen. More correctly, the electrons come from the hydride (H-).

The hydride is represented by 2 electrons on this redox diagram:

As you can see, the reduction reaction transfers a proton (H+) and hydride electrons (H- or 2e-) to NAD+. One electron goes to the nitrogen, and the other to the carbon where the proton binds. More details on the redox reaction of NAD can be found here.


where can I find a full list of examples of data types in biology? I have no background in biology and I would like to build a collection of the data types in biology. I start searching and reading bout that and found there are 7 data types:

1-Sequences: DNA, RNA, Protein
2-Structures of biological molecules
3-Gene expression profiles
4-Biochemical pathways
5-Chromosomal mapping
6-Phylogenetic data source
7-Single Nucleotide Polymorphisms (SNPs)

and I search for a schema that defines these types and found EDAM ontology http://edamontology.org/pag but it does not help me.
Do you have any idea where I can find a complete list of examples of the data types mentioned? or at least for one of those data types? Any reference will help me.

Thank you

I am also a little confused about what exactly do you mean by "data type". As far as I know in programming "data type" is something you use to obstruct 0s and 1s e.g string, int and array is the way you'd reference your own data and something that language interpreter/compiler can understand and allocate right memory for. Whereas type of data you can get in biology (bioinformatics), I think is what you are asking. The type of data you get is flat text file i.e ASCII or binary and there are few different binary formats in bioinformatics.

In genomics, which is DNA/RNA type of data you mainly dealing with ASCII files. These are the files that I know of:

FASTQ hold raw - sequenced data. The main two types of sequencing you can do is DNA sequencing (DNA-seq) and RNA sequencing (RNA-seq). Usually FASTQ files always gzip ed and file extension is fq.gz or fastq.gz I wrote this tutorial explaining FASTQ
FASTA can hold different type of sequence data, which is different to raw-sequence held in FASTQ. You can actually convert FASTQ to FASTA, but you'd loose quality information. The two broad classes of sequences you can have in FASTA file are nucleotides sequence i.e DNA/RNA sequence or  amino acid sequence i.e protein/peptides sequence. FASTA is also almost always gziped, file extension varies a bit, most common once are fa.gz or fasta.gz, but you will see fna.gz or fna or faa which tries to indicate FASTA with nucleotides or amino acids. FASTA usually used for reference files e.g reference genome. Here is a link to Ensembl repository for mouse genome
GFF and GTF files these are annotation files, used together with reference genome FASTA files. Here is another one of mine tutorials
SAM and BAM okay here is an example of binary type of data. Sequence Alignment Map, file extension .sam depending on the organism, can be very big. For mouse RNAseq data for example SAM file can be between 1 Gb - 40 Gb, makes sense to compress it. BAM is binary SAM. you need samtools to work with BAM files. Here is pure python BAM parser if you are interested.

This should cover first two of your points. Although proteomics has few more type of data, again mainly text. Mass Spectroscopy is the tool proteomics people use to get they "raw-data" and there is some finny file format(s) that I'm not aware of and there will be a few downstream file formats I'm sure.
As for gene expression, that's mainly tabular data, csv or tsv again flat text file.
One other format that I should mention that covers your point 7 is VCF which is variant calling format here is specifications for it again flat text format.

One thing that I should say; it is somewhat common and preferred, at least in the past to be able to parse biological files with Unix tools such as grep, awk and cut and therefore most of the files are tab separated text files.. I think now bioinformatician coming around and using more structured and compressed data formats.

This isn't exhaustive list of file format by any means, but I think this should give you enough to google for.

One last link to Kegg pathway which is your biochemical pathways, they might explain there the type of data they use


At any given moment, how much energy is stored in the human body as ATP? At any given moment, approximately how much energy is stored in the human body as ATP in the ADP-P-bond?

This of course depends on what type of cell it is and the activity of the individual in question. The calculation should be fairly simple, as we know that ATP hydrolysis release about 30 kJ/mol. Hence, the question could actually be re-phrased to $"$At any given moment, how much ATP does the human body have?$"$

ATP burned per minute is not a useful number because the turnover is so high. 2000 kcal/day is dozens of kilograms of ATP so obviously ATP is turned over more than once a day, but there's probably more than one molecule of ATP being passed around between all the ATP synthases.

This blog claims 250 grams. Taking the estimate of ATP concentrations(1-10 mM) from wikipedia and multiplying by a 60 kg person pops out 150 grams (for 5 mM). The ATP/ADP ratio is about 5 to 1 under physiological conditions, so I'm comfortable leaving out that source of error.

So: Probably a few hundred grams, depending on a lot of things. Which is about .2-.7 moles, for reference. 6-20 kJ is not a lot, in fact even at the upper end of estimates you're looking at maybe 8 dietary calories, and probably more like 3.


G>T transversion VS. T>G transversion? So I'm reading about how mutations in DNA can be caused by oxidative damage. An example of a product of oxidative damage is given: 8-oxo-7-hydrodeoxyguanosine

My textbook says that this product frequently mispairs with A, resulting in a high level of G-->T transversions.

What I'm not understanding is why it's a G-->T transversion. If the 8-oxo-G is pairing with A, resulting an an A-G pair, isn't this a T-->G transversion? Or does the order not matter?

Originally the position had a G:C pair. After the mutation, there is an oxoG:C pair. Upon replication, the strand with C will pair to G and the original pair will be created as expected. However, since oxoG can also pair with A, the strand with oxoG may form an oxoG:A pair. Another round of replication gives the products T:A and oxoG:A. Thus the G in the original strand is replaced by T (ie it is a G$\ce{->}$T transversion).


What is the X-chromosome responsible for? I understand that the X-chromosome is responsible for certain disorders, like red-green colorblindness; but besides disorders, what do the genes on the X-chromosome determine?

Here is the list! There are about 900 protein coding genes and about 500 non-coding transcribed sequences. It is not going to be feasible to explain you the function of every single one of those genes. Your question is hence too broad.

You will find here on wikipedia a small subset of those ~900 genes.

If your question was

  Are all genes that are on the X chromosome related to sex?

Then, the answer is "no". Most of them have nothing to do with gender specific traits.


How does TYRP1 affect the synthesis of black and brown eumelanin (on a biochemical level)? TYRP1 (aka B-locus) is a gene in dogs that determines whether black or brown eumelanin is produced (assuming eumelanin is produced at all which is determined by the MC1R gene). I've looked at many papers and flow charts and now i have a contradiction: DHI seems to be the molecule that gives eumelanin a black color and DHICA a brown color. According to many flow charts, TYRP1 seems to be involved in the polymerisation of DHICA (not DHI). Mutations that cause a loss-of-function of TYRP1 will cause dogs that carry these mutations (homozygous) to have brown fur. But if TYRP1 is important for polymerisation of DHICA to brown, why does a loss-of-function of this very protein cause dogs to have brown coat color?

Where did I get it wrong?

The actual coat color is determined by the ratio of the products of two genes: Tyr and TyrP1. The first oxidizes DHI to Indole-5,6-quinone and forms brown pigment, TyrP1 on the other hand oxidizes DHICA to Indole-5,6-quinone carbolic acid, which forms black pigment. See this pathway diagram (from here):

So loss of TyrP1 activity is not harmful to general pigmentation but prevents the formation of black color, while the inhibition (or loss of function) for Tyr will lead to albinism, since no pigment precursors (from Tyrosine to DOPA can be formed.

You may also be interested in this paper: "TYRP1 and MC1R genotypes and their effects on coat color in dogs."


Why do many cells together survive better than one cell alone? I know that one cell with no ECM is subject to anoikis. That's why in general one cell alone not in its environment is dying.

But are there advantages for a cell to live close to other cells even of the same type (for many types it looks obvious) ? If yes what are they and could you give a reference if it is possible please ?

I don't mean only what evolutionary advantages do cells together have over one cell (which is more simple, and there is a wikipedia about it), but I'm more interested if one wants to culture cells that you find generally in tissues, why is it better to take many of them (because it is better, right ?) ?

To be clearer, my point is that I want to understand the mechanisms of what happens when cells (of the same type) are in community and to understand given those mechanisms the advantages a cell has when it is with other cells rather than alone.

Thanks !

Cells can communicate with each other using chemical signals.

But do you also know about gap junctions? These are tunnels that connect cells in tissues.

Water, ions etc. can travel to and fro.

Or maybe a tight junction can connect cells together to form an an organ. No fluids pass through, which is good: The bladder is an example.


How can one create images like those in the PDB ‘Molecule of the month’? I am impressed by the illustrations for the Protein Data Bank ‘Molecule of the month’, e.g. the gorgeous image of DNA Helicase below. Does anyone know how they were made or how one might create something similar?

(source: rcsb.org)

Those (really cool) pictures are created by David Goodsell using custom-written software.
From an interview to the artist:

PDB: How do you create the illustrations?
Goodsell: Most of the pictures are created with a computer program that I developed back when I was doing postdoctoral work with Dr. Art Olson here at The Scripps Research Institute. I've been using this style of illustration--with flat colors and black outlines--for about 10 years now. I like the way that this style simplifies the molecule, giving a feeling for the overall shape and form of the molecule, but at the same time you can still see all the individual atoms. On the last page of each Molecule of the Month--"Exploring the Structure"--I always use RasMol, to give visitors an idea of the kinds of pictures that they can create themselves with off-the-shelf software.

There are good tools around if you want to replicate that look. Although it may take a bit of tweaking (and possibly programming) I would surely give PyMOL and Bioblender a try.


Are left-handed people more likely to be colorblind? My friend, uncle, and I are left handed and also suffer from Protan colorblindness. Is it more likely for left-handed people to be colorblind?

Disclaimer: I was originally Right handed and due to a physical handicap I developed left-handedness.

EDIT: We also suffer from either ADD or ADHD.

In research literature, colorblindness and handedness appear to be correlated through male-ness.

Genetic causes of colorblindness are on the X chromosome, which explains why males are much more likely to suffer from colorblindness than females, as high as 16x more likely for red-green colorblindness.

Handedness is a complex polygenic trait governed by dozens of genes. A recent paper, Brandler et al., PLOS Genetics 2013, studying handedness implicated genes in chromosome 10.

However, males appear to be 25% more likely to be left-handed than females.

I wasn't able to find any studies directly addressing whether or not handedness is correlated with colorblindness, but it appears that if the only thing you tell me is that you are left-handed, then I can guess that you are more likely to be male than female, which means you are more likely to be colorblind than a person picked at random. So yes, a correlation appears to exist through maleness.

However, it's possible that being left-handed is conditionally independent of being colorblind given that you are male. In which case, for males, there may not be a correlation between left-handedness and colorblindness - there haven't been any studies addressing this question that I have seen.

To put this another way: if you tell me that you're male and left-handed, then insufficient scientific studies exist for me to guess whether or not you're more likely to be colorblind or not.


What is this white/translucent with brown back, larva/worm creature I found, in the UK, on my lettuce? I'm in United Kingdom, East Anglia. I've just started to grow lettuce in my back garden, taking my first harvest today, I found one of these creatures:

They have a distinctive brown/white mark along the top of their behind. The black dot appears to be its front, as it scouts with that, and moves in that direction most of the time. This is about 10mm long, give or take 50% depending on how stretched out it is.

They appear to have transparent skin, as I think we can see its organs in there. It moves almost peristaltically (similar to a worm), but with direction, not just flapping around, and seems to like the undersides of things.

They're not particularly segmented, though they have those tiny, tiny ridges as you can see. And there are no legs or meaningful features to speak of on its underside. They were also slightly sticky, with a white-ish secretion.

I have since looked and found a few amongst the other lettuce, which all look incredibly similar to this. Usually hiding inside the outer leaves, but not exactly an infestation (yet!). They don't seem to be on any other plants at the moment. There's no evidence that they've eaten any leaves, or anything, currently.

I have done a lot of searching and attempts to identify, but I can't for the life of me find this online. My amateur guess is some sort vermiform fly larva, but it could be anything from a baby caterpillar to a worm, for all I know. Any help in narrowing it down, or especially in finding out if I should be worried for the plants, would be helpful.

It's a kind of hoverfly larva (don't know which one, maybe Episyrphus balteatus), they eat aphids on cabbages.

Image on wiki commons


How to translate a blood type used in Eastern Europe? What are the I-IV blood type descriptions shown below (commonly used in Eastern Europe), and how do you translate them into the ABO-system?

It is a direct correlation between the ABO blood groups and the Roman numerals.

 O: I

 A: II

 B: III

AB: IV

This numeric system was pioneered by Jan Jansky of Czechoslovakia in the early 20th century. Apparently it is still used in some former Soviet states.

Erb IH. 1940. Blood Group Classification (A Plea for Uniformity). Can Med Assoc J 42(5):418-421.


What is the name of this plant I found in a park? I found this on Garret Mountain in Paterson, New Jersey, USA. Does anybody know the name of this plant?

I think this is Lysichiton americanus,  skunk cabbage. It has these large, rolled-up leaves and grows in wet habitats as you describe. In Europe, it is an invasive species, but in America it is native. I am not 100% sure, because I don't know if there are any similar species in the US.

EDIT
As Anongoodnurse pointed out, I was right to be unsure. This is Eastern skunk cabbage, Symplocarpus foetides. This species occurs in the Eastern parts of the USA.


What is this microscopic image from Peter Gabriel's New Blood album cover? This image appears on the cover of Peter Gabriel's album New Blood.  It appears to be a photograph of some microscopic biological cell.  But it doesn't look like a blood cell to me.   What kind of cell is it?

This is an embryonic stem cell on the tip of a needle photographed on a scanning electron microscope (SEM). The image was taken by Steve Gschmeissner, see here for the original.


Watering plants with soaked forest soil I am thinking of mixing forest soil with water and water plants with that.

I was hoping that nutrients from soil would get released into the water, so in effect, fertilize the soil.

I am not sure if this works, since I am not aware in what chemicals P, K, Ca, Mg is "stored" in forest soil. If it is oxides that it should dissolve rapidly.

So, overall, is it beneficial to the plant to water them with water in which forest soil was dispersed?

Plant in question are tomatoes, peppers.

You are thinking about something like "compost tea".
http://www.homecompostingmadeeasy.com/composttea.html

The problem is that a random piece of forest soil may or may not be rich in nutrients.  If that soil has water soluble nutrients in it, wouldn't the rain have already rinsed them out?

If you make tea out of compost, there has been no chance for rain to rinse out nutrients because the decomposed stuff has been in your compost bin.

Last piece: if you are making tea out of forest soil or compost, when you are done you will have a soaked clump of wet soil or compost.  What are you going to do with it?  Probably throw it on the ground somewhere.  It might make more sense and be much less messy to skip the tea step, put the forest soil or compost on the ground next to your plants, and then water them.


Is there a difference between "cell line" and "cell strain"? I'm translating one Russian text where a cell line is transfected to produce a drug. I wonder if I can sometimes use "cell strain" or simply "strain" instead of "cell line" or instead of "producer" (продуцент, meaning "the producer of the drug", i.e. the cells that produce the drug).
I googled and found this answer on Yahoo answers:

Cells in culture can be passaged a finite number of times before reaching a crisis which can be compared with aging. The number of passages, before reaching crisis, has been termed the Hayflick limit and is related to the longevity of the species from which the tissue was originally derived.
Within the Hayflick limit, the cells are referred to as a cell strain.
Cells that survive the crisis and continue to grow are referred to as a cell line. Cell lines can also be derived directly from cancer cells. There are many properties that distinguish cell lines from cell strains, including altered chromosome number, changes at the cell membrane, and reduced requirement for certain growth factors.
Therefore:
A cell strain is defined as an euploid population of cells subcultivated once or twice in vitro, lacking the property of indefinite serial passage. Cell strains ultimately undergo degeration or death (senescence).
A cell line is an aneuploid population of cells that can be grown in cultures indefinitely.

Is this true? Is a cell line always aneuploid and capable of indefinite growth, as opposed to being euploid and incapable of indefinite growth?

"Strain", in general, is usually used for whole organisms (whether they are unicellular or multicellular). For example, there are mouse strains.

"Cell line", on the other hand, is a very specific term that is used to refer cultured cells obtained from a multicellular organism. They need not be necessarily aneuploid.

  Is a cell line always aneuploid and capable of indefinite growth, as
  opposed to being euploid and incapable of indefinite growth?

Aneuploidy does not have any causative relationship with indefinite growth. Most cancerous cells evade the cell cycle checkpoints, which allows them to grow out of control. Some of these checkpoints also ensure proper segregation of chromosomes. Bypassing them leads to aneuploidy.

  Are cell lines essentially immortal?

Usually primary cell cultures are not referred to as "cell lines" these days. However, originally, any cultured cell that grows in vitro is called cell line. From Freshney (Basic Principles of Cell Culture):

  When cells are isolated from donor tissue, they may be maintained in
  a number of different ways. A simple small fragment of tissue that
  adheres to the growth surface, either spontaneously or aided by
  mechanical means, a plasma clot, or an extracellular matrix
  constituent, such as collagen, will usually give rise to an outgrowth
  of cells. This type of culture is known as a primary explant, and the
  cells migrating out are known as the outgrowth (Figs. 1.1, 1.2, See
  Color Plate 1). Cells in the outgrowth are selected, in the first
  instance, by their ability to migrate from the explant and
  subsequently, if subcultured, by their ability to proliferate. When a tissue sample is disaggregated, either mechanically or enzymatically
  (See Fig. 1.1), the suspension of cells and small aggregates that is
  generated will contain a proportion of cells capable of attachment
  to a solid substrate, forming a monolayer. Those cells within the monolayer that are capable of proliferation will then be selected at
  the first subculture and, as with the outgrowth from a primary
  explant, may give rise to a cell line.

Elsewhere, a cell strain is defined as positively selected subpopulation of cells:

  A cell strain is a subpopulation of a cell line that has been positively selected from the culture, by cloning or some other method.  A cell strain will often have undergone additional genetic changes since the initiation of the parent line. Individual cell strains may, for example, have become more or less tumorigenic than the established line, or they may be designated as a separate strain following transfection procedures.

This definition does not say anything about what kind of selection was used. You can select for cell that express GFP, for instance. So that strain would be simply designated as GFP+.


Neuron repair inhibition in the CNS Evolution provides different myelin sheathing cells (Oligodendrocyte and Schwann cells) in mammalian CNS and PNS. Damaged neurons in the CNS have little chance of recovery whereas damaged neurons in the PNS have an excellent chance of recovery. When ruptured, olidodendrocytes release Nogo that signals the damaged neuron cell body to stop any attempt at regrowing its axonal stump. Ruptured Schwann cells in the PNS do not release Nogo. Why should nature behave like this? Is it because the wiring density of the CNS is orders of magnitude greater than that of the PNS?

Or could it be because in the PNS the nerve is encased in a perineurial sheath that can readily self-repair and provide a framework for axon regeneration? There doesn't appear to be any similar sheath in the tightly packed CNS. Therefore to prevent unstructured axon regrowth, that could cause chaos in the brain, such a possibility is actively prevented?

I almost got it right. The consensus as of 2018 appears to be that it's a Faustian pact between providing the CNS with our unique mental powers at the cost of poor damage repair. This is not an issue in the PNS where damaged neuron repair is, in the main, impressive.

Quote (1): Principles of Neural Science 5th Ed (2013) (Eric R Kandel et al)
“ ... the regenerative capacities in the peripheral nervous system are impressive.
In contrast, in the central nervous system regeneration after injury is poor.”
“Is it the ability of peripheral axons to regenerate that is unusual, or the inability of central axons to do so? It is in fact the latter.”
“Maintaining constancy in the face of small perturbations in connectivity may therefore have the unavoidable consequence of limiting the ability of central connections to regenerate in response to injury. In this view our limited regenerative capacity is the Faustian biological bargain we have made for the possession of many precisely wired circuits that underlie our superior intellectual powers.”

Quote (2): Transl Psychiatry (2017) 7, e1214; doi:10.1038/tp.2017.170 www.nature.com/tp
“Reticulon 4 receptor (RTN4R) [aka NgR and NgR1] plays an essential role in regulating axonal regeneration and plasticity in the central nervous system ...”

Quote (3): A.R. Walmsley, D. Bourikas And A.K. Mir, 15 - Myelin Neutralization For Spinal Cord Injury And Stroke, In CNS Regeneration (Second Edition 2008)
“ ... the environment of the CNS is highly inhibitory to axonal regeneration and plasticity. In recent years, great advances have been made in our understanding of the molecular components contributing to the inhibitory environment of the CNS. The majority of these have been identified as membrane proteins present in CNS myelin, such as myelin-associated glycoprotein, Nogo-A and oligodendrocyte-myelin glycoprotein, that inhibit neurite outgrowth by binding to the multimeric Nogo-66 receptor (NgR1) complex on the neuron ...”

Quote (4): https://en.wikipedia.org/wiki/Reticulon_4_receptor

Reticulon 4 receptor (RTN4R) also known as Nogo-66 Receptor (NgR) or Nogo receptor 1 is a protein which in humans is encoded by the RTN4R gene. This gene encodes the receptor for reticulon 4, oligodendrocyte myelin glycoprotein and myelin-associated glycoprotein. This receptor mediates axonal growth inhibition and may play a role in regulating axonal regeneration and plasticity in the adult central nervous system.


Are SLC52A2 and GPR172A really the same? The official HUGO gene nomenclature page says that GPR172A (Gamma-hydroxybutyrate receptor) and SLC52A2 (riboflavin transporter, member 2) are the same. The sequence reported by Andriamampandry seems to be the same, but I find no other evidence. Can anyone enlighten me?

(I'm wondering if I should add the SLC52A2 information to the GHB receptor Wikipedia page.)

This isn't a case of gene splicing causing different protein variants.  In the studies that identified these two functions (GHB sensitivity and riboflavin transport), they were using DNA derived from mRNA (cDNA), which means what was being expressed in their experiments did not have introns, so there was no chance for alternative splicing.

This gene has a weird history, here is the summary:

Takeda et al. 2002: Identification of G protein-coupled receptor genes from the human genome sequence

Takeda and co. download a copy of the human genome and translate it looking for GPCRs.  They look at all the ORF that DIDNT have introns: "We collected intronless open reading frames (ORFs), which were long enough to cover GPCRs from the human genome". They also only look at things with 6-8 transmembrane helices as determined by the prediction program SOSUI.  One of the GPCRs they found was named hGCRP41 (hypothetical protein similar to GPCR) accession number: AB083623.  They report it probably has 8 transmembrane helices, and 418aa.  This protein probably doesn't exist because they read straight through two introns in their analysis.  The protein also terminates in the middle of a frame-shifted exon.

Ericsson et al. 2003: Identification of receptors for pig endogenous retrovirus

Next, Ericsson et al come along looking for receptors for the pig endogenous retrovirus and find this gene.  They used cDNA to make a bunch of transduced cell lines that had difference human cDNAs expressed.  They found two related proteins that could serve as receptors to the pig endogenous retrovirus.  They named the first one HuPAR-1, which is 445aa long and has 11 transmembrane helices.  This is the length of one of the proper splice variants of this gene.

Andriamampandry et al. 2007: Cloning and functional characterization of a gammahydroxybutyrate receptor identiﬁed in the human brain

Andriamampandry is looking for gammahydroxtbutyrate (GHB) receptors by using cDNA and seeing which cDNA-transduced cells become sensitive to GHB.  They find two nice proteins that are sensitive to GHB, GHBh1 and C12K32.  GHBh1 is identical to HuPAR-1, it has 445aa and 11 transmembrane helices.  C12K32 is a frameshifted version of GHBh1 that is slightly longer, but has the same number of helices. They had previously found a 512aa ortholog in rats, in 2013.

Yao et al. 2010: Identification and Comparative Functional Characterization of a New Human Riboflavin Transporter hRFT3 Expressed in the Brain.

Finally, we have Yao et al, who searched for homologs to their Riboflavin transporters.  They found one in a cDNA library, and it was 445aa long.  But they noticed upon BLASTing it that people had been calling it a GPCR.  They point out that this is weird since it has 11 transmembrane helices, and go on to show that it is a Riboflavin transporter, concluding: "The molecular function of GPR172A has yet to be determined. We designated it hRFT3 (GenBank accession no. AB522904) based on its functional characterization as shown below."  This paper is in pretty poor form, because somehow they don't address the Andriamampandry paper which presented data supporting its function as a GPCR.

So this protein, in this specific spliced formation, has been shown to be a virus receptor, a GHB G protein-coupled receptor, and a riboflavin transporter.  It is very weird that it is a GPCR with 11 transmembrane domains... they very rarely have more or less than 7.  I'd wait for more studies to confirm both of these findings before I'd accept that this protein is an XXL GPCR moonlighting as a riboflavin transporter.


Spermatogenesis question I found this diagram in my textbook regarding the process of spermatogenesis. But, I doubt if the labelling done is correct or not. Especially, I can't figure out any difference between the cells labelled as spermatids and those as spermatozoa. Also, I doubt the labelling of Sertoli cells.
Please help me clarify my doubt.

As per my textbook,

  The spermatids are transformed into spermatozoa (sperms) by the process called spermiogenesis. After spermiogenesis, sperm heads become embedded in the Sertoli cells, and are finally released from the seminiferous tubules by the process called spermiation.

Notice the cell labeled "spermatid" is still attached to the Sertoli cell. Once released from the Sertoli cell, spermatids are called spermatozoa.
This process (release of the spermatid to form a spermatazoon) is called spermiation
EDIT
The text you added is still correct, but not well explained. Spermiogenesis is the development of the spermatid, the haploid 1N gamete produced by the second meiotic division, into a cell with a long flagella with a small amount of cytoplasm. Spermiation is the release from the sertoli cell. Both spermiogenesis and spermiation are involved in the development of a spermatid to a spermatozoon, but the specific point where we stop calling them spermatids and start calling them spermatozoa is release by the Sertoli cell, or spermiation, a substantial process in its own right. Both spermiogenesis and spermiation are important steps in the conversion of the haploid 1N gamete to a motile, free spermatozoon.


What is the evolutionary tradeoff against primates producing multiple offsprings (litter)? If we evolved to have multiples all the time we would more likely have extended families living together in 1 house. This would be better than the spouses by themselves for multiple reasons including money.

And during prehistoric times it would have been better for several reasons including that 1 would be more likely to survive than if it was born without any siblings.

Most mammals have litters of at least 2. An extreme of this is the cheetah which has litters of up to 9 cubs. They evolved to have litters because they were in conditions where 1 is likely to starve. Lions evolved this for a different reason since lions are not likely to starve. They evolved it because of the fact that they live in prides.

So for primates including us wouldn't it be better if they had litters often instead of single babies?

There is a tradeoff between having multiple progeny, with relatively low parental investment in each, and few progeny, with high investment in each.  This used to be called "r" and "K" selection respectively, though the terms are now used less.  Very simplistically speaking, long-lived species within a fairly stable environment tend to produce few offspring and invest large amounts of care in each; this description fits primates very well, and so it's not surprising that they follow this paradigm.  The bottom line is that because of primate life history, having small litters is a more successful evolutionary strategy.

The Wikipedia article on r/K selection theory is reasonably good and points to updates and some further reading on the subject.


Serotonin - Does being aroused make you sleepy? My Psychology text book says Serotonin causes "Sleep, arousal levels and emotion"

Does this really mean that when you are being aroused, Serotonin is released, which in turn makes you sleepy? If so, what evolutionary benefit would that have??

According to this article [1], serotonin (5HT) inhibits sexual arousal:

Dopamine is generally facilitative to male sexual
behavior; however, 5-HT is regarded as inhibitory.
Antidepressants of the selective serotonin reuptake
inhibitor class (SSRIs, including Prozac and Zoloft)
impair ejaculatory/orgasmic function and frequently
inhibit erectile function and sexual interest as well.

However, serotonin can also facilitate erections:

Systemic administration of the 5-HT1B receptor agonist
anpirtoline impaired ejaculation in male rats. On the
other hand, stimulation of 5-HT2C receptors with mCPP
impaired ejaculation but facilitated erections in male
monkeys, suggesting an increase in parasympathetic
influence.

Serotonin release also causes sleepiness after ejaculation in males (source):

5-HT is released in the LHA at the
time of ejaculation and promotes sexual quiescence during
the postejaculatory interval

There are many signalling molecules used by the human body that have a different effect depending on the cell type they are detected by and the receptor type they activate.
I would also like to touch on your question about evolutionary benefit. Evolution does not care about you after you have reproduced. As long as an individual reproduces, evolution is "happy". For example, you think falling asleep after sex is counterproductive on the evolutionary scale? What about Mantises where the female will sometimes eat the male during or immediately after copulation. Falling asleep seems like a pretty small thing compared to that (source):

Although the praying mantis is known for its cannibalistic mating process in actuality it only occurs 5-31% of the time. Especially in laboratory conditions of bright lights and confinement, the female is more likely to eat the male as means of survival. "In nature, mating usually takes place under cover, so rather than leaning over the tank studying their every move, we left them alone and videotaped what happened. We were amazed at what we saw. Out of thirty matings, we didn't record one instance of cannibalism, and instead we saw an elaborate courtship display, with both sexes performing a ritual dance, stroking each other with their antennae before finally mating. It really was a lovely display". (7) There is one species, however, the Mantis religiosa, in which it is necessary that the head be removed for the mating to take effect properly. (5) Sexual cannibalism occurs most often if the female is hungry. But eating the head does causes the body to ejaculate faster. (3)

Anything that makes an individual less likely to reproduce will be selected against. Things that happen after reproduction do not affect the survival of the species and will not be subject to selective pressures.
References

E. M. Hull, J. W. Muschamp, S. Sato, Physiology & Behavior 83 (2004) 291 – 307


Japanese Crab Identification? I saw a crab walking home from work the other night. We're by a river, but I was probably 500 feet away from the river when I saw this one. I apologize for the image quality, all I had was my terrible Ipad camera and no flash. I have provided the original image and one with brightness and contrast modified to make the crab easier to see. It's about 2.1 inches from leg to leg, I threw a 500 yen coin by the crab as a reference, but cropped it from the image.

I am located directly across from Haneda airport, which is on Tokyo bay. The river is close enough to the ocean that we get tides. I'd say the river level varies by as much as a meter, and there are many many crabs on the exposed riverbed at low tide. But again, this crab was far away, and would have needed to climb a three foot tall vertical wall at the river's edge.

The carapace shows the distinctive lines of Chiromantes dehaani (Kurobenkei-gani in Japanese). This species can be found quite far away from the ocean, commonly in brackish streams and rivers. The size fits your description, the width of the carapace is approximately 3-4 cm, giving the entire body roughly the same size as you observed. These crabs are also most active at night.

I have seen these crabs in sheltered areas slightly inland from the sea. Here is a photo of C. dehaani that I took in Tokyo:

While there is a slight possibility that this is Chiromantes haematocheir (Akategani in Japanese), your photo does not show the distinctive red claws and this species is less common in Tokyo Bay due to development and loss of its natural environment of mudflats. Therefore, I think it is save to identify this as C. dehanni.


Names and abbreviations in biology After one year in college, I am quite surprised with the number of different abbreviations used in biology for the same thing.

I wonder if there are any rules for naming something new in biology, for example new genes, or if it is just up to the researchers without restriction?  If there are rules, how did the confusion arise?

Elsewhere on SE Biology I have answered a related question regarding enzyme names. Here I will restrict myself to genes, as it seems that this is the main concern of the poster. (In talking about ‘abbreviations’ I think he is referring to what are generally termed gene ‘symbols’.) The answer from @KarlKjer addressed current recommendations regarding gene nomenclature; mine addresses the causes of the current confusion.

Summary

Rules (actually recommendations) did not appear until a late stage in
the development of the field of genetics, when the problem was
already there and there was a need to do something about it.
Historically in animal systems the naming of new genes tended to
relate to mutant phenotypes as this was how they were discovered. The function of the gene that had been mutated was generally unknown.
Sometimes different mutants of the same gene caused different
phenotypes, either because of severity of damage to the protein, use
of animals from a different development stage, or different growth
conditions for bacteria. These mutants appeared to be of different genes, which
were given different names.
Sometimes the same gene was discovered at about the same time by
different workers and given different names in the laboratory while work was in progress and, hence, on publication.
Later it became possible in some cases to identify the products of
genes for which there was no clear mutant phenotype — perhaps just
lethality — and one method of naming was on the basis of the size of the
protein, preceded by the letter ‘p’ (e.g. p63)
The current trend is to try to rename genes according to the function
of their products, where these are known, i.e. to replace the name of a
mutant phenotype by the name of an enzyme or structural protein.
The implementation of such rules or recommendations is imperfect,
depending on the cooperation of authors and editors.

Illustration using some Drosophila genes

I shall use Drosophila melanogaster (the fruit fly) to provide some illustratations of the history of genetic nomenclature, because this was the organism used by Thomas Hunt Morgan (he of the centimorgan) to perform genetic studies after the rediscovery of Mendel’s work in 1900.  His laboratory was responsible for the discovery in 1910 of the first Drosophila mutant, a spontaneous sex-linked mutant that resulted in males having eyes that were white, rather than the normal red. The gene responsible for this mutant was named white, initiating the custom of naming genes after their mutant phenotype. (Drosophila gene names became italicized by convention.) What else could they have done? Not only was the protein product of this gene unknown, the whole idea of genes encoding proteins did not yet exist. The abbreviation (symbol) for this gene was merely w. Clearly, nobody anticipated that another 17,000 genes would follow, or suggested that a committee on gene nomenclature should be set up.

It is interesting to note that the product of the white gene was not identified until almost 90 years later. In 1999 it was established that this was a member of the ABC transporter family, responsible for bringing  into cells the guanine and tryptophan  needed to make the red pigment so characteristic of the eye of the wild-type Drosophila. The human version of white was identified roughly contemporaneously by sequence homology, and although it was initially referred to as hW (human homologue of white) is now named according to its gene product: ATP-binding cassette sub-family G member 1 (ABCG1). Its function in humans — who only have red eyes in flash photographs — is in lipid transport.

The era of of molecular genetics in the late twentieth century brought an avalanche of new genes, many not associated with a particular phenotype. The culture — accepted by scientific journals — was that if you discovered a new gene you had the right to name it as you pleased. A generation of young scientists were pleased to chose names that reflected twentieth century, rather than classical, culture. Flip through the names of Drosophila genes (try the autocomplete here) and you will find alien, bazooka, cactus, Dorothy, ether a go-go all the way to zucchini. Nor was it only the Drosophila geneticists that were responsible for this. The hedgehog segmentation gene, discovered in Drosophila, has three human homologues. One of these was named ‘sonic hedgehog’, which I am informed is the protagonist of a children’s video game. O tempora, o mores!

A couple of final points will be made to illustrate the problems of nomenclatue of Drosophila genes. Several other mutations of the white gene have been observed which have different phenotypes (e.g. result in different eye colour). This is because they involve insertions into the gene rather than its complete deletion. This also illustrates one historic difficulty that could result in several names for the same gene. The other point is that many of the genes identified by genome sequencing, at least initially, were associated with no mutant phenotype and had no known function, and were so named simply be an accession number (CG1234 etc.). As functions emerged they would be renamed. And an example of the nomenclature situation can be seen in the NCBI entry for Drosophila gene TfIIS (RNA polymerase II elongation factor):

  Also known as: BG:DS00929.12; br52; CG3710; Dmel\CG3710; DmS-II; DmSII; l(2)35cF; l(2)35Cf; l(2)br52; l35Cf; RnpSII; TFIIS; TFIISA; TFS-II


What is the name of this big plant with a purple trunk and green to purple berries? I have photographed the following plant in our garden in Pittsburgh, PA.

Do you know the name of the plant?

The plant looks like Pokeweed (Phytolacca americana) to me, a common "weed" in the U.S.


Why is the gene regulation in eukaryotic cells needs multiple level of control than in prokaryotic cells? That "eukaryotic cells are more complex" and "compartmentalized" are used to justify the need of more level of control of gene expression. I get the basic idea but can't convince myself why complexity or compartmentalization leads to more complex control (i.e. multiple levels) of gene regulation!

In control theory, we often use multiple level of control to minimize the variance (there are few other benefits as well from design perspective); probably that is what eukaryotic cell would also do. Moreover, simple combinatorics suggest that two level of control with $n_1$ and $n_2$ molecules involved at each level respectively would give me $n_1n_2$ possibilities of output which is higher than $n_1 + n_2$ distinct output I might get if I were to use these molecules with 1 level of control/regulation.

I was wondering if such simple reasoning are correct and can be used in the context of evolution? Are there other reasons as well?

I think you need to consider the overall amount of information that is needed to implement a proper control system in living organisms.

In prokaryotic cells, in most of the cases, you will find that one gene code for one enzyme, so if a simple organisms need 500 enzymes to stay alive you can expect 500 genes that code for that enzymes.
A more complex organism may need 100 times more enzymes to stay alive and so theoretically 100 times more genes. Now, evolution wise, to have a linear increase of DNA vs complexity is not a good option for very complex organisms. To keep everything compartmentalised in one single membrane is also not a good idea if you need to run millions of chemical reactions using thousands of enzymes that can cross react and need different optimal conditions to work properly, so multi-compartimentalization is a must.
Linked with it arises the problem of sending the right enzyme in the right place and this has been solved by adding tags, transporter enzymes, etc... in the pot... So, lots of more information is needed to make everything run smoothly.

It turned out that an efficient way to code for all that enzymes, tags, promoters and other regulators without increment the size of the DNA too much is by multi level control of the expression of a gene i.e. the same gene can be used to produce different enzymes (splicing etc...). The tradeoff to pay to have a more compact genome is to increase the complexity of its control system.

Lastly, consider that differently from normal electronic controllers, the biological one do affect each other. A biological controller system may produce an output molecule that interact with the system under control but also with other reactions going on all over... that is another burden that require an increase of complexity in the control system to make it work.


Evolution of the (phenotypic) facial features of the indigenous people of (west/central) Africa I am not even remotely an expert in this field; I just got curious, so help me.

First of all, let us remove all human sentimental attributes from this question (such as connotations of scientific racism or emotional reactions thereof) and ask it from a purely scientific point of view. The typical facial feature of a West/Central African person (the so-called broad African type) exhibits a wide nose, a lack of nasal bridge projection (similar to many Asian noses) and a prognathous skull shape that resembles more closely to our ancestor Homo Heidelbergensis than many other indigenous phenotypes from other parts of the world do.

I agree that this claim sounds anecdotal, and is certainly not true of all Africans (for example, Ethiopians), but one cannot dismiss it simply on grounds of ethical policing. I cannot help but notice that many of my African friends remind me of our shared ancestry (with no disrespect meant whatsoever), as is clear from the photographs below, one of a supposed Homo Heidelbergensis and one of a random African Homo Sapiens of today.

My question is the following. What is the reason behind this seeming resemblance? Is this appearance an illusion and possibly a construct of a prejudiced mind, or does this have a valid scientific answer? For example, are most Africans closer to our ancestors than the rest of humanity is? How does evolution answer this question?

Thank you for your help.

Note that I had never heard of the expression "broad african type" and could not find much reference to this term when googling. But anyway, I'm happy to use it to refer to a particular set of typical facial features.

  What is the reason behind this seeming resemblance?

Note that the Homo Heidelbergensis image is not a picture (obviously) and much of what is being depicted was open to artistic interpretation. It is possible that some of the feature you are thinking of are not real. Have a look at the post In reconstructions, how are various shapes of facial features determined from skull only?.

You list several phenotypic traits and it would be too broad of a question if you were expecting an explanation about the evolution of each of these traits. I will just pick one classic trait; the nose.

One of the role of the nose is too even up the temperature of the air that we're inhaling. As such, the shape of the nose is under differential selection pressures depending on the environment. So if the nose of Homo Heidelbergensis looked alike (assuming it really looked like on the facial reconstruction) today's "broad African type", it is probably because of shared environment. Note however that nose shape vary a lot among african lineages and also among non-african lineages. You might want to have a look at this popular article.

A big point of ressemblance is the skin color that you don't talk about. Have a look at the posts Why do we assume that the first humans were dark-skinned? and How did some humans evolve to be white? to learn more about skin color

  Is this appearance an illusion and possibly a construct of a prejudiced mind, or does this have a valid scientific answer?

First, see my above point about facial reconstruction.

H. Heidelbergensis lived in Africa and in this resepct shared an environment that is like the environment that modern african are encountering that what modern Han Chinese are encountering. In this respect, we could expect some ressemblance.

  For example, are most Africans closer to our ancestors than the rest of humanity is?

No, they're not and they cannot be. The MRCA of all humans today is more recent than the MRCA between any human and H. Heidelbergensis. You should have a look at this intro to phylogeny to understand a little bit better how different lineages relate evolutionarily speaking.


Diffusion approximation to genetic drift I am reading from the classical textbook Principles of Population Genetics, Hartl and Clark (pdf here).

Introduction

Let $f(p,x,t)$ denote the distribution of allele frequency $x$ at time $t$ knowing that at time $t=0$ the frequency was $p$. One can model the change in this distribution with time using the Kolmogorov forward equation

$$\frac{\partial f(p,x,t)}{\partial t} = -\frac{\partial [M(x) \cdot f(p,x,t)]}{\partial x}+\frac12\,\frac{\partial^2[V(x) \cdot f(p,x,t)]}{\partial x^2}$$

where $M(x)$ is the "drift parameter", which represents natural selection (thus, in the absence of the selection $M(x)=0$), and $V(x)$ is the "diffusion parameter", which represents genetic drift. The diffusion parameter is $V(x) = \frac{x(1-x)}{2N}$, where $N$ is the population size.

Question

Why is it true that $V(x) = \frac{x(1-x)}{2N}$?

I welcome intuitive explanations and mathematical proof.

Thoughts

I would think it derivates from the Wright-Fisher model of genetic drift where the distribution of allele frequency at the next generation is given by a binomial distribution.

It does indeed proceed from the Wright-Fisher model, specifically from its diffusion process approximation.

If the population is size $N$, then at generation $t$ the number of alleles is $A(t)$, and so the frequency of alleles is $x(t) = A(t)/(2N)$, assuming the diploid case. Then Wright-Fisher says that:
$$ A(t+1)\mid A(t) \sim \text{Bin}(2N,x(t)) $$
So the distribution of the next generation's count, given the last one, is binomially distributed (under random mating).
One can find that, for a binomially distributed random variable $b\sim \text{Bin}(m,p)$, the mean and variance are given by:
$$ \mathbb{E}[b]=mp\;\;\;\;\;\;\&\;\;\;\;\;\;\mathbb{V}[b]=mp(1-p) $$
Thus, we get that
$$ \mathbb{E}[A(t+1)\mid A(t)] = 2N x(t)
\;\;\;\;\;\;\&\;\;\;\;\;\;
\mathbb{V}[A(t+1)\mid A(t)] = 2N x(t)[1-x(t)] $$
Applying $x(t)=A(t)/(2N)$, we see that
\begin{align}
\mathbb{E}[x(t+1) \mid x(t)]   &= \frac{1}{2N}\mathbb{E}[A(t+1)\mid A(t)]= x(t) \\
\mathbb{V}[x(t+1)\mid x(t)] &= \frac{1}{(2N)^2}\mathbb{V}[A(t+1)\mid A(t)] = \frac{x(t)[1-x(t)]}{2N}
\end{align}
using the fact that $\mathbb{V}[cX]=c^2\mathbb{V}[X]$.

We can relate this to forward Kolmogorov as follows. Recall that the binomial distribution can be approximated by a normal distribution, with mean $\mu$ and variance $\sigma^2$ given by the mean and variance of the binomial. This tells us that: $$ x(t+\delta t)\mid x(t) \sim \mathcal{N}(x(t),(\delta t)x(t)[1-x(t)]/(2N)) $$
The properties of the normal distribution then imply that $$ \Delta x_t=x(t+\delta t) - x(t)\sim\mathcal{N}(0,\sigma^2(x_t)\delta t) $$
where $\sigma^2(x_t) = x(t)[1-x(t)]/(2N)$.
This implies the following equality (in distribution):
$$ \Delta x_t = \sigma(x_t)\Delta W_t $$
where $\Delta W_t\sim \mathcal{N}(0,\delta t)$. As $\delta t\rightarrow 0$, we get a stochastic differential equation,
$$ dx_t = \sigma(x_t)dW_t $$
where the solutions are Markov random processes (unlike e.g. ODEs where there is only one solution and it is a deterministic path; think of it as a noisy ODE), specifically in this case an Ito diffusion. Note the SDE has no $dt$ component since the increment mean was $0$. If we then consider the density function for the random process $p(x,t)$, it must satisfy the Fokker-Planck (Forward Kolmogorov) equation: $$ \partial_t p(x,t) = -\partial_{xx}[p(x,t)\sigma^2(x)/2] $$
which gives a probability distribution over the allelic frequency value at each time point (given some initial value I've not specified here).
Note that $V(x)=\sigma^2(x)$.

In terms of intuition, I'm not really sure. Essentially $V(x)$ measures how much perturbation in the allelic frequency you can expect to happen each generation due to purely random effects, i.e. genetic drift. Notice that there is no perturbation when $x=0$ or $x=1$, i.e. no random changes can happen if no one or everyone has the allele. Notice also that this variance is exactly the variance of a Bernoulli distribution. It's like we've distilled the individual-level model to a population-level model that simply looks at the frequency of the binary choice of allele presence, I guess.
The variance (noise) is maximal when the frequency is $1/2$. It's sort of pushing the allele away from the middle, by increasing noise when one goes there; one might expect that (if run long enough) any such model will hit and get stuck at $0$ or $1$ (not sure if this is true).
I looked a bit if there were any other interesting interpretations of the sde considered here (e.g. in physics), but couldn't find any. Basically, it would be equivalent to a heat equation, spreading under some potential function controlled by $\sigma$.

Your question is closely related to this one. My answer largely follows Tataru et al, Statistical Inference in the Wright–Fisher Model Using Allele Frequency Data.


Is Hemoglobin binding to oxygen the same as Adsorption I have recently been reading about Hemoglobin and came across how it binds to oxygen. This seems very similar to Adsorption. Is the process of Hemoglobin binding to oxygen through Adsorption ?

From the Wikipedia article you cite the answer to your question is clearly NO. They seem very different: absorption is described as a surface phenomenon, whereas oxygen binding occurs in a single internal pocket in each globin subunit and forms a specific bond to an Fe(II) atom. The chemical nature of this pocket is quite different from that of the surface of the protein.

The Wikipedia article states:

  Adsorption is the adhesion of atoms, ions, or molecules from a gas, liquid, or dissolved solid to a surface.[1] This process creates a film of the adsorbate on the surface of the adsorbent.

and

  Similar to surface tension, adsorption is a consequence of surface energy. In a bulk material, all the bonding requirements (be they ionic, covalent, or metallic) of the constituent atoms of the material are filled by other atoms in the material. However, atoms on the surface of the adsorbent are not wholly surrounded by other adsorbent atoms and therefore can attract adsorbates.

However if you consult a text-book which describes the biochemistry of haemoglobin, such as Berg et al. you will find the specific chemical nature of the binding clearly described, as indicated by this extract:

  The iron atom lies in the center of the protoporphyrin, bonded to the four pyrrole nitrogen atoms. Under normal conditions, the iron is in the ferrous (Fe2+) oxidation state. The iron ion can form two additional bonds, one on each side of the heme plane. These binding sites are called the fifth and sixth coordination sites. In hemoglobin, the fifth coordination site is occupied by the imidazole ring of a histidine residue from the protein. In deoxyhemoglobin, the sixth coordination site remains unoccupied...The binding of the oxygen molecule at the sixth coordination site of the iron ion substantially rearranges the electrons within the iron so that the ion becomes effectively smaller, allowing it to move into the plane of the porphyrin (Figure 10.19).

The only similarity I can see is that in both processes the interaction of the gas with the material to which it binds is controlled by the pressure of the gas. However in the case of haemoglobin there is a distinct difference from absorption in that the dependency on pressure exhibits a sigmoidal curve, specifically suiting it for the role of quantitative delivery of oxygen to the tissues at a particular small reduced pressure range.

You sound as if you come from the physical sciences. If so, prepare to be surprised at how smart a chemist Mother Nature is.