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Hardy Weinberg Equilibrium; Homozygous individuals
I have the following exercise that I can't solve:
In a sample there are 16 homozygous A1 allele carriers
(A1/A1) and 24 heterozygous A1/A2 allele carriers. How many homozygous A2 allele carriers (A2/A2) would you need to get an HWE=1 in the sample?
I think there is some information missing, probably an assumption should be made so that the equation can be solved...

Welcome to SE Biology! While you're here, it may be a good idea to take the tour and learn more about how to participate. One feature of the community is that we do ask people to do some minimal research or attempts to answer their questions. For example, I was able to find a variety of resources on understanding HWE with an internet search, e.g. https://www.nature.com/scitable/definition/hardy-weinberg-equation-299/. What have you already tried?

This question is similar to: Solving Hardy Weinberg problems. If you believe it’s different, please edit the question, make it clear how it’s different and/or how the answers on that question are not helpful for your problem.

As per H-W:
a^2 + 2ab + b^2 = 1
where: a + b = 1

We are given:

16 homozygous (A1/A1). So: a^2 = 16/x
24 heterozygous. So: 2ab = 24/x

where x is the total population size (which we don't know)

Rearranging the two equations above:
x = 16/a2
x = 24/2ab
b = 12a/16

Substituting this into a + b = 1:
12a/16 + a = 1
a = 16/28 ~ 0.57
b = 12/28 ~ 0.43

x = 16/a2 = 16/0.57^2 = 49

Therefore:
b^2 = homozygous (A2/A2) / x
homozygous (A2/A2) = b^2 * x = 12/28 * 12/28 * 49 = 9
(which is also 49 - 16 - 24 = 9)

So the population has 49 individuals, comprising 16 homozygous (A1), 24 heterozygous and 9 homozygous (A2).

Thanks for answering. This appears to be a correct answer. I appreciate that you're trying to help this person out, but in the future, I'd recommend the method of helping them to work it out themselves, rather than doing it for them! They haven't really met the bar for an answer according to the homework policy. Side note: LaTeX formatting your equations might make them easier to read.


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Examples of species whose extinct common ancestor is well documented?
If we follow the ascendence line of two closely related species we can build a
"Theoretical" common ancestor, whose characteristics were inherited with few differences by the offspring.
         _______ species 1
Ancestor/
        \_______ species 2

Are there examples of extinct ancestors that we can be almost 100% sure they correspond to the ascendant of the two distinct species?
Are these examples well documented with fossils and the inherited traits well understood?

Not with fossils.
Very very few organisms ever fossilize and most of the organisms tissues are not represented in fossils. Less than 0.01% of all animal SPECIES have left a single fossil and most of those have not been found yet.
Because of how incomplete the fossil record is we can never say a species is definitively part of a lineage. in fact the basic assumption in paleontology is that you never have a direct ancestor (individual or lineage) and extraordinary evidence would be needed to demonstrate otherwise.
Only direct observations or high genetic sampling would allow something to be considered definitively a common ancestor at the species level. Now we do have this for some species. We also have fossil localities with really high resolution making common ancestors highly likely, but never definitive.
Part of the issue is also defining species, the definition for species used in paleontology is very different than the one used in say population genetic. Species are nota real things but a human category stuck onto what is basically a continuous spectrum, it only works because most of the spectrum is dead. There is no concrete point at which two groups are definitively separate species. Its a bit like trying to define the exact cut off between two colors. Some groups of biologists favor definitions which increase the number of species others ones that decrease it, and both work because for the actual practice of biology whether two closely related populations are or are not separate species really does not matter.

This phenomenon appears to be called "pseudoextinction", with dinosaurs as the classic example of an ancestor (of modern avians). We know tons and tons about dinosaurs and avians, such that we can be pretty damn sure that modern avians are the descendants of dinosaurs.
Granted, almost by definition no fossil evidence could yield conclusive evidence of such a relationship, as the fossil is just a fossil.
For example, I am not sure that anyone could point to a specific dinosaur and say "this is probably the ancestor of modern avians A and B." Though I could be wrong about that.

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how to culture mc38 cells
I work at a start up company in a vivarium. My boss would like me to start working with MC38 Cells. I bought all of the equipment (recommended by a colleague) and should be ready for the cells. Could anyone recommend a good place to learn how to do this fast? He has surprised me and already ordered the cells. I do have some knowledge on the subject ( from bachelors degree in Biology), but it is not enough. I need somewhere that can teach me even the little steps. I have tried looking at scientific papers, but they typically skip over much of the steps that are common knowledge (to most).

actually, this question may be a duplicate of this question: https://biology.stackexchange.com/questions/36255/textbook-lab-manual-for-mammalian-cell-culture.

Does this answer your question? Textbook/lab manual for mammalian cell culture

Edit: Similar questions have been asked before: Textbook/lab manual for mammalian cell culture
Cell culture reagent/consumables suppliers can have good step by step recommendations for how to use their products. For example Thermo has some guidelines that you may find helpful. Specifically, cell culture maintenance would seem to be helpful.
These folks also have what superficially look like good resources.
Reviewing MC38 culture requirements is also always a good idea.
Good luck!

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How can the recurrence risk ratio be calculated?
The recurrence risk ratio is calculated as follows:
$$ \lambda_s = \frac{\text{risk of sibling}}{\text{risk in population}}$$
where the risk of sibling refers to the risk that a sibling has to get the disease and the risk in population is the risk that the disease occurs in the population.
I do not understand how it is possible to calculate the numerator. I saw a video here that discusses how it's calculated for simple diseases that follow Mendel's laws. However, my lecturer was discussing this in the context of multifactorial traits.
How would we calculate the risk of the disease occurring in a sibling without simply forcing the parents to breed thousands of times?

If we look at web resources, what we will notice is that this ratio is not deployed at the family level but at the population level.
In other words, when we look at a population, we can ask:

What proportion of these people have the disease?

That is the denominator.
Taking that group of people, we can then ask:

Of those people that have the disease, what proportion of this affected group has a full sibling that also has the disease?

That is the numerator.
So if we have a population of 100 people, say 10 people have the disease. The denominator is then $0.1$. We might then observe that 4 of those cases are two pairs of siblings (and there are no other siblings). So
$$risk\ in\ sibling = Pr(sib\_has\_disease | person\_has\_disease) = \frac{4}{10} = 0.4$$
And thus
$$ \lambda_s = \frac{\text{risk of sibling}}{\text{risk in population}} \
= \frac{0.4}{0.1} = 4$$
It's worth pointing out that we are not controlling for environment or for pedigree or anything like that here. The null hypothesis of what $\lambda_s$ should be without any genetic risk is a complex function of prevalence and family structure (what if everyone is an only child, or the whole population is all siblings?). So it's not even clear how to interpret it, except to say that you might intuitively guess that a disease that strikes purely randomly might have $lambda_s = 1$. But I'm not even sure that that's true! All that this ratio is measuring is a rough estimate of how clustered the disease is within families within a population.


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If you want to understand evolution from a genetics standpoint what are some must reads be it books or textbooks?
The question basically sums it up. I'm looking for books/textbooks that explain evolution from a genetic perspective.

So your question is about your problem, not a problem in biology. I suggest re-reading the [Tour] for examples of the types of biological questions that are on-topic here.

https://en.wikipedia.org/wiki/Modern_synthesis_(20th_century)

Dawkin's selfish gene is still a nessisary starting point if you don't know much about evolution.

For a historical perspective and summary, see here.
For a textbook that works through the math from a very simple foundation, see here. (Felsenstein, J. Theoretical Evolutionary Genetics, 2019).

Excellent, thank you

Depends on the level you are after. Science is constantly changing our understanding of fields. To you want to secure the "established basics" or do you want to "find bleeding edge perspectives" of evolution?
The better the question is asked the better the answer.
Since evolution has been a major focus since the 60s, any textbook would bring you upto date on stuff that has been acceptably proven. However, Evolution in popular terms is generally gravely misunderstood, and you don't want to read the zealots opinions (e.g
Dawkins).
To get a popular overview of the current state, I would recommend the book "How Life Works, Philip Ball". (honestly haven't read the whole thing, but seems to bring up some critical common missunderstandings..)
What many biologist forget is that evolution is a theory without a complete foundation. Classical evolutionary reasoning cn explain anything, true or not. It's a theory, and definitely a phenomena, but not an explanation.
I'm not rejecting evolutionary theory, merely emphasising some of it's shortfalls.

Evolution has been a major focus since long before the 60s! The convergence of genetics and evolution itself goes back to the 20s-30s with regard to the Modern Synthesis (see wiki comment above). I am not sure what to make exactly of your statements about a complete foundation, that is neither here nor there with regard to this question. I'd suggest trying to edit your question to target it a little bit more directly to the matter at hand, rather than evolution at large.

I highly recommend "Evolution" by Douglas J Futuyama. It covers evolution from every angle including genetics.


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What is the minimum number of chemical elements required for life on earth? Does it vary between kingdoms?
As a non-biologist, I assume that there are certain elements that occur in all life forms as we know them. Examples might be carbon, hydrogen, oxygen and so forth. There are also elements that are rarely, if  ever, required for life on earth. My question is not about what elements might be required for life (although such information might be interesting for me and other readers). Rather it is about what the minimum possible number of elements that any life form on earth has, if we know the answer to that question. Also, if it is known, (how) does this differ between the plant, animal and other kingdoms?

You are far more likely than me to know what tags might be appropriate here. Please feel free to edit.

What are you defining as life? Viruses? Prions? bacteria and above certainly, but where's your cut-off?

@bob1 Whichever entities/notional kingdoms that an answerer might consider to be forms of life are fine, so long as it is explained in the answer. (Although, I wasn't thinking of prions and barely know what they are).

Prions are self-replicating proteins that can turn other proteins into more prions, they cause diseases like Creutzfeldt-Jakob disease (vCJD is also known as "mad-cow disease"), they replicate, evolve etc... don't worry, they aren't really alive, but then neither are viruses technically, which can't replicate themselves independently of another organism and always need some part of that organisms replication machinery to function. However, if you accepted prions as life, the minimum would be C, H, O, N, S I think.

I think I would add P to the list provided by @bob1 (ATP/NAD)

Hmmm. Four downvotes, but no constructive comments to explain how to ask a better question. Sigh ...

@user338907 Is that an answer perhaps?

@Araucaria - The reason for the down-votes is likely that it is impossible to define because there is such a variety of life that there will be no 1 magic number of elements. The most we can do is list a minimum of elements that are found in all life-forms, which would presumably make life possible, but that is specifically not what you asked for.

@bob1 +1 But presumably if there are elements that are found in all life forms, there are life forms that don't need any or many more than those elements. The vastness of different life forms that exist doesn't really have too much effect on this. For example, if we know of a life form that only needs those elements that are necessary for all life forms plus two others, then every other life form requiring more than that is out of consideration. No?

minimum to have any life or life as earth currently has?

@John I suppose that it's probably best to restrict it to life as earth currently has.

then you will need basically every element aside from the very unstable ones and the noble gasses, very few are not used in some life somewhere. even fluorine occurs in some life. it would be easier to list the elements NOT used in life.

@John I meant the minimum for a life form that currently exists on earth! (Narrow scope meaning of (any). I misunderstood the 'any' in your comment.

If we change the question to "what is the minimum number of elements common to every form of life?", my lists would be as follows. (I am not considering either viruses or prions to be 'alive').
The following elements are surely common to all forms of life (List 1):

H (1), C (6), N (7), 0 (8), Mg (12), P (15), S (16) [#7].

In addition, the following elements are very likely to be common to all forms of life (List 2):

Na (11), Cl (17), K (19), Ca (20), Fe (26), Cu (29), Zn (30) [#7].

If we broaden things to include elements occurring in any form of life I would add (List 3):

B (5), F (9), Si (14) [!Seemingly], V (23), Cr (24), Mn (25), Co (27), Ni (28), Se (34), Mo (42), Cd (48), Sn (50) [!Maybe], I (53) , W  (74) [#14].

No element in either list has an atomic number greater than 74 (Tungsten). (In the list given by Frieden (1972), the highest is I (53)).

For List One (and as pointed out by @bob1), H (1), C (6), N (7), 0 (8), S (16) are all present in proteins. P (15) is present in ATP and NAD. We must surely also include Mg (12), as the true substrate of almost all ATP-requiring enzymes is a complex of Mg++ and ATP. I can't see that any element can be removed from this list, but it could be argued that we need to add some from List 2.

For List 2, Fe (26) is present as haem in haemoglobin and the cytochromes, and (not necessarily complexed to heme) in other components of the electron transport chain. It might be possible that anaerobic life is possible without iron, in which case Fe (26) needs to be demoted to List 3 (but I doubt it). Zn (30) occurs in many enzymes (including yeast and liver alcohol dehydrogenase). It might be possible for a life form to exist without requiring Zn, but I don't know of any examples.

If we restrict consideration to plants, then Mn (25) needs to be promoted to List 1 (Mn is an essential component of Photosystem II, the enzymic system responsible for the 'splitting' of water in photosynthesis). As life as we know it would be impossible without PS, Mn (25) should possibly be in List 1 without qualification.

List 3 will probably always be contentious, but here are my thoughts:

B (5) is present in boromycin the only naturally-occurring compound containing Boron (as far as I am aware). It has long been considered essential for some plants, but this is contentious. See The importance of boron in biological systems and Boron: the essential element for vascular plants that never was
Edit B (5). @john has pointed out that B is required by some cyanobacteria, and has provided the following reference: Boron Requirement in Cyanobacteria. Its Possible Role in the Early Evolution of Photosynthetic Organisms.
The authors (Bonilla et al.) point out that B is a trace element that "although required in higher plants, has no role in animals or fungi". They suggest that B (possibly as boric acid?) can stabilize membranes by forming cis-diols with glycolipid -OH groups, a role previously suggested to account for B requirement in plants. (References to the original plant research may be found in Bonilla et al.).

This, I think, justifies B being included in List 3: required for some forms of life (but not a minimum requirement for life).

F (9) occurs in fluroacetate (See also The natural production of chlorinated compounds by G W Gribble)

Si (14). A paper in Science in 1972 suggests that Silicon is an essential element for the chick (news to me!). Frieden (quoted below) has this to say: "Possible structural unit of diatoms; recently shown to be essential in chicks. "

V (23). Occurs in haloperoxidases (See Coordination environment changes of the vanadium in vanadium-dependent haloperoxidase enzymes.  The vanadate ion is very similar to phosphate. See The role of vanadium in biology)

Cr (24) Whether Chromium is an essential trace element is controversial. It may play a role in insulin action (see Wikipedia) but this is not universally accepted (the Wikipedia article gives a good summary of the current position). Some bacterial can reduce chromium but this seems to be a detoxification mechanism (See also Chromium: is it essential, pharmacologically relevant, or toxic?). Frieden states "Essential in higher animals; related to action of insulin." but this, it appears, is still controversial. Possibly Cr (24) needs to be deleted from List 3.

Co (27) is a component of Vitamin B12

Nickel (28). Urease, the first enzyme crystallized (by Sumner in 1926), an accomplishment that played an essential role in establishing that enzymes are proteins, was shown in 1984 to contain Nickel (see Urease (Wikipedia))

Se (34) Selenium (as selenocysteine) is directly incorporated on the ribosome into some enzymes (SelenoCys is considered "the twenty-first amino acid")

Mo (42) is a component of quite a number of enzymes, including xanthine oxidase and is often associated with a pteridine cofactor.  See Molybdenum and Molybdenum-Containing Enzymes

Cd (48) A carbonic anhydrase from the marine diatom Thalassiosira weissflogii contains cadmium. It is thought that in oceans depleted of Zn, diatoms can use Cd as a zinc substitute. (See Biochemistry: a cadmium enzyme from a marine diatom and
Structure and metal exchange in the cadmium carbonic anhydrase of marine diatoms)

Sn (50) There have been some reports that Tin is an essential trace element for rats and humans (see Case study: bioavailability of tin and tin compounds and Frieden (quoted below)), but the evidence appears to be very scanty. Tin probably should be deleted from List 3.

I (53). Iodine is known to be a component of the thyroid hormones

W (74) Tungsten The first enzyme to require tungsten, a NADP-linked formate dehydrogenase from Clostridium thermoaceticum was purified and characterized in 1983. Since then a number  of tungstoenzymes (at least ten) have been identified, including acetylene hydratase. In many cases (and in a similar fashion to molybdoenzymes), W is often bound to a pterin cofactor. (See Tungsten in biological systems)

I think The chemical elements of life by E.Frieden, published in Scientific American in 1972, is still relevant, and I have relied heavily on the table on p55 of this publication in compiling the above lists
I haven't considered Sr (38), Nb (41), Ba (56) or Ta (73) but from Tungsten in biological systems  it appears that there is a case for these elements to be included in List 3

Should I take it, then, that there may be life forms that have only around 14 elements (list 1 + list 2)?

Note boron is important in cyanobacteria. http://www.plantphysiol.org/content/plantphysiol/94/4/1554.full.pdf and there a few notable organoboron compounds. https://www2.chem.wisc.edu/areas/reich/OrgMet/boron.htm

I think you can safely move Fe into list 1, even if heme (or haem) had never existed, Iron-Sulfur cluster proteins are ubiquitous among all cellular life, including obligate anaerobes. I can only think of one synthetic biology experiment in which E. coli was engineered to grow (very slowly) without making new Fe-S clusters, but they didn't even attempt to show growth in iron-limiting conditions. You're also probably right about being able to move Mn and Zn up to list 1 without further qualification.

@MikeyC Thanks. I agree with all you say, especially about non-heme iron. (Will update again over the weekend)


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Evolution from Mating types to different sexes
Imagine a lineage of multicellular organisms that had mating types and evolved their mating types into sexes. What are the possible mechanisms that might have brought this lineage to evolve sexes from mating types?
To my understanding of the definitions of sexes and mating types, the only diffenece between the two is that sexes imply gametes of different sizes. Is it correct?

Another important reason to have mating types is to prevent self-fertilization or self-polination that produces less capable offspring. Because of this requirement, mating types may evolve also for species that produce both types of gametes, or does not differentiate them into male and female gametes. Fertilization is only possible if gametes have different mating types.
It may be more than two mating types, but if there are only two, they are probably similar to "sexes" even if gametes do not look different.

Thanks for you answer. It is interesting so to explain the evolution of mating types. But I don't think it answers the question though in the sense that it does not address the evolution from mating types to sexes. In my question, I am mostly interested in the evolution of gamete size differentiation and of number of gametes from a lineage/species where there is different mating types but no difference in size of number of gametes.

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Source of information on the evolution of aging/senescence
Do you know a good review (published peer-reviewed or an online course or whatever) that offers a good overview of all hypothesis explaining the various patterns linked with aging?
I'd like this review to make the following things clear; antagonist pleiotropy, Gompertz and Weibull models and what theoretical explanations are underlying these models, mutation accumulation, reliability theory, eventually group selection, age-specific efficiency of natural selection, telomere length, the definition of senescence, and all not-cited hypothesis to explain the patterns of aging/senescence.

this is one paper which covers some of that - http://www.cosmoid.de/zajitschek/papers/Bonduriansky2008FunctionalEcology.pdf - you've asked for quite a lot of coverage there so I'll throw together a few papers tomorrow.

@Remi.b: Have you found the book?

I don't know about just one source that fits everything you've asked, so here's a custom bibliography to get you started instead.
General Sources
I first learned about biogerontology from the excellent series of introductory essays at João Pedro de Magalhães' website, senescence.info; I definitely recommend starting here.
A short book written by two experts, for Scientific American Publishers, is Finch and Ricklefs' Aging: A Natural History. "The" book on the Evolutionary Theory of Aging is Michael Rose's Evolutionary Biology of Aging. "The" book on comparative biogerontology is Finch's Longevity, Senescence, and the Genome. A "pop" account of recent research (esp. to do with caloric restriction and long-lived mutants, which have people excited right now, and the search for longevity drugs) is David Stipp's The Youth Pill. A constantly-updated-with-new-editions-reference is The Handbook of the Biology of Aging. In 2008 (just missing the 2009 rapamycin excitement), Cold Spring Harbor Press published a collection on Molecular Biology of Aging. The Gerontological Society of America has an e-textbook out, that I think is going to be updated on the regular, called Molecular and Cellular Biology of Aging.
The Definition and Measurement of Aging
Usually, people define senescence as an increase in "mortality" with age. Mortality roughly means vulnerability; the older you are, the easier it is to die. Mortality is measured/estimated demographically, in terms of (hypothetical or actual) cohort survivorship. There are two quantities usually used: one for discrete-time, and one for continuous-time. Where $N_x$ the number of survivors still alive in a cohort at age $x$,
$q_x = \frac{{N_x}-{N_{x+1}}}{N_x}$ discrete-time; The Age-Specific Probability of Death.
$\mu_x = -\frac{N^{'}_{x}}{N_x}$ instantaneous; The Force of Mortality.
The first one is the fraction, of those alive at age $x$, who will die before age $x+1$. This estimates the probability that an individual aged $x$ will die before age $x+1$. This is intuitive: to age means that an 80-year-old is less likely to make it to 81, than a 20-year-old is to make it to 21. Notice that $q_x$ is bounded between 0 and 1.
The second one is the instantaneous rate of death, normalized against cohort size at that instant (whereas the first was the number of deaths in an interval, normalized against cohort size at the beginning of the interval). It is the instantaneous, age-specific, per-capita death rate. It can be visualized as the slope of the survivorship curve, divided by its height, times -1 to make it positive. It is not a probability. It has a dimension of rate ("per-second", "per-hour", etc) and it has no upper bound.
This way of defining senescence is described in Nature Scitable's Aging and its Demographic Measurement (although the authors give an erroneous definition of the force of mortality). It is discussed and justified intuitively, and at length, in Peter Medawar's The Definition and Measurement of Senescence.
Sometimes, you might want to count a decline in fecundity as aging, too, even if mortality wasn't changing. Or, you might want to define senescence in terms of various kinds of physiological performance. This is really a matter of taste, I suppose, or of what kinds of question you're trying to answer. Ageing or Senescence is just the part of getting older which, on top of having more birthdays, is somehow or other "bad" for you.
But the most common criterion is that $q_x$ or $\mu_x$ grows with age.
Mainstream Evolutionary Theory of Aging:
The mainstream idea is that aging evolves because of the declining force of natural selection with age. Natural selection "cares less" about things that happen late in life, than about things that happen early in life.

Mutation Accumulation (MA): the theory proposed in Peter Medawar's An Unsolved Problem of Biology. (Theory that aging is due to genes that are silent or neutral in early life, and deleterious in late life.)
Antagonistic Pleiotropy (AP): the theory proposed in George C. Williams' Pleiotropy, Natural Selection, and the Evolution of Senescence. (Theory that aging is due to genes that are beneficial in early life, and deleterious late in life.)
Disposable Soma: Proposed by Thomas Kirkwood and Robin Holliday; sometimes considered a version of AP. (Theory that aging is due to a tradeoff, in turn possibly due to allocation of limited resources, between reproduction and maintenance; selection favours less than perfect maintenance. Can be considered a version of AP where the "early beneficial effect" is increased maintenance, and the "late deleterious effect" is decreased survival.)

Summarized in Nature Scitable's The Evolution of Aging. Note that both MA and AP could be partly true; both kinds of genes could exist.
Both MA and AP are commonly cited as predicting that higher extrinsic mortality should lead to the evolution of earlier / faster senescence; but things may be more complicated than this.
The Declining Force of Natural Selection: Hamilton's Formalization
Medawar's and Williams' insights were verbal. William Hamilton did the math, and showed that certain formal indicators of the strength of selection on a genetic effect, necessarily declined with the age at which that effect occurs. These indicators were I think: 1) the partial derivative of $r$ (the intrinsic rate of increase / malthusian parameter, which he took to be fitness) with respect to the force of mortality at age $x$; and 2) the partial derivative of $r$ with respect to fecundity at age $x$. (The first starts declining at the age of first reproduction; the second starts declining immediately.)
In passing, this also demonstrated that a remark R. A. Fisher had previously made, and which Medawar had accepted, was fallacious. Fisher and Medawar had assumed that the strength of natural selection was proportional to age-specific reproductive value; but since reproductive value can increase with age, and Hamilton's indicators can't, reproductive value can't be measuring the sensitivity of $r$.

Hamilton's paper: The Moulding of Senescence by Natural Selection.
Charlesworth summarizes Hamilton's results and puts them in context in Fisher, Medawar, Hamilton and the Evolution of Aging.
Charlesworth's book Evolution in Age-Structured Populations is supposed to be quite important and to have furthered and refined stuff in this area.
Apparently things might be a bit more complicated than this? Baudisch has claimed that although Hamilton's indicators must decrease with age, other indicators, which aren't obviously unreasonable, can increase.

Gompertz, Weibull, and Gompertz-Makeham
The Gompertz equation is intended to describe how the Force of Mortality $\mu_x$ grows with age. The Gompertz equation was come up with empirically, not for any theoretical reason; it just seemed to Benjamin Gompertz to fit the data quite well, for a good stretch of adult lifespan. The same goes for the Weibull equation, as far as I know, and for the Gompertz-Makeham equation.

Gompertz is an exponential growth equation: $\mu_x = \mu_0 \cdot e^{Gx}$ (where $G$ is a parameter). It looks like a straight line when graphed on a semilog plot.
Weibull is a power growth equation: $\mu_x = A \cdot x^B$ (where $A$ and $B$ are parameters). It looks like a straight line when graphed on a log-log plot.
Gompertz-Makeham adds a constant to the Gompertz equation: $\mu_x = \mu_0 \cdot e^{Gx}+C$. This ruins the elegance of the semilog-graphing, alas; it doesn't look like a straight line.

Apparently some people have tried to show how eg. Gompertz can evolve in MA models, but the generality of this is questionable (see Box 2 in this Trends in Ecology and Evolution paper). Gavrilov and Gavrilova (proponents of the "reliability theory of aging", have said something about Gompertz and Weibull being special: ("Both the Gompertz and the Weibull failure laws have their fundamental explanation rooted in reliability theory... and are the only two theoretically possible limiting extreme value distributions for systems whose life spans are determined by the first failed component... In other words, as the system becomes more and more complex (contains more vital components, each being critical for survival), its life span distribution may asymptotically approach one of the only two theoretically possible limiting distributions—either Gompertz or Weibull (depending on the early kinetics of failure of system components).") I don't know what that means.
Gompertz is the most commonly cited / used equation, I think. It's supposed to be more accurate than Weibull. Gompertz-Makeham I guess is more accurate, but of course it would be - it has an extra adjustible parameter, which, if it isn't helping, you can just set to zero!
Sometimes these equations are erroneously presented in terms of $q_x$ instead of $\mu_x$. This is erroneous historically, but also because $q_x$ has an upper bound of 1 and couldn't possibly obey any of the equations, at least not indefinitely.
Sometimes people find it more intuitive to describe Gompertz' exponential growth in terms of how long it takes $\mu_x$ to double; in humans, this "Mortality Rate Doubling Time" is about eight years.
Note that the equation does not accurately describe early life; mortality often starts high in infants, before falling to its minimum, and then starting to grow again. Thus $\mu_0$ isn't the actual mortality rate at age 0, but the backwards-extrapolated mortality rate you would have had at age 0, if you were perfectly Gompertzian (or whatever).
It also may not describe very late life. A hot topic right now is "late-life mortality deceleration", where the exponential growth seems to slow down such that Gompertz overpredicts mortality in the very old; whether this is so, and why, is debated.
Reliability Theory and the Reliability Theory of Aging
"Reliability Theory" itself is just a mathematical framework for describing survival / failure rates and stuff. (Engineers use it to quantify stuff like, the rate at which parts have their first breakage, or whatever.) Some of the quantities it describes are basically the same as some analogous quantities in demography / life histories, if "first failure" is taken to mean death. For example, the "Survival Function" $S(t)$ is the probability, at time $0$, that failure will not yet have occurred by time $t$; this is obviously analogous to the probability $l_x$ that a newborn will still be alive at age $x$.
Systems can be made of parts; if you know the survival/reliability patterns of the parts, and how they go together, you can tell something about the survival/reliability of the whole system. To illustrate, compare two kinds of reliability structure:

A "series reliability structure" is one where, if any part fails, the system fails. An example would be a block held up by a chain; if any link breaks the block falls.
A "parallel reliability structure" is one where, if all parts fail, the system fails. An example would be a block held up by a number of individual rings, attached separately; only when the last ring breaks, does the block fall.

"The Reliability Theory of Aging and Longevity" is a specific theory proposed by Leonid Gavrilov and Natalia Gavrilova, intended to explain patterns of organismal failure ("death") in terms of component failure, and how the components are put together. If I recall, they propose that aging organisms are made up of redundant blocks of non-aging components; supposedly, this can explain near-Gompertzian aging over most of adult life, as well as apparent late-life mortality deceleration.
Group Selection
Heresy! Most evolutionary biologists / gerontologists, I assume, are happy with the mainstream theory and don't take the group selection theory seriously. Iunno, try Mitteldorf? Here's a paper and he also wrote a pop book with Dorion Sagan. On group selection in general as an explanation for altruism, I think David Sloan Wilson's the guy trying the hardest to defend it (or "a new version of it").
Molecular Mechanisms
Iunno, try The Hallmarks of Aging? The trouble is we really don't know what mechanisms cause aging. There's some good ideas, but finding evidence is haaaaard. One problem is that, if you want to know why some species live longer than others, and you're looking for physiological correlations, body size is a huge confound (elephants and whales live longer than mice and dogs), and so might be phylogeny.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Heterozygosity and overdominance
Consider $m$ loci with heterozygote advantage (overdominance) such that the fitness of the two homozygotes is $1-\frac{s}{2}$ and the fitness of the heterozygotes is $1+\frac{s}{2}$, where $s>0$. We'll assume that the fitness of an individual is given by the multiplication of the fitness component on each locus. In consequence, the fitness of the best possible genotype is given by $\left(1+\frac{s}{2}\right)^m$.
According to this book, an individual is heterozygote at $j$ of these $m$ loci with probability
$${m\choose j}\left(\frac{1}{2}\right)^m$$
and the equilibrium population mean fitness $\hat w$ is
$$\hat w = \sum_{j=0}^m {m\choose j}\left(\frac{1}{2}\right)^m  \left(1+\frac{s}{2}\right)^j  \left(1-\frac{s}{2}\right)^{m-j} = 1$$
I don't understand any of these two equations! Can you help me to understand how they have been calculated?

For the moment I just enjoyed proving that $\hat w = 1$. We can reformulate $\hat w$ as
$$\hat w = \left(\frac{1}{2}\right)^m  \sum_{j=0}^m {m\choose j} \left(1+\frac{s}{2}\right)^j  \left(1-\frac{s}{2}\right)^{m-j} = 1$$
,then using the binomial identity
$$ \hat w = \left(\frac{1}{2}\right)^m \left(\left(1+\frac{s}{2}\right) + \left(1-\frac{s}{2}\right)\right)^{\space m}$$
$$\hat w = \left(\frac{1}{2}\right)^m 2^m$$
$$ \hat w = 1 $$

Am taking another stab at this. I think that derivations in the refs are simpler and overall it's an interesting question.

If the fitness of a heterozygote is $(1+s/2)$ and of a homozygote is $(1-s/2)$ then why is the probability for a given state $(1+s/2)^j(1-s/2)^{m-k}$
$$\binom mj (1/2)^j(1/2)^{m-j}= \binom mj (1/2)^m~~ ?$$
As you pointed out earlier, in the general case it need not be true that $p = q = 1/2$ but that is what the form of the probability above implies. So the threshold question is why this particular heterozygous-dominant model implies equilibrium probabilities $p = q = 1/2.$ I think the ideas below begin to address this.
The simplest case is for one locus, two alleles, and there are many good derivations online. I think if you understand the situation for one locus you can generalize to higher numbers. (Hopefully I will supplement this answer, time allowing. I think a shortcut would be to assume $p = q = 1/2$ and use your fitness weights. That gives us $\bar{w}=1$ as a denominator. Now for reasons of symmetry I think you can show that the relative frequencies of $p$ and $q$ are equal and so $p' = p.$ Then you have to show that this equilibrium solution is unique.)
For a single locus the derivations of `heterozygote advantage' I have found,(1)(2), assign fitness weights as follows:
AA = (1 - s),     Aa = 1,       aa = (1 - t )
in which $s,t > 0, s \neq t$ in general, from which they derive as a condition for equilibrium
$$\Delta q = \frac{pq(sp-tq)}{\bar{W}}  = 0$$
so
$$\hat{p} = \frac{t}{s+t} ~~~\text{and}~~~ \hat{q} = \frac{s }{s+t}$$
in which $\hat{p}, \hat{q}$ are equilibrum frequencies for each allele, respectively, and s and t are rates of mutation. Nowhere did I see a model in which they had assigned the same fitness to both homozygous cases (AA, aa) but it's just a special case of the heterozygote advantage model.
fitness (AA) = fitness(aa) = (1 - s/2), fitness(Aa) = (1+ s/2).
So if we subtract s/2 from each fitness score (or normalize with respect to Aa to the same effect), we get:
fitness(AA) = fitness (aa) = (1- s ) and fitness (Aa) = 1 as in the two references above, except that now the two homozygous states have equal fitness.
But then we have $$\Delta q = \frac{pq(sp-sq)}{\bar{W}} =  \frac{pqs(p - q)}{\bar{W}} $$
and the only nontrivial solution is $p = q = 1/2.$
So what I am suggesting is that when you assign the same fitness to both $AA$ and $aa$ you no longer have the general case. As for the value of s being forced, the following seems relevant.
The full expression from (2) for the equilibrium condition is
$$p' = \frac{p^2 W_{AA}+ pq W_{Aa}}{\bar{W}} \hspace{10mm}(1)$$
in which$ W_{AA} = W_{aa} =  1- s$ and $W_{Aa} = 1$ and
$\bar{W} = p^2 W_{AA}+2pqW_{Aa}+q^2W_{aa}$
If the homozygotes are assigned the same fitness and $p = q = 1/2$ , equation (1) above becomes:
$$p' = \frac{\frac{1}{4} + \frac{1}{4}(1-s)}{\frac{1}{2} + \frac{1}{2}(1-s)} $$
The program on page 583 of (1) is helpful. Let h:= heterozygous and m:= homozygous. If $p = q = 1/2$ then as long as fitness(h) and fitness(m) are equal the system is in equilibrium immediately.
If $p\neq 1/2$ then as long as f(h) = f(m) the system reaches equilibrium at $p = 1/2$ asymtotically. If $p = 1/2$ but f(h) $\neq$ f(m) the asymtotic limit has to be calculated.
See also http://evol.bio.lmu.de/_teaching/evogen/Evo8-Summary.pdf

Thanks a lot for your answer. I'm traveling right now and I don't have time for reading up your answer. I'll read it wednesday or thursday probably.

Great answer. In addition to your (now deleted by yourself) other answer, you perfectly answered my question. Thank you. +1

@Remi.b: Appreciate the feedback. It was an interesting question and I am still learning about this broad subject.


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Is Haemoglobin a positively charged Sol?
My book NCERT(Class 12, Surface chemistry) claims that hemoglobin is a positively charged sol.

The cytosolic pH in human cells is around 7.4, but fluctuates through the cell cycle
according to this article the isoelectric point of Hemoglobin behaves as follows:

The more nearly free a preparation of hemoglobin is from
nonhemoglobin protein the more nearly does the isoelectric point
approach 6.8,

So if the isoelectric point is 6.8 for Hemoglobin and pH of cytoplasm is 7.4 so wouldn't be Hemoglobin a negatively charged sol?
As we know in blood, proteins exist as negatively charged species so blood is termed as negatively charged sol, so is there a point I am missing?

This may be more appropriate for chemistry.stackexchange.com.

@MaximilianPress protein structure of membranes  is determining the charge here, as biology is more concerned with things like protein structure, I thought it might be better to post here

It's a bit of a value judgment. For the record, I would suggest looking into the different forms of Hb (oxy, deoxy, carboxy) and their ternary structure as oxygenation reduction status etc. should play a role. I am not a chemist but there are a variety of publications in chemistry journals investigating isoelectric behavior of these different forms: https://www.sciencedirect.com/science/article/pii/S0021925818745547/pdf?md5=e2e6c1800015a0907b237e8b32f49569&pid=1-s2.0-S0021925818745547-main.pdf, https://www.jbc.org/article/S0021-9258(18)61920-9/pdf, https://pubmed.ncbi.nlm.nih.gov/7324711/

There is a major problem with the item list, hemoglobin is not the same as "blood". In blood, hemoglobin is contained with RBCs  and not floating everywhere. Let me show how this can cause a HUGE difference:

Whether hemoglobin is negatively or positively charged will not affect the blood; because it is contained with RBCs whose membrane is negatively charged and doesn't depend to a large degree on its contents. However, blood is actually negatively charged and the main contributor to this is Heparin (negatively charged anticoagulant protein), the RBCs membrane is negatively charged preventing adhesion to themselves and negatively charged membranes of other cells (anti-coagulation mechanism)
intracellular pH of RBCs is around 7.1 (1). the isoelectric point of haemoglobin is a bit of trouble to agree on because actually the alpha chain of hemoglobin has isoelectric point of (7.5–7.8) while beta subunit is (6.1–6.7) (2). I didn't find a source assessing the in-vivo charge of hemoglobin or electrophoresis at physiological pH, even though if electrophoresis at physiological pH is present, it won't be a good indicator because isoelectric point can vary in-vivo as there are many acids other than H+. I would like to quote the following paragraph from National Academy of Sciences (US) and National Research Council (US) Division of Medical Sciences. Conference on Hemoglobin (3):

Near the physiological pH probably all of the charges on hemoglobins
come from their constituent amino acids. Neutral amino acids
contribute one terminal carboxyl and one terminal amino group to each
polypeptide chain which is not a ring. Additional positive charges are
contributed by the nitrogenous groups of the three basic amino acids,
Rb. Additional negative charges are contributed by the second
carboxyl group of aspartic and glutamic acids, Ra

pH at which several amino acid in Hemoglobin ionize:

References :

Swietach, P., Tiffert, T., Mauritz, J. M., Seear, R., Esposito, A., Kaminski, C. F., Lew, V. L., & Vaughan-Jones, R. D. (2010). Hydrogen ion dynamics in human red blood cells. The Journal of physiology, 588(Pt 24), 4995–5014. https://doi.org/10.1113/jphysiol.2010.197392
Devineau, S., Inoue, K. I., Kusaka, R., Urashima, S. H., Nihonyanagi, S., Baigl, D., ... & Tahara, T. (2017). Change of the isoelectric point of hemoglobin at the air/water interface probed by the orientational flip-flop of water molecules. Physical Chemistry Chemical Physics, 19(16), 10292-10300.
National Academy of Sciences (US) and National Research Council (US) Division of Medical Sciences. Conference on Hemoglobin: 2–3 May 1957. Washington (DC): National Academies Press (US); 1958. THE STRUCTURAL BASIS OF DIFFERENCES IN ELECTROPHORETIC BEHAVIOR OF HUMAN HEMOGLOBINS. Available from: https://www.ncbi.nlm.nih.gov/books/NBK224284/

Ok ,then can you explain then if the isoelectric point of haemoglobin in 6.8 , how can it have a net positive charge at physiological ph of cytoplasm of 7.2, Is the data of isoelectric point for Haemoglobin incorrect?

@Samardeepsingh, I edited the answer


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Molecular biology - Lewin's Gene Xi vs Molecular Biology of the Cell by bruce albert
I am an undergraduate and want to start reading about molecular biology. to anyone who has read both books please let me know your thoughts. which one should I go with?
Lewin's Gene Xi or Molecular Biology of the Cell by Bruce Albert

They are both good books and standard texts, but they are not equivalent. Albert's "Molecular Biology of the Cell" is an overview of many aspects of cell biology: metabolism, genetics, cellular structure, intracellular communication, cancer, etc. Lewin's "Gene" really only covers genetics. It's a subset of the material in "Molecular Biology of the Cell", but it goes into more depth on many of the topics that it does cover.
Which book you should choose will depend on whether you are interested exclusively  in genetics, or if you want to cover other aspects of cellular biology too.


text:
CRISPR-Cas9 system, DNA repair
As a critical stage in the CRISPR-Cas9 system, two different mechanisms of DNA repair can occur in the target DNA after RNA has been introduced: non-homologous end joining (NHEJ) and homologous recombination (HR).
Can these repair mechanisms be intentionally controlled or manipulated, and if so, what effects do they have on the target DNA? If the repair mechanisms cannot be controlled, how can we determine which mechanism has been employed in the target DNA, and if an undesired repair mechanism has been performed, can it be distinguished from the desired one?

This is a pretty broad question. From the [help/dont-ask]: Your questions should be reasonably scoped. If you can imagine an entire book that answers your question, you’re asking too much. The regulation of DNA repair is a huge subject, and books have been written about it. Please [edit] your post so that it focuses on one discrete, specific question that can be answered in a few or several paragraphs. Additionally, please include the research you've done so far to try to answer the question on your own.

I would recommend reading some basic resources on current Cas9 technologies. Here is one such review on prime editing, which illustrates one mechanism by which you can force cells to use a favorable precise repair mechanism. The way that you do this is by providing a repair template as part of the guide RNA that can be directly incorporated (see figure illustrating mechanism).
Properly, this mechanism uses neither of the two pathways that you mention:

Since almost all precise repair strategies generally require repair templates, they must exploit the endogenous HDR machinery, restricted to dividing cells. This has been a bottleneck in therapeutic applications of gene editing, especially for the many neurological diseases involving mutations that affect post-mitotic neurons. However, as [prime editing] bypasses the need for HDR machinery, precise genome substitutions were observed (albeit at low frequency) in primary mouse cortical neurons.

Note that this is only one example of how you can control repair mechanisms. I suggest reading that review (Scholefield and Harrison 2021, Gene Therapy), which includes information on other methods such as base editing.
As for distinguishing NHEJ vs HDR, there are a variety of references on this that can easily be found by google, such as this one. I'd recommend doing some cursory research there as well.


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Why are plasmid genes not already incorporated into bacterial chromosomes if necessary for stressful situations?
If plasmids are important for bacteria to express specific genes under stressful conditions, why are these genes not already incorporated into their chromosome to begin with? What is the evolutionary significance for this?

Plasmids do have the advantage that they replicate independently of the cells chromosome and that they can be transferred between different bacteria. This spreads the gene encoded by the plasmid to other bacteria, which then can also survive.
Think about antibiotic resistance. Bacteria which have a plasmid which allows protection against the antibiotic will survive. They can transfer this protection to other bacteria which then also become resistant. This can either happen through pili which develop between bacteria or also via the uptake of plasmid DNA from the environment in a process called horizontal gene transfer.
Additionally mutations on the plasmids are not as dangerous on the plasmids than on the chromosomal DNA, where essential genes might be damaged. Plasmids can also get lost, if they are not needed by the bacteria due to a missing selection pressure, which is also much harder for genes encoded on the chromosome.

Thank you. Would you mind clarifying on how exactly they get "lost"? Do the plasmids still remain inside the bacteria or do they get transferred when unneeded?

I am not sure, if the exact mechanism is known, but I can look into it.

How many copies of a plasmid get made can vary, and then how those plasmids segregate into each daughter after mitosis can vary. It is possible for one of the daughters to wind up with no copies of a plasmid. If that is the cell you or evolution picks to replicate, the plasmid is lost in all descendants.


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Why does enteral carbohydrate yield higher energy than parenteral?
The following is written in a well-known textbook of surgery:

Each gram of enteric carbohydrate provides 4.0 kilocalories (kcal) of
  energy. Parenterally administered carbohydrates (eg, intravenous
  dextrose) yield 3.4 kcal/g

What is the explanation for this?

Is the textbook refering to the same type of carbohydrate in both case ?

The 3.4 refers to dextrose. What other carbohydrate is given iv?

@Frédéric unfortunately, this is not elaborated upon.

@GrahamChiu theoretically one can also administer fructose or inverted sugar syrup etc., but I don't think they are widely used.

Parenteral carbohydrate is usually dextrose which is actually D-Glucose monohydrate. Monohydrate implies coupling with a water molecule, such that 1 gram contains a lower relative component of glucose, resulting in a lower kcal yield.

The value of 4.0 kcal per gram of dietary carbohydrates is simply a convention used by the Atwater System, which took a single averaged value for each of the available macronutrients found in food. I believe it was meant to represent an average composition of dietary carbohydrates at the time.
However, not all carbohydrates have the exact same heat of combustion. In other words, the amount (weight) of carbohydrate needed to yield a specific amount of energy differs depending on the molecular form of the carbohydrate (1). More specifically, monosaccharides (glucose and fructose) have ~3.75 kcal per gram, disaccharides (sucrose and maltose) ~3.95 kcal per gram, and longer polysaccharides (starches) have 4.15 to 4.20 kcal per gram (2).
The reason for this is again caused by water, specifically the dehydration (loss of water) that occurs as a result of the condensation reaction which forms the glyosidic linkage between monosaccharide monomers (1). For each additional monosaccharide subunit added to a carbohydrate chain, a water molecule is lost (see the example below).

Image credit: https://ib.bioninja.com.au/
So...going back to the original example. The heat of combustion of anhydrous glucose is 3.75 kcal per gram. Glucose (180 g/mol) makes up ~ 90.9% of the weight of dextrose monohydrate (198 g/mol). So, take the heat of combustion of glucose (3.75 kcal/g) multiplied by it's relative proportion in composition of dextrose monohydrate (0.909) and you get 3.75 * 0.909 = 3.4 kcal per gram. The 4.0 kcal per grams of dietary carbohydrate is simply a convention derived from an average value based on work that's over a century old.
References:
1: FAO FOOD AND NUTRITION PAPER 77. Food energy - methods of analysis and conversion factors; Report of a Technical Workshop, Rome, 3-6 December 2002. FOOD AND AGRICULTURE ORGANIZATION OF THE UNITED NATIONS.
2: Agricultural Handbook No. 74. Energy value of food; basis and derivation. Merrill, A., Watt, B. USDA Agricultural Research Branch.


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How to decide if genes are linked in an unordered mapping problem?
From what I understand, if the tetrads resulting from a cross exhibit the same number of parental ditypes as there are nonparental ditypes, then the genes under consideration are said to be unlinked.
For example, say I cross two gametes containing $ab^+$ and $a^+b$, respectively, and get 170 tetrads exhibiting parental ditype (all offspring are $ab^+$ or $a^+b$), 165 exhibiting nonparental ditype (offspring are $a^+b^+$ or $ab$), and 30 exhibiting tetratype (offspring one of $a^+b^+$, $a^+b$, $ab^+$ or $ab$).
I'm not sure whether to classify these genes as linked or unlinked. I want to say yes, they are indeed linked, but 170 and 165 seem like close enough numbers to suggest they may be unlinked.
I would think the ratio of parental to nonparental ditype has to be considered close enough to 1, but how do we decide a threshold for that?

I'd use a chi-squared test.  You calculate what you expect to see if your hypothesis is true, and you take what you do see, and the chi-squared result tells you how likely it is that your results are different enough from what's expected to indicate that your hypothesis is incorrect.

Okay that makes sense to me. Is there a way to know the expected distribution for the tetrad genotypes?


text:
How to tell if a given gene is a tumor suppressor or oncogene?
This is a problem taken from "Concepts of Genetics", Klug et al, 10e. I'm given the following table about the mutations in the BRCA1 gene:
$$\begin{array}{c|c|c|c|c}
\text{Kindred}&\text{Codon}&\text{Nucleotide}&\text{Coding}&\text{Frequency in}\\
&&\text{change}&\text{effect}&\text{control chromosomes}\\
\hline
1&24&-11\text{ bp}&\text{Frameshift or splice}&0/180\\
2&1313&\text{C}\to\text{T}&\text{gln}\to\text{stop}&0/170\\
3&1756&\text{Extra C}&\text{Frameshift}&0/162\\
4&1775&\text{T}\to\text{G}&\text{met}\to\text{arg}&0/120\\
5&\text{N/A}&?&\text{Loss of transcript}&\text{N/A}\end{array}$$
Footnote: "*N/A indicates not applicable, as the regulatory gene is inferred, and the position has not been identified."
Using this information, how can I decide whether the gene is a tumor suppressor or an oncogene?
I already know that BRCA1 is a tumor suppressor, so put another way, how can I arrive at this conclusion given the data above?

I assume these are all carcinogenic mutations. Because some them are clearly recessive loss-of-function mutations (like loss of transcript), you can conclude that the function of the gene consists of "holding back cancer". When these mutations occur, they can generally be complemented by a healthy allele on the sister chromosome.
Oncogenes on the other hand, require gain-of-function mutations, like translocation to a more active promotor or dominant negative mutations (like a loss-of-function mutation in a protein which forms multimers, which get "polluted" by the mutant and thus can not be complemented by the other allele). In most cases this "increases" their stimulation of cell division and thus cancerous growth.
Loss of transcript of an oncogene would not cause cancer.


text:
Listing Cluster of Differentiation (CD) markers (immunology)
I hope this question is appropriate for this SE. When listing multiple cluster of differentiation (CD) markers to define a cell population, e.g. CD3+CD8+CD45+CD4-, is there a default order to put them in? I was recently told to list them numerically with the negative populations after the positive ones (i.e. CD3+CD8+CD45+CD4-). However, I have seen different orders in the literature and would personally prefer to order them by whatever I would consider most logical (e.g. CD45+CD3+CD8+CD4-).

There is no convention like that AFAIK.

WYSIWYG is correct, and I would tend to agree with your personal preference - order the markers in the manner that makes the most sense, not necessarily in any numerical or positive/negative order.


text:
How do molecular recognition features work?
The occurrence of relatively short (10–70 residues), loosely structured protein regions bind within longer, largely disordered sequences that were characterized as bound to larger proteins. These regions are MoRFs. But how do these high specificity regions combined with low affinity proteins?


text:
How to predict a mRNA secondary structure with a large sequence?
When I use some web servers to predict a mRNA secondary structure, I find they always required in a small size sequence. If I use a long sequence and cut it into small parts, do these small parts change the energy or thermodynamic data from the origin sequence when predicting? Is there any effective way to find the right sites when cutting the long sequence?

I would think that it would matter.  Can you list the tools you have used and their constraints?  Have you tried http://rna.urmc.rochester.edu/RNAstructureWeb/Servers/Predict1/Predict1.html ?

Yes, the structure predicted by splitting up the sequence may not represent the actual structure of the full-length RNA. A simple hypothetical case would be that of an RNA whose 3' and 5' UTR interact to cause circularization.
I am afraid there is not clear rule for choosing the subsequences such that the assembly of the individual secondary structures is closest the the actual structure.
We may expect that, with better computational power, the limitation on the size of the sequence for secondary structure prediction, can be overcome.
However, there are experimental techniques using RNA-sequencing that can determine the actual secondary structure — SHAPE-seq (ver 2.0; Loughrey et al. 2014) and structure-seq (Ding et al. 2014). Structure-seq in-fact, tries to determine the RNA secondary structures in-vivo and hence may be a more powerful tool.
However, you said you are working with mRNAs. I guess for mRNAs you can predict the structures of UTRs and the CDS separately. Actually depends on what you are interested in. CDS usually does not harbour any structural motif and any secondary structure in the CDS is usually resolved by the helicase activity of eIF4A. However, secondary structures can slow down the translation elongation rate (Mao et al. 2010, Gorochowski et al. 2015).

Loughrey, D., Watters, K. E., Settle, A. H., & Lucks, J. B. (2014). SHAPE-Seq 2.0: systematic optimization and extension of high-throughput chemical probing of RNA secondary structure with next generation sequencing. Nucleic acids research, 42(21) e165.
Ding, Y., Tang, Y., Kwok, C. K., Zhang, Y., Bevilacqua, P. C., & Assmann, S. M. (2014). In vivo genome-wide profiling of RNA secondary structure reveals novel regulatory features. Nature, 505(7485), 696-700.
Mao, Y., Liu, H., Liu, Y., & Tao, S. (2014). Deciphering the rules by which dynamics of mRNA secondary structure affect translation efficiency in Saccharomyces cerevisiae. Nucleic acids research, 42(8), 4813-4822.
Gorochowski, T. E., Ignatova, Z., Bovenberg, R. A., & Roubos, J. A. (2015). Trade-offs between tRNA abundance and mRNA secondary structure support smoothing of translation elongation rate. Nucleic acids research, gkv199.


text:
Plasmid choosing
To design a experiment in feeding of C. elegans. It has to choose a plasmid vector to insert the gene of interest that can feed to C. elegans. Many paper are using pL4440 for the feeding vector, saying it is the first used in feeding C. elegan and because of the two T7 promotor, so it easy to perform the experiment. There also paper saying T3 promotor is not fit for feeding in C. elegans. I am curious about why T3 is not fit? and because I didn't see many paper using other vector to perform the feeding experiment in C. elegan. So I wonder that is it ok if I choose a plasmid that has two T7 promotor and is used to express in worms like pLT61, will it influence the feeding or the efficiency so that people use pL4440 for feeding in C.elegan? Or is people use pL4440 vector because it is specific designed to the feeding experiment of C. elegan? Thank you!

PREFACE:
There's a text, C. elegans: Methods and Applications, specifically doi: 10.1385/1-59745-151-7:109. They outline this exact experiment in it's essence, and one of the diagrams (page 110) notes that for the purposes of RNAi in C. elegans, the T3 promoter specifically doesn't work for the bacterial feeding method, but works for injection or soaking procedures. I absolutely can't figure out why that is specifically, but i'll keep researching.
UPDATED:
Much thanks to mdperry for clearing things up! As it turns out, this is a matter of experimental design. Using information from Ingestion of bacterially expressed dsRNAs can produce specific and potent genetic interference in Caenorhabditis elegans, and Source Bioscience:
HT115 (DE3) is a feeding strain engineered like so,

The genotype is as follows: F-, mcrA, mcrB, IN(rrnD-rrnE)1, lambda -, rnc14::Tn10(DE3 lysogen: lavUV5 promoter -T7 polymerase) (IPTG-inducible T7 polymerase) (RNase III minus). This strain grows on LB or 2xYT plates (and is resistant to tetracycline, see below), and competent cells can be made using standard techniques.

We can go through these and look at the changes as well:
F- means no F plasmid for conjugation. mcrA/B refers to mutations made which reduce the ability of the E. coli to attack foreign DNA. IN(rrnD-rrnE)1 is an inversion in the region of some rRNA operons that I'm unsure as to the effect. Lambda- removes the lambda lysogen. You can see that they have the lavUV5 promoter for an IPTG-inducible T7 polymerase which is important for getting the E. coli to begin producing T7 polymerase to express the associated cloning vector. You can also see that HT115 (DE3) is deficient for RNase III, however, which normally degrades dsRNA, making it suitable for the feeding experiment.

The L4440 (pPD129.36) cloning vector contains two convergent T7 polymerase promoters in opposite orientation separated by a multicloning site and was made using standard cloning techniques (Timmons and Fire, 1998).
pLT61 contains 0.8 kb of unc-22 inserted into the L4440 vector.

I think the L4440 plasmid is probably easy to optimize for this experiment, and cheap. If you can access the article I linked above, they catalogue some additional plasmids. In conclusion though, it'd seem that if we in fact had a system where the E. coli themselves could produce T3 polymerase, it'd be fine to use those promoters. In the case of this experiment, the genotype of the feeding strain of bacteria nicely complements the vector being used.

One also needs to use the appropriate bacterial host. As I recall HT115 is engineered to carry a copy of the gene for bacteriophage T7 RNA Polymerase, and this polymerase is being driven by the lacUV5 promoter. So in the absence of an inducer for the lac operon the T7 RNAPol is not made, and the dsRNA is not made. When you add IPTG the polymerase is turned on, and the insert in pL4440 is transcribed from both strands. The reason you can use the T3 promoter for injections or soaking is because the T3 RNAPol is added to the test tube.

Is there a molecular explanation for why T3 isn't fit for feeding ,i.e. the same inducible system doesn't work for T3 polymerase? Or is it just a matter of experimental design?

The bacterial cells carry a prophage, lambda DE3 integrated into the bacterial chromosome at the att site. This phage is the source of the T7 RNA Polymerase. If you had some way of producing T3 RNA Polymerase then a plasmid carrying T3 promoters should work fine

The pLT61 contains 0.8kB 0f unc-22, on the internet saying it is a gene influence the muscle in C. elegans. does it mean that it will influence the effeniency of the experiment? Such as if I put the my gene of interest that is relevant to function of pumping, after it either injected or fed into the C. elegans, will it have a conflict or will it interrupt the experiment? to be clear, like will it express both of the genes? Thanks

This article shows the effect of a stem-loop GFP-unc-22 structured dsRNA in RNAi. Basically, it can potentially knock down both GFP and unc-22, and what this does to the worms is induce a twitching phenotype because it alters the contractility of the muscles. It also produces issues with egg laying.

If your endgame is to simply knock down GFP expression and visualize that and be done, there may not be a huge effect, but prolonged exposure to unc-22 knockdown might be deleterious to the numbers of worms in your culture. Let me know if anyone more experienced has input!

In that article, though, they did find that unc-22 dsRNA exposure had to be rather continuous to evoke unc-22 knockdown, so injection with a specific amount of dsRNA didn't work for long.


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Is ribosome denser and smaller than nucleus. Also sone relations in centrifugation related to size and density
I want to know that if ribosomes are denser than nucleus. If so, then they should settle at the bottom of tube in centrifugation (following a density gradient) before the nucleus.
Secondly, if ribosomes are smaller than nuclei than they should settle after the nucleus (which they do) but they should also have a smaller Svedberg value (I don't know whether they do or not).
More simply, I want to know whether density or size is responsible for their sedimentation after the nucleus.
I also want to know the relationship between size and Svedberg value of organelles in general.

I think that the higher speeds necessary to collect ribosomes by ultracentrifugation are likely to disrupt the nucleus. See for example this extract from a well known textbook:

This treatment separates cell components by size and density: in general, the largest units experience the largest centrifugal force and move the most rapidly. At relatively low speed, large components such as nuclei sediment to form a pellet at the bottom of the centrifuge tube; at slightly higher speed, a pellet of mitochondria is deposited; and at even higher speeds and with longer periods of centrifugation, first the small closed vesicles and then the ribosomes can be collected (Figure 8-8). All of these fractions are impure, but many of the contaminants can be removed by resuspending the pellet and repeating the centrifugation procedure several times.

See the image they reference, which shows that the supernatant from spinning out nuclei will then yield ribosomes upon subsequent spins:

Ribosomes are much smaller! Recall that Svedberg units are indirect measures of size. I am not sure that many of the large organelles have Svedberg values per se. Even the ribosome falls apart into subunits upon ultracentrifugation after all, it doesn't really have a singular S value I don't think?


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request for peer reviewed articles using Markov Chains tools
I am a mathematician setting up an REU for next semester. Students have background in modeling with ODES (population growth models, predator-prey relations, neuron firing models; stability analysis of linear and nonlinear systems, stable limit cycles). They have expressed interest in learning about Markov Chains, so I'm currently preparing some material on probability and textbook applications of Markov Chains techniques in the life sciences. I'm having more trouble identifying recent-ish peer reviewed important publications where Markov Chain techniques are used in a substantial way for important questions in biology or medicine. Any field of bio/med works, I just want to come up with a few recent (i.e. last decade), impactful examples of how these techniques are relevant.

Markov chains are so fundamental to many approaches that they are unlikely to be explicitly called out. MCMC is very commonly used (e.g. phylogenetics), Just about any model of biological sequences uses a Markov chain somewhere (e.g. Hidden Markov Models). The issue may be that the tools are older/more fundamental and less explicitly about MCs than you want.

This question is better for https://bioinformatics.stackexchange.com - you will certainly not get downvotes there and likely get a reasonable answer

Not recent, but here are several references for MrBayes, a classic phylogenetics program using (MC)MCMC. The links page there also has some tools for visualizing MCMC chains. Structure is another neat program taking advantage of MCMC. (FWIW, I wouldn't have necessarily called these applications bioinformatics, but maybe today they would be.)

I’m voting to close this question because this is not a question about a specific problem in biology, the remit of this site, as laid out in the [Tour].

Basically if you post the question on bioinformatics SE I'll answer it for you. Your call.


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Plant growth regulators for Grape berry elongation?
I want to make a formulation for grape berry elongation, planning to use

GA3,
NATCA (N Acetyl Thiolidine Carboxylic Acid),
IAA (Indole-3-acetic acid),
IBA (Indole-3-butyric acid)

What else can I use?
Ultimate goal is to increase auxin level in plants.
All auxins are compounds with aromatic ring and a carboxylic acid group so will it be helpful to use carboxylic acids as a solvent with the above plant growth regulators?

Actually I am new to this site,

For any elongation like purpose for example elongation of sugarcane, apple, grape etc we use gibberellins.
You can get this result by just a single Google search.
My source: Biology NCERT Class 11 chapter 15 (2021 edition) and this site

Actually I am new to this site, I have used GA3 + NATCA N Acetyl Thiolidine Carboxylic Acid + IAA Indole-3-acetic acid + IBA Indole-3-butyric acid all these are dissolved in aceton & water. ok results, is there more pGRs I can use?


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What is the advantage of being tired after having a sex?
When we have a sex with partner, we feel so tired that we don't have any power to do anything. Then it would be disadvantage to the animals, of course humans too, for they are exposed to danger. For example, the predator's atack. But you know, we cannot help having a sex. Then what is the advantage of being tired after having a sex?

Why do you think there should be an advantage to everything that exists? And not everyone feels exhausted after sex.

The reason why we feel relaxed / sleepy after having sex is probably the release of endorphins, i.e. morphine-like chemicals. This is part of what makes the experience pleasurable. In a sense, we are rewarded with endorphins for having sex. Probably, a reason why we evolved this way is we would not mate as much if there was no reward for the behavior, hence the trait favors reproduction. We must sleep anyway. It is more advantageous to do so after having sex (or having eaten for that mater) than to sleep at other times, which would possibly make one miss an opportunity to mate or feed.


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Name/Examples of Traits whose benefit is non-obvious and/or which evolve despite apparent mal-adaptivness?
I'm a graduate student in cognitive science doing work on people's explanations and learning, particularly having to do with natural selection.
Often, students misunderstand natural selection as a "goal-directed" process, one in which organisms are directed to adapt towards beneficial traits. This kind of thinking can be tempting, since most evolved traits are beneficial in obvious and straightforward ways.
However, I'm very curious about traits whose benefits are NOT at all obvious, and can only be understood under careful consideration of the evolutionary process.
An prototypical example would be the evolution of altruism, or of homosexuality. But I'm looking for more examples like these, and preferably ones that are more specific/concrete (e.g., the existence of a specific trait/behavior, rather than someone general like altruism).
Any help would be appreciated.

Sounds like something to do with Saltationism and "hopeful monsters". https://en.wikipedia.org/wiki/Saltation_(biology)

Altruism is absolutely beneficial.

@MattDMo the user is looking for examples where the benefit is not obvious, given that an individual might sacrifice itself under altruism I'd say it's a good example. Also ageing http://biology.stackexchange.com/questions/17077/why-does-evolution-not-make-our-life-longer/17091#17091

I got some excellent answers on my cross-post here: https://www.reddit.com/r/biology/comments/3durzm/help_biologists_trying_to_brainstorm_traits_that/


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Loss of function in inflammation
The Wikipedia-article about Inflammation says

The five classical signs of inflammation are heat, pain, redness, swelling, and loss of function (Latin calor, dolor, rubor, tumor, and functio laesa).

What does 'loss of function' mean? And how does it occur?

TL;DR: It originally referred to abnormality in "secretion" by the inflamed tissue and later became used to mean any abnormality at all.
This fifth cardinal symptom of inflammation seems to be rather mythological as laid out in detail by Rather (1971, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1749862/?page=3). This source explains that the term seems to have been invented at some point in the 19th century without proper definition. Later authors seem to have interpreted it as basically just meaning "not functioning properly" (although this is literally the definition of unhealthy as opposed to healthy, and not specific to inflammation).
According to Rather, the original source of the confusion may have been the phrase: "...heat, redness, tumour and pain; to which should be added an alteration or suspension of the natural secretions of the part." by Macartney in 1838 (page 8 of the same document). Various versions of mentioning a fifth cardinal symptom that involved altered function made their way through pieces of writing, until it received the Latin term "functio laesa" in the late 19th century (Rather cites a piece from 1882), lending it credibility as an established concept. The passage by Macartney was later cited by Marchand in 1924, who was trying to clear up the confusion around who established the four and potentialy fifth cardinal symptoms of inflammation. Marchand rephrased it into a "fifth cardinal symptom the alteration or disappearance of normal secretion (thus a functio laesa)", trying to explain what, according to Macartney, is the fifth symptom, and adding why it could be called a "loss of function".

Usually, loss of function means some sort of limitation in physical performance. Either force, range of motion, or some other aspect of movement. In this context, loss of function can occur by at least two mechanisms:

mechanical loss of function due to swelling of the tissue around the joint
limitation due to pain associated with movement, part of movement, or too high load.


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How to prevent mold from building on food and how to kill it along with neurotoxins?
I have some food/fruits chopped in very small parts, whatever it is that needs to be conserved during long time, when it is given to me it can be somewhat wet or humid, after some time of keeping it in a plastic Sterilite it builds mold.
After reading a bit I've learned that an autoclave can kill mold at 100°C at 10psi (68.9kPa) for an hour, but it won't kill toxins. My All American pressure cooker with gauge says it can reach 120°C at 15psi (103.4kPa), however this is not much of a difference.
Vinegar, bleach and borax can all be used, but food becomes unusable.
So here are the two questions:

How can I safely keep that food without building mold?
If mold does appear, how do I exterminate it along with toxins safely for human health?

I think this is possibly better asked at Cooking.SE - you are basically asking for something like canning , though there are other approaches too - it mostly depends on the type of food you wish to preserve and how it handles each approach. Vinegar, for example, works well for some foods: though it's not as simple as just soaking your food in vinegar, we typically call it "pickling."

@BryanKrause Then take the approach at industrial level, suppose the food is blended rice, could something be done? Disposal is not an option.


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What kind of insect eggs are these (found in Malaysia)?
What kind of eggs are these?
Found outside on a window, when I removed them via scraping, whitish oozy fluid came out. I've seen this before but they've been appearing more frequently, always appear in a straight line and are brown.
This is in Malaysia, in South East Asia. More specifically Johor. The entire line measured about 1 inch, and in terms of individual egg size, 0.3 inches.

This eggs belong to Mictis profana which is a species of insect in the family Coreidae known by the common names crusader bug and holy cross bug. It is distributed in Australia, Indonesia, and the Indo-Pacific.


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Does the yolk sac for Danio rerio form at the vegetal pole?
Does the yolk sac in general form always at the vegetal pole?
If so, is this the case for Danio rerio (the zebrafish)?

Generally, yes, yolk is at the vegetal pole. There may be exceptions but I am not aware of them.
You can read about zebrafish (Danio rerio) embryology in great detail in this paper. Figure 3 from this paper (see image) shows the immediate post-fertilization zygote, in which the animal-vegetal axis is first set up by the migration of non-yolk to the animal pole.

UPDATE: very explicitly labeled yolk figures.

Thank you! I read a paper but it was not clear to me where the yolk sac was eaxctly.

See new figures from paper in update.


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What type of genetic changes occurs when ovaries or uterus are removed from female body?
I saw so many women which have present dermoid cysts in their ovaries or uteruses. Doctors operate and mostly the ovaries and uterus can not be saved and the doctors remove the ovaries or uterus.
Which type of genetic changes occur in such type of women?

welcome to biology stackexchange!
In the classical way we think of the body, there won't be a lot of genetic changes if the ovaries, uterus (or the testes for that matter) are removed from the body.
The main effect would be that the sex hormones that are produced in these organs would no longer be present and this would have a profound effect. So the broad answer might be 'no genetic effects but large endocrine changes'.  Endocrinology is the study of glands and their function in the body. Growing cysts, tumors as well as other effects seem like reasonable effects to see for such a drastic change in the body as removing the reproductive organs.
If I were hard pressed though probably this might end up with some small genetic effects compared to an individual who had never had the organs removed.  Mutations happen frequently in many of our tissues and also they respond to the environment to methylate the genome and modify it in non-genetic ways ( known as epigenetic effects).  This is purely conjecture but its also found that nearly everything has some effect on the cells.
hope this helps.

Answer simplified to match OP level
There are two different parts of biology in this question:

Genetic changes, only happen when the DNA changes (in a person's genes). But in general, this is fixed before your birth (when you are conceived), and what happens in your life does not change it any more.More accurately, genetics can change, or be changed, but not just by removal of a body part like this question asks.
Removal of organs like the ovaries and uterus will mean that hormones they produce, and actions they are involved in, may be reduced or stop.  That can change a persons life a lot, because hormones and other functions play a major role in our body. But it doesn't change the person's genes, or genetic makeup.

A way to think about this is, if a doctor had to remove your leg, or your tonsils, and then you had a child, your child would have the leg, or tonsils, even if you didn't. Because that is in your genes, and has not been changed.


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How do I determine an acceptable $F_0$ value in sterilization?
Here's a sample question:

The sterilization process using moist heat is used to kill B.stearothermophilus by heating to 115 degrees C and holding it for 30 mins.
For B.stearthermophilus, it is given that $D_{115} = 11$minutes and z=10 degrees C.
  Determine the sterilization process equivalent time at 121 degrees C. Is this an acceptable $F_0$ value ?

By using formula $F_0 = \Delta(t) \cdot L$
I found $F_0 = 7.5$minutes.
How do I know what is the acceptable $F_0$ value? I've been told it's 15minutes. Is it 15 mins for ALL sterilization methods or is there a method to calculate this regulatory requirement of $F_0 = 15$ ?


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What spider is that?

It was scared because my cat was playing with it. I saw it tonight (22 October) in Slobozia, Romania. I never saw something like it. The back is white with no points or marks or lines.

need a better picture from the top to help identify.

This is the only picture I have. It was big and I was kind of afraid

@Cataleya could you estimate the size?

okay I am not expert but I think the title is low and bad ,d oyou think

It's pretty clearly an Araneid of some kind, based on the large, globular abdomen, the eye arrangement at the front of the 'head', and the characteristic defensive posture when out of the orbweb.  All known orbweavers are completely harmless to both cats and humans, so nothing to worry about!
Unfortunately, I'm not familiar enough with central European spiders to tell you exactly what it might be, but I can assure you that it is not the only problem biter in your area - one of the Black Widows.  I include a photo I found of a common orbweaver in Europe (the Cross Spider) which was also caught out of its web, and in a similar position (although clearly not having been attacked by a cat..).  Whether yours is normally a plain white species, or yours is a leucistic (all-white or partially-white) variation of a normally darker and patterned species, I have no idea.  As I say, I'm not familiar enough with European spiders to be confident about something like that.


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Berries ID - Can someone help us identify this plant?
Found it in the hilly areas of Meghalaya - a state of India.
Not sure if is edible or not, we haven't tried it but it gives a beautiful blue color when used for dying.
The seeds are big and there is not enough fruit except its like the skin covering the seeds.


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How does evolution explain the apparation of different group like: mammals, insects etc
When I am learning about evolution I barely see any source that explains how insects, mammals, reptiles and fish came to be. Can someone show me a source where I can learn about this? Especially insects and mammals - I want to know how those 2 distinct group came to be.
And I have a related question: can a fly evolve into a rabbit given enough time with the necessary condition? (I know the question sound stupid but please can someone explain me that)
I have a layman understanding of evolution. So please can any of your source or explanation be simple? Thank you.

Re a fly evolving into a rabbit, theoretically yes, practically no.  Insects (and invertebrates in general) made some evolutionary "choices" like having an exoskeleton & breathing through trachea that put serious limits on their maximum size.  (And vertebrates, particularly warm-blooded mammals & birds, likewise have limits on their minimum size.)  So to get a rabbit-sized fly (in Earth gravity & atmosphere) you'd have to make a bunch of major changes, with no obvious environmental niches for the intermediates.
But where the size limits and other constrants overlap, convergent evolution can produce remarkably similar results.  I think perhaps the best example is the hummingbird https://en.wikipedia.org/wiki/Hummingbird and the hummingbird moths https://en.wikipedia.org/wiki/Hemaris  They're about the same size, live in the same habitat with similar lifestyle, and from a distance are almost indistinguishable, yet evolutionarily speaking, they're about as different as animals can be.

Insects and mammals diverged from one-another over 500 million years ago. For most of Earths 4.5 billion year history, life was single-celled, or organized into colonies of single-celled organisms. Likely sometime shortly before the Cambrian, multicellular animals evolved. The first multi-celled animals were likely a kind of colony that was not differentiated into tissues. It didn't have a head, or tail, or look much like an animal. From these simple undifferentiated, multi-celled building blocks, came most of our animal phyla, during a burst of innovation called the "Cambrian explosion". At this time, one lineage headed down a path that would lead to insects, and another lineage, toward mammals. Although theoretically, it is possible, given enough time (as in billions of years) for a fly to evolve into a rabbit, this is highly unlikely. Evolution works with what it starts with and modifies it under natural selection to favor fitness. So having six legs and wings works pretty well for flies, and having 4 legs and fur works pretty well for rabbits. The hurdles to go from one form to another, given that these lineages are already well adapted, would be enormous. It was much easier, 500+million years ago, to go from one colonial lump of cells to a rabbit, and another lump to a fly. As an example of how evolution works with what it starts with, virtually all tetrapods (amphibians, reptiles, and mammals) have 5 digits on their limbs. This is because they share a common ancestor that did. Not because 5 is somehow special. Another example, humans choke to death because we share a common ancestor with fish, and fish share a tube that connects both the mouth with their swim bladders and their gut. Swim bladders were modified into lungs, but the common connection from our fish ancestors remains (a really bad design, but we are stuck with it).

The two groups that you mention belong to two separated branches in the animal kingdom. The fly and all insects are protostomes and the rabbit and all mammals are deuterostomes. In the first, the embryonic opening (the blastopore) becomes the mouth, while in the second, it becomes the anus. Wiki
At first glance, it seems like a simple difference. But it became a total change in terms of body structure and allow the appearance of animals whit the nervous system in the back, like us (insect have a ventral nerve cord).
In theory, it is possible for a population of flyes to accumulate the mutations to become something similar to a population of rabbits. All the intermediate forms should be viable and able to reproduce them self.


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What is the evolutionary advantage of getting hard nipples when being aroused? Why can they even be stimulated sexually?
I try to understand the evolutionary advantages of the body reactions of nipples and penises/vaginas. I'm confused, because I can explain the evolutionary advantage in a logical & consistent way for penises/vaginas, but not for nipples.
arousal causes stiffness
Penises are getting hard when aroused. I can make sense of that - it is evolutionary advantageous, because sperm is more likely to reach the uterus; therefore the likeliness to get pregnant is higher; therefore providing an evolutionary advantage.
But I can not make sense of nippels getting hard. I don't see any advantage that could provide. I mean, breast feeding causes stiffness through stimulation; but that is not sexual, I guess? I guess, breast feeding woman don't experience arousal because of the breast feeding?
sexual stimulation
Furthermore, why does nipple stimulation even cause arousal? I mean, why does it cause evolutionary advantages that we feel arousal when they are stimulated? Again, I can understand this part for penises/vaginas.

Are you talking about female body only, or male body as well? :)


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Do we find protein not of cellular origin in nature?
I read once that we have two sources for proteins:

Protein that is made in cells
Protein that is made in labs

However, based on Miller–Urey experiment, it's argued that amino acids can be made from initial Earth's condition, and from this link, it seems that protein-first world is a hypothesis.
Yet if we accept that proteins could be made before cells, then the process that made proteins in the first place is still out there. This means that we should be able to find proteins outside cells or labs in nature.
Do we find protein not of cellular origin in nature?

I would suggest rewording your question to refer to proteins/peptides/amino acids not of cellular origin instead of "in nature".

Viruses are composed of proteins. They exist outside of cells freely in nature.

Vituses reproduce in living cells and use host cell's machinery to replicate. Thus they don't count.

On our planet, there is such an incredibly massive amount of protein creation by biological organisms (as well as smaller peptide constructs) that it would be essentially impossible to identify any that was created by a natural non-biological process.
Moreover, now that there is life, any location with the right conditions for non-biological creation of protein would likely also be a good place for modern microbes  to take advantage of those same resources to grow themselves, diverting the necessary inputs or quickly eating the outputs.
It is for this reason that we search for precursors of life in space, and have long ago found the basic building blocks. This is also why probes to other planets are carefully sterilized, because otherwise we will never know if life found on Mars is just hardy colonist organisms transplanted from Earth.
To the best of my knowledge, however, no non-Earth molecule has yet been found that has the full complexity of a protein, as opposed to just isolated amino acids.

@user1136 Sure. But if you found material with L-amino acids, you wouldn't know.

We're in agreement: finding proteins based on D-amino acids would be interesting.  I'm saying that if we didn't sterilize spacecraft and we found proteins based on L-amino acids, we might have a hard time determining if it came from the planet or the spacecraft.


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Blood groups - why is O the universal donor and AB the universal recipient?
I do not understand why individuals with type O- blood are often called universal donors and those with type AB+ blood are called universal recipients.
My thoughts on this are:

It should be that because O+ blood has all antibodies but no antigens that all other blood types including O- would be incompatible making O not a universal donor - so why is O the universal donor?
Also if O is the universal donor, it should be O+ that is the universal donor and O- that isn't because Rh+ is compatible with Rh+ and Rh-, not just Rh+ or Rh-.
It should also be that because AB- has all antigens and no antibodies that AB is not the universal recipient - so why is AB the universal recipient?
Here is what I would expect from blood group mixtures:
O-A: A clumping in O
O-B: B clumping in O
O-AB: AB clumping in O
and that being true for the reverse order as well
AB-A: AB clumping in A
AB-B: AB clumping in B
as well as the one that everybody knows which is A-B: A clumping in B and B clumping in A
I would also expect for Rh compatibility:
Rh- with Rh+: Rh- clumping in Rh+

@Arsak Nominating for re-opening does not happen automatically. This needs to be done by you and decided by the community.

@Chris Thank you for the feedback! I've found that the reputation threshold for close and reopen votes is at 3000, so I'll leave it's up to the higher-rep user to decide.

In blood groups you always need to consider two things: The antigens present on red blood cells (RBC) and the antibodies present in plasma, which lead to clumping of RBCs if they match. Don't mix up the words antigen and antibody! A healthy individual will never have antibodies against the antigens on their own RBCs, but they will have antibodies against antigens which are not present on their own RBCs. (*)
Also always remember that blood transfusions consist only of RBCs! The plasma and antibodies are removed. If you mix blood of two people directly, all combinations will coagulate unless the blood types are identical. Thus, when thinking about donor and acceptor match, you have to consider the acceptor's antibodies and the donor's antigens - nothing else.
Finally, Rh+ means RBCs have the Rh antigen, Rh- means they don't.
A universal acceptor will thus be someone who has no antibodies at all (because their antigens don't matter - they receive no antibodies from the donor). This is the case if the RBCs have all antigens: AB+
A universal donor will be someone whose RBCs have no antigens at all (because their antibodies don't matter, they get removed before transfusion): O-
As a side note: The ABO system and Rh are only the two most dangerous blood groups when they are mismatched. There are many more RBC antigen types (around 35) and in fact hospitals will consider several of these when matching donors and acceptors.
(*) We don't completely know why we make antibodies against antigens not present on RBCs yet. One hypothesis is that the bacteria in the intestines produce antigens which 'look' similar to our blood antigens. Also, this only applies to the A/B/O antigen. All other antigens work like normal antigens such as bacterial ones - after your immune system has seen them the once, you have antibodies against them.

O- should be the universal donor not O+because when rh- blood is given to rh+ person ,the rh+ person can not make antibodies against rh- blood because there are no rh antigens in the rh- blood.(So what will rh antibodies be made against ?)
Now I think u can figure out about why AB+ is the universal recipient !

this I think is why it should be O+ that is the universal donor. You see O- is only compatible with O-, B-, A-, and AB- from the Rh compatibility and ABO compatibility combined whereas O+ is compatible with O+, B+, A+, AB+, O-, B-, A-, and AB- as far as donating and as far as recieving these are the compatibilities.                                             O+: O-, O+ and O-: O-  so already O+ is compatible with more blood types than O- is on both the donor side and the receiving side.

No..if you give O+ blood to a person with -ve blood group, that person will make antibodies against the rh antigens on O+ RBC. But if you give O- blood to any blood group they can not make antibodies (reason explained above. ) so your notion that O- is compatible only with negative blood groups is wrong.  Receiving and donating compabilities for a blood group are different. You can NOT say that if O+ can receive blood from O-, it can donate blood to O-..

ah but negative blood types have antibodies against Rh antigens in positive blood already there so that means less making of antibodies. Plus when you have a blood transfusion you get an RBC transfusion and a plasma transfusion so there comes the problem of antibodies in plasma. You might also get a WBC transfusion or a platelet transfusion.

Various  factor are considered before blood transfusion. Not only abo and rh+  and -  blood group... I am unable to understand what you are asking in the first statemen of the above comment.