text:
Why are fatty acids consisting of even number of carbons predominant?
Most of the fatty acids in animal biology consist of even number of carbons in its parent chain. What property of such fatty acids cause the biological systems to prefer them over the odd counterparts? What's so bad about fatty acids containing odd number of carbon atoms in their parent chain?
Why are fatty acids consisting of even number carbons in their parent chain predominant?

you might want to justify your underlying claim.

What does TL:DR mean? Don't tell me, it isn't English. Replace it.

@David Are you opposed to all abbreviations?

@canadianer — In general I discouraged my students from using all but the most common (RNA, SDS) or any that came up repeatedly. There is nothing to gain from abbreviating a word that only occurs a couple of times, and there is likely to be someone unfamiliar with it. In this case, the abbreviation is some sort of internet slang which I looked up once but forget. It is not in the Collins English Dictionary on my iPhone and I regard its use as inexcusable.

It actually was added to Oxford Dictionaries as an abbreviation in 2013! "TL;DR, abbrev.: ‘too long didn’t read’: used as a dismissive response to a lengthy online post, or to introduce a summary of a lengthy post." (https://blog.oxforddictionaries.com/august-2013-update/). Also in Collins English (https://www.collinsdictionary.com/us/dictionary/english/tl-dr). But, regardless, I can understand that abbreviations can be hard to keep up with.

@canadianer — My funamental point remains. I did not know what it meant. I did not want to do an internet search. Half the people who post here apparently do not know how to do an internet search. There is nothing to gain by it and something to loose. Avoid it. Incidentally, this is one of the first rules of public speaking. And one of the reasons I advised my students agains using lab slang is an external examiner hates it if a student (who is not as smart as him) uses some obscure abbreviation to demonstrate he is a member of some in-group. It's terrible psychology.

because they are made from two carbon blocks and also the building blocks are even.

In short, it's because fatty acids are made from two-carbon blocks.
The way that most organisms make fatty acids is by the successive addition of two-carbon units (acetyl-CoA). So we usually get even-numbered fatty acids just because the building blocks are also even.
In plants and in synthetic contexts, we can have some reactions that can produce odd-numbered fatty acids (by building with two-carbon units three times to get six, and then breaking that six in half to get three, for example). Such odd fatty acids are seen in some organisms, but humans are usually thought to get them from other sources (e.g. microbiota, diet).
EDIT:

Point 1: Fatty acids are generally built two-carbons at a time.
The European Bioinformatics Institute has a really good explanation of fatty acid synthesis. The quote below is from that (https://www.ebi.ac.uk/interpro/potm/2007_6/Page2.htm):

"Whether existing as one complex or as independent enzymes, the
  reactions catalysed by types I and II fatty acid synthases are the
  same.  Both systems are primed with acetyl-CoA, and then add 2-carbon
  units to the growing chain using malonyl-CoA as substrate."

Point 2: Odd-numbered fatty acids can be produced by various organisms, and can be linked to dysfunction in humans.
doi:10.1038/srep44845 talks about the importance of odd chain fatty acids in disease as a preface to its findings about the sources of such fatty acids. They try to narrow down where odd-chain fatty acids come from, but they definitely seem to be building their case on the pretense that odd chain fatty acids are not great in humans.

"According to the literature, the origin of C15:0 and C17:0 has long
  been attributed to the diet, specifically from ruminant fat as the
  main contributor in a typical Western diet. This has been explained by
  the fact that these two OC-FAs are produced by the rumen microbiome
  and then incorporated into the fat deposits of the host animal
  destined for human consumption."

Point 3: Plants produce odd-chain fatty acids
An established/old paper (doi:10.1006/abbi.1994.1110) mentions this, and there's a Wikipedia article (https://en.wikipedia.org/wiki/Odd-chain_fatty_acid) that paraphrases in a nice way:

Some plant-based fatty acids, however, have an odd number of carbon
  atoms, and Phytanic fatty acid absorbed from plant chlorophyll has
  multiple methyl branch points. As a result, it breaks down into three
  odd numbered 3C Propionyl segments as well as three even numbered 2C
  Acetyl segments and one even numbered 4C Isobutynoyl segment.

You may be correct, but how are we to know? On SE you have to demonstrate why your answer is correct. In this case you could provide a reference to a Wikipedia article or, better, the section in Berg online. Even better would be a chemical equation. Read the Help on How do I write a good answer.

Thank you for the correction! I've added a bottom component with a few sources that hopefully help to make my answer a little more rigorous.

Fine now. This is a question that is likely to come up again, so making it more comprehensive will make it more useful to many people.


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why has evolution favored sexual reproduction using two mates over sexual reproduction using three mates?
Many animals species require two members — a male and a female — to sexually reproduce. Why has nature (or the process of evolution) chosen to favor the form of sexual reproduction which requires two members? Why didn't nature encourage the form of sexual reproduction which involved three members?
The reason for sexual reproduction being a better choice over asexual reproduction is justified by saying that sexual reproduction involves mixing of genetic information from two living beings and hence if one set of them had an error, the other would compensate for it. With the same kind of reasoning, we can argue that sexual reproduction involving more than two organisms coming together would cause better genetic variation, shuffling of mutations, etc. and thereby produce a better offspring.
However, most of the organisms as we see today have evolved to reproduce sexually using two beings of the same species.

Consider an animal species which has 24 pairs of chromosomes.
Sexual Reproduction Type 1:
There are two sexes: male and female. During the event of sexual reproduction, the male transfers 24 chromosomes to the female where the chromosomes from both the sexes are mixed to produce an offspring.
Sexual Reproduction Type 2:
There are three sexes: male, female and [insert word]. During the event of sexual reproduction, each member transfers 16 chromosomes to the female where it gets mixed to produce an offspring.
We don't observe sexual reproduction of type 2 (or it is rare). Doesn't the type-2 form of sexual reproduction cause better mixing of genetic information than type-1 form of sexual reproduction? Despite the aforementioned advantage, nature has chosen to encourage the type-1 form of sexual reproduction. Why is the type-1 form of sexual reproduction more common than the type-2 form of sexual reproduction?
This question can be extended to "Why has evolution favored sexual reproduction involving two mates than sexual reproduction involving $n \space (n > 2)$ mates?

i think it's an interesting question

Are you asking about species with more than two sexes/mating types or situations where more than two sexes are involved in a single reproductive event?

@fileunderwater I edited the question. Is it clear now?

I think this falls under the "why don't some traits evolve?" Question: http://biology.stackexchange.com/questions/35532/why-do-some-bad-traits-evolve-and-good-ones-dont

@kmm I don't think so - the dynamics behind the evolution of sexes and multiple mating types is an active field of research.

Because it's a lot easier to get two sexes together than three?  Especially in the more primitive types of mating, where eggs/sperm are simply released into the water.  (Or pollen into the air.)

@fileunderwater Do you know of any references for this field of research? I would be interested to look into it. See my related question: https://biology.stackexchange.com/questions/59715/is-there-a-theoretical-maximum-on-the-number-of-sexes-an-organism-could-have

As an aside, it might be interesting that science fiction author Iain M. Banks in "The player of games" describes an alien species with three sexes. If I remember correctly, procreation is a two-stage process where one sex transfers sperm to the second, which then transfers it in modified form to the third. As author, Banks is more interested in how a developed society would work with three sexes and what kind of power relations would develop.

I suspect the double strand nature of DNA is intrinsically more suited to mixing of genes via two parents but would not suit three. Although science fictional three sexes often have two contributing their genes with the third as incubator - at least one such story posited evolution from parasitic species.

Why do you feel evolution favors sexual reproduction in the first place? I've never really understood this premise and presume it somehow vindicates Darwin's theory. The most prolific organisms are either asexual or sexual/asexual and, based on previous answers, increasing the number of mates shows sexual reproduction to be an inferior method.

Have you ever thought of X as a partner to X being a third sex in some sense of your question with Y being second? It might be a matter of compatibility, reciprocity, in some mathematical logic.

"Dominance" might allow to establish various "sexes" as phenotypes. Thus, two is a minimum in number. Assuming there is maximum pressure of evolution to establish a maximum of similarity in a search for the better. There can only be one sex that is the best in copying one other (as it occurs to me: there is just one maximum of similarity in a multitude of elements).

Why do you say "more common"? Are there any processes you describe in real life?

Let's break it down: The chance that two individuals of distinct gender meet at one location in space time is tremendously higher than for three. We could do some math here (assuming biased random walks of points in three classes on a 2d surface etc.) but that is not necessary I guess. As far as we know sexual reproduction evolved long before complex sensory systems and/or brains (namely 1250 million years versus 500 million years) that allow for active search behavior beyond chemotaxis. Therefore a random walk would be a reasonable first approximation for organism behavior to simulate the situation back then. Having two genders seemed to have been a good trade-off between the chance to meet and advantages in terms of mixing the genetic information. Note that this answer might not be valid for organisms being able to reproduce in both ways, sexual as well as asexual.

Your first sentence ("chance... meet at one location in space time...") makes me think of the pair, two as a number, as a mathematical maximum of compatibility if the premise were one and only one rule of "dominance". Underlying question: What is the mechanism that safeguards existence and identity of one and the same sex (best answered in some logical context)?

Quite simply two mates is simpler both functionally and logistically. It is basic statistics you are far more likely to find 1 individual from 50% of the population once, than 2 individuals each representing 33% of the population at the same time. That's three factors making two sexes statistically easier.  Also most sexual organisms do not have chromosome counts divisible by 3, some don't even have numbers evenly divisible by 2.
There is still debate about why sex is favored at all, so it is difficult to go into greater detail for other possibilities, but it is far more likely for two individuals to cross paths than three or more, that alone would be enough for a selective pressure favoring two over three most of the time. And of course not now most sexual organisms are built to handle that 2 individual mating they inherited and could not mechanically handle a third.

Can you please further on the claim that two mates is simpler both functionally and logistically and eventually back up your claim with a citation? If you google the question why is there two sexes, you'll get plenty of popular science article to inspire an answer. I don;t if they cite much trusty sources though.

"... likely to find 1 individual from 50% of the population once, than 2 individuals each representing 33% of the population..." - I think you should state your assumption that there is non-compatibility. I guess you do NOT assume that there is compatibility of any of those sexes with each and every other.

@PeterBernhard I do not understand what you mean, the OP specifies 2 mates, over 3 mates, encountering 1 individual will always be more likely than encountering 2 individuals at the same time, unless you resort to special pleading.

@Remi.b its just math, P(A) will always be more likely than P(A and B) or P(A)(A)

Ah, now I now why you do not understand. I did not understand your premise. Your premise is that any one gender - e.g. of three - does NOT fit any other. What you are assuming is  that  A matches B, but does not match C, right? - That ain't necessarily so. Every one of three might match any other of the box. That's what I meant without knowing.

@PeterBernhard no it doesn't matter if they match or not, if you need all three to breed which is what the OP asked.

Thank you for understanding me so well. This, in fact, did not cross my mind. Would deleting my comments be appropriate? Such processes do not exist in nature, at all, do they?

No need to delete, I do know there is a 3 sexed worm in mono lake, but I don't know any details.

Though some would disagree, sexual reproduction has distinct advantages over clonal reproduction specifically because it provides a way to shuffle homologous blocks of genes within a population.  But increasing the number of parents required beyond two would not provide enough greater "shuffling" power to compensate for the logistical impediments to n-parent matings.

I find "... shuffle homologous blocks of genes within a population ..." unobtrusively alluding at the clone, the clan; "the population" is "my universe". Imagine different diploid "races" that know no interaction between them, then imagine a mitotic individual mingling within itself. With  diploid non-sexual reproduction there is mingling of genes - the "problem" is  the clone that stemes from Adam mingling only Adam's genes, not even Eve's, no mating. Nothing specific to mating, mingling, will happen in diploid cell. Any separate clone will "stay like that".

Currently unable to delete my commente above which is not bad : "shuffling" of genes does not happen in one individual of a population, although logically it could ("imagine"), as those beings are all diploid in their cells. So what is the advantage of refraining from shuffling in mitosis?

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How does natural selection affects seasonal polyphenism in animals?
How does natural selection affects seasonal polyphenism in animals?
In this Wikipedia article there is a following statement:

Since these animals in widely separated groups have evolved
separately, the similarity of coloration is due to convergent
evolution, on the presumption that natural selection favours a
particular coloration in a particular environment.

By looking at e.g. snowshoe rabbits, how can it be that natural selection "favors" a particular coloration during winter and summer? Is not the environment causes coloration without any "benefit" for these animals? How can it be proved, that these animals change their coloration because it is useful for them?

Thanks, the article focuses on social aspects only, but I will read it anyway. I'm more interested in ecological impact on coloration, though. And yes, I'm looking for the articles providing evidence. I.e. I want to see natural selection in action.

I think that the textbook case of Peppered moths is a good example of how an environment can influence coloration and of evolution in action. It is not seasonal change but the principle is similar. https://en.wikipedia.org/wiki/Peppered_moth_evolution

[H]ow can it be that natural selection "favors" a particular coloration during winter and summer?

Camouflage for example. In regions, where it snows some animals would take advantage to have a fur colour that match the substrate in which they live and they may therefore be selected for having a white fur in winter and a non-white fur in summer.
Consider for example Lepus lepus in summer

vs in winter

How can it be proved, that these animals change their coloration because it is useful for them?

There are a whole lot of possible experimental design.
Considering seasonal coat colour in response to predation, a simple and obvious approach would be to experimentally dye the individuals and see how their survival varies depending on the colour they have been dyed.
Sometimes, you may have a sister clade that is non-plastic which it might be of interest to test against (depending on the exact question at play).

I'm more interested in ecological impact on coloration [..] I'm looking for the articles providing evidence

Cases of local adaptation (such as Hoesktra 2006 for example) or other evidence of natural selection on coat colour such as differential selection among lineages are probably way more common. But if you are specifically interested in seasonal variation then, here are a few papers I could find with a quick google scholar search showing selection on seasonal variation for fur colour.

Zimova 2013 and Zimova et al. 2016 in snowshoe hares (which is listed in the wikipedia article)
Turner 1961 in pastry larvae
Maybe Ornborg et al. 2002 on blue tits

Thank you for the quick response. I'd agree coloration is due camouflage, but it is hard for me to believe in that without evidence. Also, in summer they are more visible, but they are also visible in winter, though little more less. As to the testing method you proposed, I think it would be a good way to test natural selection in action. By the way, could this coloration happen without natural selection?

Ok, is there a specific species for which you are looking for an original paper? (I picked Lepus lepus quite randomly, I do not mean that there is evidence for this specific species).

Any of the species from that list in the Wiki article I've provided would be interesting for me.

Please see edit in my answer.

@user35970 I think the issue is not about whether you can see the animal in its summer camo in the summer, especially in pictures of that animal (presumably selected by the photographer when you can see the animal..). The issue is that if it wore its winter coat in summer, it would stand out white against a non-white background; if it wore its summer coat in winter, it would stand out against a white background. It's certainly fine to have some skepticism, but being harder to see seems like it carries a pretty obvious benefit for any species, prey or predator.

@Remi.b Thanks, this is what I was looking for. Still the information present in those articles is not convincing enough to be sure that the camouflage is due natural selection, the difference in numbers of survival rates are too small, the testing methods are not good enough. There could be also a lot more factors influencing the decreasing/increasing of animal survival probability, not just their coloration and background.

What I've realized though, is that it is very difficult to test natural selection - is it really that acquired characteristics benefits the animal or it is simply a coincidence that these characteristics promotes better survival and thus it only seems to us that it brings a significant benefit for the animal.

@BryanKrause Yes, that is logical assumption, but in initial stages of acquiring characteristics there is seems no natural selection, if it is so, then natural selection cannot be a driving and creative force of evolution (as per Darwin, Modern synthesis), it is simply that species with certain characteristics tend to survive and reproduce and these characteristics are "stabilized" in time.

@user35970 Sounds like you are being extremely opinion-based. You are selecting a specific trait (fur colour seasonal variation) and ask for evidence that it is adaptive, you read the paper and (whether or not your have much knowledge in data analysis but it does not sounds like you do reading your comments) you conclude that the paper is not good enough. There are tens of thousands of evidence out there (see for example the Hoekstra paper; I'm about to publish one more myself), it is not so hard to give an evidence that a trait is beneficial over another one.

Also, calling selection a creative force sounds like you you would take advantage of having a look at an intro course to evolutionary biology such as Understanding Evolution by UC Berkeley for example

@user35970: Differences in survival rates don't have to be large to have an effect, when they act over many thousands of generations.  A practical way to test this would be to e.g. find a closely-related species (or even the same species) that lives in an area with little or no winter snow cover, and observe whether the same color changes occur, and their timing.  Or (if you have sufficient time and funding, move color-changing species to a different location, and observe whether the change becomes less common over time.

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Does science have an explanation of how the first "common ancestor" formed in evolution?
I always have this question on my mind and I need a better explanation on this. Does Charles Darwin's theory explain it or are there any other theories which explain it better than Charles Darwin's theory?

This is a very broad question you will have to narrow down. Are you asking about  molecular mechanisms of evolution or the molecular development of an organism following fertilization?

Molecular mechanisms of evolution

Which Darwin theory? I suggest doing some research and improving your question with more information and demonstrated effort to answer the question

Let me explain it further, as we all know we all were descended from a single common ancestor. I just need a better explanation on how the first common ancestor had formed before the evolution occurs

The you are looking for Abiogenesis not evolution, you need a replicator before you can have evolution.

@hamilthj I don't see how "molecular mechanisms of evolution" is any better than what user54581 wrote originally. I don't know what "molecular mechanisms of evolution" means but if I had to guess I would guess the mechanisms of DNA mutation, not abiogenesis (which doesn't involve mechanisms of evolution, or at least insofar as evolution is involved it's not the hard part that makes it an actual question) and definitely not "how an organism is formed on a molecular level".

Darwin's theory of evolution (and the modern theory of evolution) explains how the current diversity of life developed. Remember, the title of Darwin's book is On The Origin of Species, not the origin of life.
As for how the current diversity of life developed, or how species originate, the theory of evolution states that life forms change and diversify gradually, and species arise and differentiate from related species, via the processes of random mutation at the time of reproduction and natural selection. The ToE is a complex set of theories with many different semi-independent aspects but that's what it basically comes down to.
Clearly all this requires life, or imperfect reproduction at least, to exist; it says nothing about the first life, and it cannot say anything about it because given what we know of the processes that lead species to arise and life to diversify and aquire its form, those processes cannot possibly have been in play when going from abiotic stuff to the first living systems.
In other words, the Theory of Evolution is how life develops once it starts existing; it would work equally well if the first life appeared via natural chemical processes or was created by alien tinkerers or the result of a time paradoxical sandwich dropped in the wrong place on primordial Earth. The study of how life could start existing is usually called "abiogenesis".
The issue isn't actually as clear-cut as it may seem, since there is a very wide unknown space between what we consider the most archaic forms of life, and any entity that could plausibly arise via purely abiotic processes; every theory of abiogenesis does assume that a lot of the features we consider essential to life must have arisen after some kind of replication appeared, meaning those features would have evolved. So there definitely is some evolutionary biology involved in investigating abiogenesis, and maybe if we ever solve abiogenesis it will be folded into the ToE (like I said, the ToE is actually a complex set of theories and observations, not one single thing. So while our understanding of what the theory says and can say currently excludes abiogenesis, our understanding and definition of the theory could evolve). But we haven't, and it currently isn't.
You need to edit your question however, because it is completely unclear from the title or text that you are asking about abiogenesis. Your question sounds like it's about embryonic development or biochemistry. Those are the current instances we have of organisms forming; whatever processes were at work in creating the very first life, well for one thing maybe we wouldn't want to call whatever that was an "organism", but more to the point those processes cannot happen today. The atmosphere is wrong and too full of oxygen, there are organisms everywhere vaccuuming up whatever resources those original biochemical processes might have used, basically there is likely no chemical environment on modern Earth that's anything like the chemical environment life originated in.
To answer your question though, abiogenesis is currently an unsolved question, so no, Science does not have an explanation of how the first organisms formed. But if you want to have an idea of how things could have happened, what the challenges are in figuring things out, and what things Science currently considers likely or impossible, there is a lot of active research in the field and many different hypotheses. The Wikipedia page for Abiogenesis has a fairly comprehensive rundown on this.
This video describes one of them (my favorite and the first I've found actually convincing, I have no expertise whatsoever to base this on but I plug it anyway; if nothing else it gives an appreciation for what kind of things the researchers in this field look at when thinking abiogenesis) :
https://www.youtube.com/watch?v=av98Brx23_4
(disclaimer: youtube throws up an error for this video for me right now but I've watched it before, I don't know if the video's down or if the problem's on my end)

Thanks for the explanation. Your explanation leads me to the next level of the theory of evolution

Darwin is quite explicit that his theory does not attempt to answer the question of how life originated.  Rather, it takes one (or a few) original forms as a starting point, and explains how diverse species arose from that start.  In his own words:
"Thus, from the war of nature, from famine and death, the most exalted object which we are capable of conceiving, namely, the production of the higher animals, directly follows. There is grandeur in this view of life, with its several powers, having been originally breathed into a few forms or into one; and that, whilst this planet has gone cycling on according to the fixed law of gravity, from so simple a beginning endless forms most beautiful and most wonderful have been, and are being, evolved."


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single use traits
Are there any known traits (in any organisms) that serve exclusively one purpose?
(Counterexample: Giraffes long neck help them reach less available food AND communicate sub-sonically).
If so is that the exception rather than the rule?
This will be used for a human evolution paper, in which I would suggest that the descended hyoids in hominins and modern Homo sapiens could have serve multiple purposes, such as size exaggeration and language. I want to debate an argument that a similar descension in deer evolved, or was selected for, for only one use (i.e. size exaggeration) and that this correlates to human larynx evolution, by citing literature (if available) that demonstrates that organisms use features for multiple purposes more often than not.

Comments are not for extended discussion; this conversation has been moved to chat.

if you mean a physiological trait, a butterfly wing with a fake eye is only there to look like a fake eye. when moth species turned black during the coal peaks of the industrial revolution, it was to make them hide against the black backgrounds.

There is no rule to this, advantage is advantage however it is achieved. Slection does not care how it yields a net advantage just that it does.

If by trait you mean any phenotypic trait there are boatloads of enzymes which have only one function.  Phosphofructokinase-1 is good only for adding another phosphate to fructose-6-phosphate.
If you want big things there are plenty of those too.  The gallbladder's only function is to add bile to the intestinal contents.  The quadriceps femoris has only the function of extending the leg at the knee.  The abducens nerve controls the lateral rectus muscle of the eye and that is all.  Beta cells in the islets of langerhans in the pancreas are only good for making insulin.  You can't make them do anything else but that.

Actually the rectus femoris part of the quads also crosses the hip joint and thus in involved in hip flexion as well.

You seem to be thinking only of molecular function but even an enzyme with a single molecular function can have multiple cellular functions, be involved in various pathways and processes etc. There are actually relatively few proteins involved in one and only one function and it is very likely that they too are involved in many we just don't know about. Same for the rest of your examples: that we know of only one function does not mean there are no more.

@terdon: If I play the bass drum, but with the band I play many different pieces, is my function different with each piece?  Or am I performing the same function in different contexts?

@Will that's a very, very long and complex discussion actually. The meaning of "function" in biology is very unclear. Especially when you consider the different levels one can function on (from the molecular to the cellular to the tissue or organismal, from complex systems and emergent properties down to simple chemical reactions). If a receptor kinase activates the same MAPK pathway in different tissues but results in opposite effects is it still the same function? What if the same receptor activates a different pathway?

In fact,  PFKA1 which you mention has multiple functions: ATP binding, fructose binding, metal binding, it is involved in the metabolism of fructose and of mannose, it exists with three different types of subunits in different tissues. Is that the same function? Is it even the same protein? It all depends on how you define function and after spending 4 years doing a post doc on this sort of thing, all I can say is that it is very hard to define.


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How are the wings of birds, pterosaurs and bats related to each other?
Homologous organs are organs which have same arrangements of bones, blood vessels and muscles with different functions, and analogous organs are those which have different arrangements of bones but serve same function.
I want to know whether the wings of birds, pterosaurs and bats are analogous or homologous organs. My book says that their wings serve same function and have similar structure but they evolved independently. It confuses me because this seems like a blend of both homologous and analogous organs to me. So which is it?

Here is a discussion of homology and analogy that clearly presents bat and bird wings as an example of analogous organs:
http://amrita.olabs.edu.in/?sub=79&brch=16&sim=132&cnt=1
You are right however that bat, bird and pterosaur wings are homologous in a sense, as they have similar underlying structure and a common evolutionary origin - the front limbs of tetrapods.
One could perhaps say that bat, bird and pterosaur wings are homologous organs as front limbs, but analogous organs as wings.
This page has pictures of the skeletal structure of each:
http://www.ucmp.berkeley.edu/vertebrates/flight/converge.html
As you can see, they are similar front limbs - made of a common set of bones and muscles. But those bones have been arranged into wings in different ways: Pterosaurs have a lengthened pinky finger maintaining a flap of skin that makes up the wing; bats have three lengthened fingers with a flap of skin around them; and birds have small, fused finger bones with the surface of the wing being made up of feathers.
And it is in fact the case that as far as their evolutionary history goes, bat, pterosaur and bird front limbs have a common origin in the front limbs of tetrapods, but have separate independent origins in terms of how those front limbs evolved into wings. Or put another way, the common ancestory of bats, birds and pterosaurs had front limbs, but those front limbs weren't wings.
Compare with the "wings" of flying fish, which does have a common origin with that of birds/bats/pterosaurs: both developed from the pectoral fins of their bony fish common ancestor. Obviously they became wings independently, and they also have a very different evolutionary origin as "limbs". On the other hand when you look at the wings of insects, there is no common origin between those and the wings of vertebrates at all. The common ancestor of insects and vertebrates had no limbs at all, not even bones or an exoskeleton. Both lineages developed limbs and hard support structures independently, and then adapted some of the structures they had for flight.
Interestingly it seems a book recently came out on the flight of bats, birds, pterosaurs and insects: On the Wing: Insects, Pterosaurs, Birds, Bats and the Evolution of Animal Flight by David E. Alexander. It could be an interesting read to anyone interested in the question. Here are some reviews of the book:
http://www.bioone.org/doi/pdf/10.1642/AUK-15-210.1
https://academic.oup.com/icb/article/56/5/1044/2420642
ETA: If you want to bend your mind a bit around the question of homologous vs analogous organs (or homology vis homoplasy), look at these two questions from the sidebar:
The pectoral fins of a whale and a shark. Are they analogous organs?
How large is the range of 'same origin' when determining whether two organs are analogous or homologous?
Which ask similar questions you did, but of the fins of whales vs the fins of sharks. And that's a funny one isn't it! Because where in the pterodactyl example we have a common ancestor who had front limbs but didn't have wings, in that case the common ancestor of whales and sharks did have pectoral ("chest-level") fins, that the fins of whales and sharks descend from! So, homologous? But the fins of whales spent so much of their evolutionary history not being fins at all that it does make one want to say the homology is at the "front limb thingy" level not the "fin" level. I mean, as far as evolutionary distance goes, the wings of flying fish and of bats are actually more closely related to each other than the fins of whales and of sharks are!!! (the evolutionary history there goes: jawed fish (Eugnathostomata) -> cartilaginous fish (Chondrichthyes; led to sharks) and bony fish (Osteichthyes; led to flying fish, bats and whales).
99% of the "shark-fin-like" appearance of whale fins developed long, long after their split from the shark lineage; and I don't know what the front fins of the jawed fish common ancestor was like but it's possible it looked different from whale/shark fins too, so the some of the "whale-fin-like" appearance of shark fins may also have developed independently after the split.

So ,what would we call them homologous or analogous organs?As homologous organs have same structure but different function and analogous organs have same function and different structure .But wings of birds,bats and pterosaurs have same function ,similar structure but yet they evolved independently. Can it be a case of convergent evolution?

@RabikJohn I thought I answered that question. If I didn't, could you explain why my answer doesn't answer your question instead of just repeating the original question?

You said that they are analogous with reference to wings and homologous with reference to front limbs .You mean wings are analogous organs ,but analogous organs have same function and different structure .And my book says they have same structure so how can they be analogous with respect to wings?

@RabikJohn they have the "same structure" in the sense that they have pretty much the same bones connected to each other like the front limbs of all tetrapods, but they have "different structures" in the sense that those bones are bent in different ways to make a wing shape. Did you look at the pictures in the link I gave? If you are confused about your book,maybe if you give the exact quote of what your book says we can clarify what the author meant.

Ok, I am writing the exact quote of my book .It is a topic of convergent and divergent evolution in which homologous and analogous organs are discussed. So the book says"An example of convergent evolution is the similar structure of wings of birds ,insects pterosaurs and bats .All serve the same function and are similar in structure yet they evolved independently".

@RabikJohn: seems like the book is just saying those organs are all wing-shaped, not saying they are homologous. Notice they include insect wings in there, whose deep structure has nothing in common with the wings of tetrapods. They do haven superficial similarities, i.e. they all look like wings. That's what the book is saying. It's not using the word "structure"" in the same way people do when they talk about homology. Did you look at the pictures of the skeletal structure of bird, bat and pterosaur wings?

I have just looked at the pictures that you had on link but ,not their skeletal structure .But I'll do that .So eventually ,it seems that they are superficially alike and have different structure of their skeleton. And by similar structure may be my book just mean superficial structure.


text:
Location of microbes causing eliminated diseases
Do eliminated diseases like polio, smallpox etc still exist in locations they have been eliminated from or in the wild or did we just make them go extinct like the dodo?

Whether a disease can be eradicated or not depends on its reservoir. To be eliminated it needs to be eliminated in all places and organisms it can thrive in and spread from. This makes diseases like rabies for example hard to eradicate altogether because it can exist and spread in many different animal species.
Polio and smallpox however both have no non-human reservoir, which makes it possible to eradicate them. There is no "in the wild" for them to persist in because humans are "the wild" for them. So smallpox the disease has indeed been made extinct like the dodo; polio we're not quite there yet but we seem to be close.
I said "smallpox the disease" because "smallpox the virus" still exists in two laboratories in the US and Russia.
Polio, as I said, isn't an "eliminated disease" yet (as of May 2017), but since you mentioned it, the main places it persists now are Afghanistan and Pakistan.

so lets say tommorow we get vaccine which kill malaria and vacciante all human malaria will die cause it need human to survive ?

No, because it doesn't. Malaria's main host is a mosquito, and while it does require a secondary host (that the mosquito bites) to complete its lifecycle, that secondary host doesn't need to be a human.


text:
Is the bipolar neuron of the retina considered a sensory neuron?
Any neuron that participates in sending impulses from receptors to the CNS are referred to as sensory neurons. But I often see bipolar neurons of the eye (which according to the above definition should be called sensory neurons) being called interneurons. Same is the case with the amacrine cells and the horizontal cells.
So what are sensory neurons? Are all the following retinal neurons sensory?

rods/cones,
bipolar neurons,
amacrine cells,
horizontal cells &
neurons of the optic nerve (ganglionic neurons)

Are all the neurons of brain interneurons? Obviously, there are neurosecretory cells in the hypothalamus that I wouldn't consider interneurons. But, still.
Wikipedia tells us that only 20% of neurons in the cortex are interneurons.

Unlike the peripheral nervous system (PNS), the central nervous system, including the brain, contains many interneurons. In the neocortex (making up about 80% of the human brain), approximately 20-30% of neurons are interneurons.

Shouldn't that be way greater than 20%?

In short, yes. Any neuron that is involved in conveying sensory information from the periphery to the CNS is a sensory neuron. So I would consider all of those neurons in the retina sensory.
Arguably amacrine and horizontal neurons do not convey information "towards" the CNS, but they are involved in the processing of sensory information, therefore I would call them sensory. However I wouldn't split hairs about it if the consensus on amacrines/horizontals was interneurons, not sensory.
I guess the confusion is that many categories of neurons are not mutually exclusive, so neurons can be both sensory and interneuron.
Once reaching the optic lobe (I assume you mean areas in the thalamus, midbrain etc.), then the CNS neurons can loosely be classed as projecting/interneurons. Interneurons will remain within a region of the brain, often inhibiting activity in other cells within the region (or exciting). Projecting neurons will carry information to a different brain region, or back out to the periphery. These are very loose, in a nutshell classifications though.
Once you start looking at a specific region, e.g. the Lateral Geniculate Nucleus, then the neurons will be further classified, either by shape, function, neurotransmitters, inputs or outputs, or a combination of the above depending on the requirements of the system.
Edit: To elaborate, the types of neurons in the brain will usually be described in an area specific fashion, e.g. the lateral Lateral Geniculate Nucleus has 3 major classes of neurons, magnocellular, parvocellular and koniocellular, as well as some interneurons and supporting cells. Whereas about a dozen types of neurons have been described in the cochlear nuclei, including pyramidal, stellate, giant, golgi etc. But at this level, you would be looking at very specific differences that are not necessarily relevant to the pathways involved.
I would argue that interneurons are small and restricted to individual brain regions, e.g. the visual/auditory cortex, many of the neurons, e.g. pyramidal neurons in layers IV and V  are generally projecting neurons that carry information around the brain. I don't have specific numbers for percentages, but about 20% interneurons sounds reasonable to me.

I like the overall message of this answer and gave it a +1, but I'd note that some people take a very narrow view of what "sensory neuron" means and intend to refer to the primary sensory neurons, which in this case would be the photoreceptors themselves. In my opinion it isn't an important distinction at all, as long as someone understands the actual functions, but sometimes textbooks or instructors can be overly precise on terminology even in cases where there is not a clear standard in the field.

I think the most generalizable definition of interneuron is what you wrote here: "Interneurons will remain within a region of the brain, often inhibiting activity in other cells within the region (or exciting). Projecting neurons will carry information to a different brain region" (though for "brain" you could substitute any component of the nervous system). By that definition bipolar, amacrine, and horizontal cells are all interneurons. Rods/cones and retinal ganglion cells are not: one is a sensory receptor cell, the other is a projection neuron.

Are projecting neurons textbook interneurons?

Thanks Bryan, that sums up the difficulties in the field. When studying inner hair cells, we would never consider them to be neurons, which would make the spiral ganglion neurons the sensory neurons, or there are no "sensory neurons" for hearing.

@DeechitPoudel, It depends on the textbook and the level of understanding you are expected to know. But in reality, no projecting neurons are neurons that carry information from one region of the brain to the other, e.g. from the brainstem to the midbrain. (In the UK, at approx. age 16, students are taught that all neurons in the brain are interneurons, which is a massive oversimplification).

@OliverHouston I agree, most people don't consider inner hair cells to be neurons: in that case I would say that spiral ganglion neurons are the sensory neurons; photoreceptors are usually considered neurons, however. It's really a developmental distinction more than anything else. I also agree 100% with what you say about projection and interneurons in your comment - for OP, if you are asking these questions because you are studying a textbook, you will simply have to familiarize yourself with how your textbook chooses to label things.

@BryanKrause It seems I am getting the picture. Although there is one thing that is bugging me. I have included that in the edited question.

@DeechitPoudel I'm guessing the 20% number is referring to inhibitory interneurons; 20% is definitely a reasonable number for inhibitory interneurons in cortex (including hippocampus). If you want to define 80% of cells as "interneurons" that probably defines interneurons to include cells that project neurons within whole regions of the brain, like neurons that project to distant areas within neocortex. I'd say that is a relatively unusual way to define interneurons, but as we have addressed already, the terminology varies by source.

Short answer
According to definitions, I can say 'yes' to all your statements.
Background

So what are sensory neurons? Are [] retinal neurons sensory?

Yes they are considered sensory neurons, because sensory neurons are defined as:

[] neurons [that] run from the various types of stimulus receptors, e.g., touch [receptors and the rods and cones in the retina] [] to the central nervous system (CNS), [i.e.], the brain and spinal cord.

Adapted from Kimball's Biology Pages and Khan Academy
Fig. 1 explains what a sensory neuron is. Note that the cell body of the sensory neuron is located in the dorsal root ganglion, just at the boundary of the peripheral nervous system. The relay neuron is located within the spinal cord, and is hence classified as an interneuron. Thus, sensory neurons are located in the peripheral nervous system.
.
Fig. 3. Sensory neurons are located in the peripheral nervous system. source: Tanya HL's pages

And, as soon as the neurons of optic nerve terminate in optic lobe, then are all the neurons in the optic lobe connected to the neurons of optic nerve called interneurons?

Per above definition, sensory neurons are located in the peripheral nervous system. Once they connect to the spinal cord (or the rhinal cortex in case of the olfactory system) they are per definition considered to be interneurons. Which answers your next question:

Are all the neurons of brain interneurons?

Yes.

Unlike the peripheral nervous system (PNS), the central nervous system, including the brain, contains many interneurons. In the neocortex (making up about 80% of the human brain), approximately 20-30% of neurons are interneurons.

All of the brain's neurons are interneurons, per the classification of neurons in sensory, motor and interneurons. As BrianKrause pointed out, often the term interneuron is reserved for inhibitory GABAergic cells, especially in the scientific literature (e.g., Markam et al., 2004).
Post scriptum
The classification in motor-, sensory and interneurons is rather a schoolbook way of explaining the types of neurons. It increases the understanding of the classification of the different neurons, but you will inevitably encounter shady areas where things fall apart; consider the fact that the retina is often regarded to be a part of the CNS, because of its embryonic development (Purves, 2002). So while I support the above answer, it's important to note that it comes down to a gross over-simplification of the nervous system. Such blunt definitions tend to fall apart when looked at more closely.
References
- Markam et al., Nature Rev Neurosci (2004); 5: 793-807
- Purves et al., Neuroscience, 2nd ed. Sunderland (MA: (2001)

I mostly like your answer, but from the perspective of someone that studies the brain (and cortex specifically), I would generalize to say that you are relying on definitions of interneurons that are used when describing the relationship of the brain to the periphery. For people focusing within brain structures, it is definitely not true that all cells of the brain are thought of as interneurons; it is also not true that interneurons are reserved for GABAergic cells, although this is common, because other cell types like spiny stellate cells in L4 of neocortex are also called interneurons.

Also by some definitions, the retina is special among sensory systems in that it actually develops from brain tissue and therefore is often considered part of the CNS. Based on that and the rest of your definitions, then, bipolar cells would not be considered "sensory" because they are already part of the CNS, so they are just as much interneurons as any of the relay neurons of the spinal cord.

@BryanKrause Considering your first comment, the question specifically relates to PNS vs CNS, so I think the approach of the answer is OK. Concerning your last comment please read the post scriptum

Oops, I should have expected better from you, I completely missed your PS. Sorry for that comment! However, "the question specifically relates to PNS vs CNS": is that true? It seems the question is about the retina, which, as your PS notes, is often considered part of the CNS. My suggestion, which of course is your decision to accept or reject, would be to amend at least your 'simple answer' to make clear up front the ambiguity or context-dependence of the term "interneuron."

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Is the promoter region of a gene transcribed?
If the RNA polymerase attaches to the promoter region of the gene, would it form the initial mRNA segment by reading the promoter region or would it slide across the DNA then read the adjoining region? Or does the enzyme span so long that its certain region attaches to the promoter while its adjacent region starts reading the DNA to form mRNA?
Does the RNA polymerase read DNA base pairs and add the complementary RNA base pairs one by one? Or, does it read groups of base pairs just like tRNA which reads triplet of bases?
Is the terminator region transcribed as well before the process of transcription ends, or does transcription end immediately after the RNA polymerase reaches the terminator region? If the latter is the case, how does transcription end just by the polymerase reading the terminator region?
So, should the promoter and terminator regions of a gene be considered parts  of the gene or separate entities?

In genomic annotations, genes are considered to begin at the first base found in a sequenced transcript, and end in the last base of a sequenced transcript.

Too many questions, too little effort.

would it form the initial mRNA portion soon after attachment by reading the promoter region?

The RNA Polymerase binds to the promoter, however since it is so large the front end of it hangs off the end of the promoter.  When Transcription begins the promoter is not included, as the transcription process occurs at the front of the polymerase.

Also, does the RNA polymerase read DNA base pairs one by one and add the RNA base pairs to the chain one by one?

The RNA polymerase adds nucleoside triphosphate (NTP) one by one.  As the picture shows below, there is only room for one NTP in the active site and once the correct NTP is placed it is added to the RNA chain.

How does the process end just by reading the terminator region?

The question of termination is dependent on the cell.  Prokaryotes terminate in either a Rho independent or dependent process.  Independently, a hairpin occurs in the RNA that breaks off the transcript, dependently, a Rho factor binds that causes termination.  Eukaryotes are less well known, but it is generally believed that after the poly-A site there are also factors that bind and induce termination.

So, should the promoter and terminator region of a gene be considered parts of the gene or separate entities?

This question is slightly more about definitions that biology.  The Oxford Engligh dictionary defines a gene as "The basic unit of heredity in living organisms".  Since the promoter, non-coding, and non-translating regions are still paramount in getting the protein made, I would argue that they are still part of the gene and the larger hereditary unit.


text:
Is a gene located in the sense or the anti-sense strand?
The given image shows a section of a dsDNA.

Suppose it's the blue strand to which RNA polymerase attaches during transcription. The resulting mRNA molecule then codes for a protein $X$.
So, which of the following is considered the gene?
a) The blue strand (anti-sense strand) to which RNA polymerase attaches during transcription and is the one that is technically read by the transcription machinery.
b) The red strand (sense strand) whose base sequence is the same as the base sequence of our mRNA molecule (except that thymine is replaced by uracil).
c) The DNA duplex as a whole, as shown in the above schematic.

As you have recently edited this old question, I assume you are keen to have it discussed. Although I have already answered, I intend to revise my answer extensively Could you therefore clarify two points. 1. Are you asking (a) Whether the term gene, as it is generally used in science (and defined in textbooks, for example), is restricted to one strand, OR (b) Should the term gene which does not normally have this stipulation, be changed or clarified to restrict it to one strand. 2. Are you sure which strand?  The strand actually copied into mRNA is the red anti-sense strand.

(a) is what I intended to ask

I've edited the question to make it more intelligible.

My revised answer specifically addresses point (a) — usage — which the answer you have accepted does not. It provides referenced examples of usage in the full gamut of scientific sophistication. It also demonstrates that the problems of defining a gene are far more numerous than gene overlap.

Short Answer
In referring to genes on a double-stranded DNA chromosome (the situation assumed in this question), the general and scientific usage of the term ‘gene’ includes both DNA strands.
The practical definition of ‘gene’ has come under scrutiny in recent years for reasons that will be discussed, especially in relation to the ENCODE project. However none of the discussions I have encountered considers restricting a gene to a single strand.
General and educational usage of the term ‘gene’
The term gene was coined in 1909 “to describe the Mendelian unit of heredity”, long before it was suggested and established that these units resided in the chromosomal DNA of organisms.
A reputable general dictionary, Mirriam–Webster, suggests a modern concept of the term, comprehensible to non-specialized readers, to be:

a specific sequence of nucleotides in DNA or RNA that is located
usually on a chromosome and that is the functional unit of inheritance
controlling the transmission and expression of one or more traits by
specifying the structure of a particular polypeptide and especially a
protein or controlling the function of other genetic material
e.g. “She inherited a good set of genes from her parents.”

And a similar definition is given to the medical profession in Morton and Spences Genetics for Surgeons.
Despite the knowledge of the complexity of genes that has accumulated in recent years, in two modern molecular biology text books the essential feature of the definition is that it is all-embracing rather than restrictive. Thus, the definition in Alberts et al. — Molecular Biology of the Cell is:

Region of DNA that controls a discrete hereditary characteristic,
usually corresponding to a single protein or RNA. This definition
includes the entire functional unit, encompassing coding DNA
sequences, noncoding regulatory DNA sequences, and introns.

And the definition in the glossary of Lodish et al. — Molecular Cell Biology is very similar.
More recent considerations of the term ‘gene’ in the context of the ENCODE project
There are several features of the structure and the regulation of the chromosomal information specifying proteins that has led to a reconsideration of the use of the term ‘gene’. This in not merely a semantic concern, as the major ENCODE Project, the purpose of which was to provide an “Encyclopaedia of DNA Elements”, had the practical task of naming the elements it describes.
I have found a couple of useful articles by others, considering the problem at length. One is by Smith and Adkinson (2010) and the other is by Portin and Wilkins (2017). A brief summary of the situation that they discuss is that there are two main problems. One problem is the deviation from the ‘one gene — one mRNA — one polypeptide chain’ concept caused by alternative splicing, multiple promoters and  alternative translational initiations sites. A second is the finding of regulation of transcription by sequences greatly distant from the transcriptional initiation site.
The general thinking is to redefine the term ‘gene’ in terms of networks or integrated interactions. Thus, Portin and Wilkins own proposal is:

A gene is a DNA sequence (whose component segments do not necessarily need to be physically contiguous) that specifies one or more sequence-related RNAs/proteins that are both evoked by Gene Regulatory Networks and participate as elements in Gene Regulatory Networks, often with indirect effects, or as outputs of Gene Regulatory Networks, the latter yielding more direct phenotypic effects.

and that employed by the ENCODE project is defined by Gerstein et al. as:

The gene is a union of genomic sequences encoding a coherent set of potentially overlapping functional products

a gene is a genomic sequence (DNA or RNA) directly encoding functional product molecules, either RNA or protein.
In the case that there are several functional products sharing overlapping regions, one takes the union of all overlapping genomic
sequences coding for them.
This union must be coherent — i.e., done separately for final protein and RNA products — but does not require that all products necessarily
share a common sub-sequence

(It is supplemented by an ontological diagram that I shall not reproduce here.)
This is complex, but in relation to the poster’s concern one thing is clear, at no time are the authors concerned with strandedness, and there is no proposal that a gene is confined to a single strand.
Two simple arguments
One might argue that nobody mentions strandedness because everyone assumes a gene is on only one strand. Really? Anyway, I‘ll finish with a couple of mundane arguments that strandedness has no place in defining genes, overlapping or not.

The Transcription Factor/RNA polymerase binding site — the TATA box — is regarded as an integral part of a gene. Both strands of the TATA box are required for binding. Likewise other transcription factor binding sites. Hence the gene cannot be on only one strand.
Single-stranded DNA viruses are found with what are called ‘positive sense’ and ‘negative sense‘ genomes. So clearly among these genomes there are heredity units which read ‘anti-sense’ as well as some that are ‘anti-sense’. On the ‘one-stranded gene’ thesis one of these could not be called genes. One would have to devise some term from them as progenitors of the gene in the complementary strand in the replicative DNA form!

None of the highlighted regions in your figure, is a gene. A gene is a section of DNA which gives rise to a product. Basically, a gene has an orientation (5'→ 3') i.e. it is essentially a single stranded region. However, the strand that mechanistically contributes to RNA synthesis (template) has the reverse-complementary sequence of the gene (in other words, anti-sense). Therefore, a gene, as it is annotated is not a functional entity but a genomic representation of a product. Some viruses (such as M13 phage) have a single stranded genome; for them the transcript is always antisense to the genomic DNA region.
Same section of dsDNA can harbour multiple genes in both orientations and this is clearly seen in viruses which have an highly compact genomes. Other prokaryotic and eukaryotic genomes also have overlapping genes.
Some related posts:

On which DNA strand is TATA box present?
Do transcription factors bind to both strands of DNA?
Which DNA elements belong to the definition of a gene?

Does that mean only the indicated region of molecule A is a gene? Or,
does the Indicated portion of molecule A + Complementary portion
present in molecule B comprise a single gene, such that A is sense and
B is non-sense strand of the same gene?

If the molecules A and B are expressed from opposite strands, then they are considered products of different genes, even if the gene region overlaps.
The situation is more unclear if both the molecules are expressed from the same strand and the transcribed region overlaps. Sometimes they are classified under the same gene (splice variants) and sometimes they are not.
These are some lines from the human genome annotation file which tells the location of genes in the genome (+ and - denote opposite strands):

chr1    HAVANA  gene    1567474 1570639 .   +   .   gene_id "ENSG00000189409.8"; transcript_id "ENSG00000189409.8"; gene_type "protein_coding"; gene_status "KNOWN"; gene_name "MMP23B"; transcript_type "protein_coding"; transcript_status "KNOWN"; transcript_name "MMP23B"; level 2; havana_gene "OTTHUMG00000074713.4";
chr1    HAVANA  gene    1590786 1594063 .   +   .   gene_id "ENSG00000272004.1"; transcript_id "ENSG00000272004.1"; gene_type "antisense"; gene_status "NOVEL"; gene_name "RP11-345P4.10"; transcript_type "antisense"; transcript_status "NOVEL"; transcript_name "RP11-345P4.10"; level 2; havana_gene "OTTHUMG00000185638.1";
chr1    HAVANA  gene    1603429 1604850 .   +   .   gene_id "ENSG00000269737.1"; transcript_id "ENSG00000269737.1"; gene_type "antisense"; gene_status "NOVEL"; gene_name "RP11-345P4.7"; transcript_type "antisense"; transcript_status "NOVEL"; transcript_name "RP11-345P4.7"; level 2; havana_gene "OTTHUMG00000182604.1";
chr1    HAVANA  gene    1604714 1605836 .   +   .   gene_id "ENSG00000269227.1"; transcript_id "ENSG00000269227.1"; gene_type "pseudogene"; gene_status "KNOWN"; gene_name "RP11-345P4.6"; transcript_type "pseudogene"; transcript_status "KNOWN"; transcript_name "RP11-345P4.6"; level 1; tag "pseudo_consens"; havana_gene "OTTHUMG00000182605.1";
chr1    HAVANA  gene    1570603 1590473 .   -   .   gene_id "ENSG00000248333.3"; transcript_id "ENSG00000248333.3"; gene_type "protein_coding"; gene_status "KNOWN"; gene_name "CDK11B"; transcript_type "protein_coding"; transcript_status "KNOWN"; transcript_name "CDK11B"; level 2; havana_gene "OTTHUMG00000078638.4";
chr1    HAVANA  gene    1592939 1624167 .   -   .   gene_id "ENSG00000189339.7"; transcript_id "ENSG00000189339.7"; gene_type "protein_coding"; gene_status "KNOWN"; gene_name "SLC35E2B"; transcript_type "protein_coding"; transcript_status "KNOWN"; transcript_name "SLC35E2B"; level 2; havana_gene "OTTHUMG00000078639.1";
chr1    HAVANA  gene    1634169 1655766 .   -   .   gene_id "ENSG00000008128.18"; transcript_id "ENSG00000008128.18"; gene_type "protein_coding"; gene_status "KNOWN"; gene_name "CDK11A"; transcript_type "protein_coding"; transcript_status "KNOWN"; transcript_name "CDK11A"; level 2; havana_gene "OTTHUMG00000000703.14";
chr1    HAVANA  gene    1634175 1669127 .   -   .   gene_id "ENSG00000268575.1"; transcript_id "ENSG00000268575.1"; gene_type "processed_transcript"; gene_status "NOVEL"; gene_name "RP1-283E3.8"; transcript_type "processed_transcript"; transcript_status "NOVEL"; transcript_name "RP1-283E3.8"; level 2; havana_gene "OTTHUMG00000183552.1";

Not evident in these examples but there are many overlapping genes in opposite strands. Anti-sense lncRNAs would be an example to have a quick look at. See Can both the overlapping genes (in opposite strands) produce proteins? for an example of antisense-overlapping protein coding genes.

Bottomline: The definition of gene is constantly changing but usually a gene has an strand orientation. Specifically, if two different RNAs are synthesized from opposite directions but from the same dsDNA region, then they are said to arise from two different genes. (check out this review for some specific examples)

I have revised my own answer and do not address gene overlap. However I am still unclear as to your conclusion. You state "The opposite strand can also sometimes synthesize a product but it is considered a different gene in that case." What is "it" in this sentence? Are you saying that the single opposite strand is the gene, or just that there are two genes sharing double-stranded DNA.

@David I mean that two genes can share the same dsDNA region. I'll clarify this


text:
Oxygen dissociation curve and temperature
Say, we have a container with a mixture of gases. The concentration of oxygen is $C_{oxy}$ and its partial pressure is $P_{oxy}$. We then introduce a sample of hemoglobin (deoxygenated) in that container. A certain fraction of the sample gets saturated  with oxygen. Afterwards, we increase the temperature of the gas in the container keeping everything else constant. $P_{oxy}$
obviously increases. Does this mean that the percentage of saturated hemoglobin increases as well with the increase in $P_{oxy}$, according to the ODC curve?
Or, will the oxygen saturation decrease, as at higher temperatures the $Hb-O_{2}$ bond starts getting denatured? If the latter is the case, does this imply the ODC curve is temperature specific? And if that is the case, wouldn't the ODC curve (partial pressure Vs saturation curve for a specific temperature) be a mere concentration vs saturation curve for a specific temperature?

Welcome to BiologySE... can you give some evidence of effort on your part to try and figure this out? where have you looked for an answer?

Added my idea. Can you help? @VanceLAlbaugh

..saturation actually depends on the concentration... If thats the case then why do we experience mountain sickness?


text:
For how long can influenza survive on a piece of paper?
Consider the following hypothetical: A graduate student would like to return a set of assignments before a certain deadline, but she currently has the flu and may sneeze or cough while grading the papers at home. Under the assumption that she has just graded the papers but is still in possession of them, how long should she wait before returning them to the students? At what point does the risk of transmitting the flu to a student via paper become negligible?

Unlikely. Because as long as she has the flu (and we're talking about the real influenza here, not just some nasty cold) she will neither grade any papers nor return them because she will be in bed being sick.

Perhaps just eight to 12 hours.

Both influenza A and B viruses survived for 24-48 hr on hard, nonporous surfaces such as stainless steel and plastic but survived for less than 8-12 hr on cloth, paper, and tissues. Measurable quantities of influenza A virus were transferred from stainless steel surfaces to hands for 24 hr and from tissues to hands for up to 15 min.

--Survival of influenza viruses on environmental surfaces.
Or, perhaps, up to 17 days, when in the presence of "respiratory mucus" (i.e. snot), although even then a couple days was more plausible. Note that this was on Swiss banknotes, which isn't standard paper.

Influenza A viruses tested by cell culture survived up to 3 days when they were inoculated at high concentrations. The same inoculum in the presence of respiratory mucus showed a striking increase in survival time (up to 17 days)....  When nasopharyngeal secretions of naturally infected children were used, influenza virus survived for at least 48 h in one-third of the cases.

-- Survival of influenza virus on banknotes.


text:
Good resource for penguin behavior for non-specialists
I just returned from Antarctica where we made many shore excursions and spent a great deal of time among penguins -  mainly Gentoo, and some Chinstrap species.
They were fascinating and there were several distinct behavioral patterns that I observed but did not understand.   I'm not really asking for explanations here, but just a good introductory source of penguin behaviours.  When I've searched online everything I've seen is either too general and basic to be helpful, or too technical and specialised for me. I have a strong general science background and I'm an AAAS member and I have one ethology course from decades ago, but reading peer-reviewed research papers on this would be over my head.   We were there in March (late summer) so the juveniles were adult-sized but still had juvenile plumage.
Examples:
(Gentoo) being on beach or snowfield where there was a dense, mainly uniform distribution of adult and juveniles standing or laying around, when in the midst of this a line (typically 4-8) of adults would walk briskly, single file, through the groups of standing individuals, and even through the groups of standing humans, all looking straight ahead and apparently with a sense of purpose.  They would walk out of sight.   Why, and are they connected or related somehow?
(Gentoo) coming up to us and grabbing anything loose like backpack straps, number tags on lifevests, or pantlegs flapping in the wind and pulling.  This was not pecking like they would trying to get an adult to feed them, but I mostly saw this with juveniles.  We were under instructions to not make any noise or motion that would alter their behavior but when one started tugging on my lifevest inflation tab I had to yell to stop him.  (IAATO guidelines are to stay 5m away from wildlife but the penguins didn't attend our orientation seminar and anytime we stood still they came up to us)  Juveniles frequently nestled between our legs if we stood still (all of us were wearing thick, insulated, multi-layers of pants), but this is easy to explain regarding chicks nestling in the adult's brood pouch, since we frequently saw adult-sized juveniles exhibiting other chick behaviours, eg, food-seeking from adults.
(Chinstrap) large groups (30-50) of individuals standing tightly together when many (but not all) would suddenly point their heads up and start to vocalise, sometimes flapping their wings.  This would go on for a minute or so and then stop suddenly. I made videos of this.  I never saw any sign of a threat, say from a skua or seal, nor did they seem to be looking at anything, and nothing obviously changed that made them stop.

Not an answer, but Michelle LaRue (@drmichellelarue on twitter)  is a penguin biologist and is always very generous about answering questions-- she encourages people to ask her questions all the time.


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What really causes cancer?
A lot of things are claimed to cause cancer, eating red meat, eggs, smoking, using phones, deodorant, breathing.
Surely these can't all actually significantly contribute to the development of cancer.
I've heard smoking is a big one to lung cancer, with someone--I can't recall--saying that most patients with this cancer are smokers.
What kind of activities/foods are sure to, or have high chances to, lead to the development of cancerous cells and how do they cause them, at a molecular level?

Do you want to know which chemical causes cancer? Or what is the general reason behind cancer?

What really causes cancer: mutations in certain genes.

@chris Chemicals, and thus activities/foods.

"Cancer" is not just a single disease. Cancers would be more accurate, but even that doesn't do justice to the vast array of different kinds of cancers at the genetic or molecular level.

As they say, in California, EVERYTHING causes cancer :p

@kmm brings up a good point. As such, this question is way too broad. Tobi, I recommend that you edit this question to focus on a particular type of cancer (e.g., perhaps lung cancer like you already mention). I also recommend doing a bit more research on your own and updating your question w/ what you find. Doing both of those things should reduce the chance that this question gets closed. For more help writing good questions, see here. Thanks!

I've sufficiently edited the question, I'd really like a proper answer.

The Guardian: The 116 things that can give you cancer – the full list

@Tobi - No, this is way too broad. You may have specified one organ system, but you're still asking for a definitive list. "What kind of activities/foods are sure to, or have high chances to, lead to the development of cancerous cells and how do they cause them, at a molecular level?" Can't be done for a number of reasons. Kind of like asking "What do I have to do to roll a 12 three times in a row with fair dice?" Answer: there is no answer to that question, because the outcome of fair dice cannot be predicted if thrown properly.

Cancer is caused by the mutations in cells.
Cancer exists because of the failure of cell cycle checks which could actually allow cells to survive with erratic genomes. However, that alone does not cause cancer.
Cancer is the uncontrolled proliferation of cells. That only happens when cells have accumulated enough errors during cell division and each cell division goes undetected to the point that cells refuse to commit apoptosis; they are no longer receptive to the body's control mechanisms.
Cancer cells are also malignant. That means that cancer cells cannot be called cancer cells until they are invasive. That means a few cancerous cells cannot be caused cancer because they don't take nutrients from the body . Also, tumour  suppressor  genes can also cause cancer when they turn proto-oncogenes into oncogenes.

"please tell me if what are said here is factually true." While it's great that you're looking for feedback, you shouldn't post an answer you're unsure of. There are, however, a lot of interesting facts here that are sure to be helpful to the OP. Please provide a source for those who want to do further reading.

You have missed the very numerous benign cancers, which, though not invasive, are still cancer.  Also, invasive doesn't quite mean what you think it means.

You are correct in that cancer is a result of escaping cell cycle checks. This is usually a result of mutations. Not always.  See mesothelioma resulting from asbestos exposure. There are some cancers that seem to be a combination of genetic and epigenetic mechanisms. Further, you can have cancer cells that have not become invasive. This is what a tumor is before it acquires the ability to extravasate and set up shop elsewhere. That is metastasis. Further confusing the issue, a benign tumor IS uncontrolled proliferation, but usually considered "non-cancerous" (can't metastasize).

@akaDrHouse - "...benign tumor IS uncontrolled proliferation, but usually considered "non-cancerous" (can't metastasize)" I disagree. The ability to metastasize is not what defines a cancer. It is what defines a metastatic tumor from a benign tumor. I can name dozens of cancers that don't metastasize.

Thanks guys for being so negative. I'm quitting stack exchange. At least I tried to help

Thanks for the correction @anongoodnurse. You are right. I was confusing malignant and metastasis. I will change my comment. Edit: it won't let me.


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How do I solve this problem related to specificity and sensitivity?
Consider an autosomal recessive disease with an incidence of 1/10,000 in
the general population of 100,000. Your best friend comes to you very
upset because he has just taken a screening test for this disease and gotten
a positive result. He is convinced he is a carrier, despite having no family
history of the disease. You try to reassure him, but he says, "Don't bother.
The Clinic said this test has 98% sensitivity and 90% specificity. With that
level of sensitivity, it must be correct!" What is the chance your friend is
NOT a carrier?
I have attempted it in this way:
The reason I used Hardy-Weinberg is because there isn't any other way to determine whether he is a carrier or  not.
Case 1: He is AA (double dominant). This has a 0.99^2 = 0.9801 chance. The chance that his result was positive is 1 - 0.90 = 0.1 since that is the chance that the specificity failed since specificity measures the chance of true negatives. Multiplying this gives us a 0.09801 probability of this case.
Case 2: He is Aa (heterozygous). This has a 2*0.99*0.01 = 0.0198 chance. Again his chance of a positive result should be 1 - 0.9 = 0.1. Multiplying this gives us 0.00198.
Case 3: He is aa (double recessive). This has a 0.01^2 = 0.0001 chance. The chance of getting a positive result is 0.98. Multiplying we get 0.000098.
Adding these up, I have 0.100088. We want the probability he is not a carrier, so 0.000098+0.09801 (cases 1 and 3) divided by 0.100088 (the total). This yields around 0.9802 or 98% chance, which isn't one of the choices. What am I doing wrong?

Welcome To Biology.SE. Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. Hint1: You have to use conditional probabilities. Hint2: The question has nothing to do with Hardy-Weinberg equilibrium (unlike you seem to think given the tags used), it is a pure mathematical probability question.

Hint 3: Seriously and truly, this question has nothing to do with Hardy-Weinberg. Hint 2 is a solid hint. Try rethinking your approach. What if your friend really has the disease? What if your friend doesn't? What is going to happen with the test in each case? What do specificity and sensitivity mean?

Does my logic make sense if I do it this way? 1-0.9 (failing of specificity to catch someone without the disease) = 0.1. 0.1*2 (since AA and Aa are two cases that are both cases without the disease) = 0.2 is the chance that he is either AA or Aa. The third probability is 0.98, the sensitivity to aa having the disease. Adding these we have 1.18, and AA + aa = 1.08. 1.08/1.18 giving 0.915.


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Plant determination: Lilium monadelphum versus L. szovitsianum
Lilium monadelphum, L. szovitsianum and L. armenicum belong to group of yellow flowering Lilium species and they are both often cultivated.
These species come from Caucasus area, so the first two are both described in the Flora of SSSR (4th volume). However, I find the dichotonic key description incomplete, and, based on the key, I am not able to clearly distinguish these species. Lilium armenicum is described by some authors as a variety of L. szovitsianum or as a subspecies of L. monadelphum.
What are your experiences with determination of these species?


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Why do people feel shame when exposed nakedly?
Why do people feel shame? Meaning the kind of shame specifically related to exposing 'private parts'.
Where does it come from (i.e. social factors due to upbringing, inherent in our genes etc.)?
What is its evolutionary purpose?

Is your question specific to nakedness or was that just an example?

Note the field of knowledge you question fits in is called evolutionary psychology which is very theoretical and very little empirical test were actually perform. So, one can, at best formulate a hypothesis but you will hardly find any evidence for one or another hypothesis in this field.

Not a native speaker. I meant the kind of shame specifically related to exposing private parts. I'll adjust the question.

You should know that evolutionary psychology is very controversial, in part for the reasons @Remi.b states and in part because of the potential for misuse of those hypotheses, in particular to defend as "natural" certain behaviors that are deemed socially unacceptable. I think the field of eugenics is a reasonable historical analogy. In other words, tread lightly and skeptically.

@Bryan Defending certain behaviours as "natural" on the basis of evolutionary psychology is not "misuse". You may not personally like the idea of promoting certain behaviours on the basis of their theoretical naturalness, I'm not entirely keen on it either, but it's just as valid a hypothesis for how to decide what behaviours to promote as any other. If we wish to oppose horrors like eugenics we do not not need to pretend their hypotheses are invalid, it's enough that we don't agree with their conclusions. Pretending they are invalid just plays into their hands.

@Isaacson The problem isn't the hypothesis, the problem is the use of unscientific arguments posing as scientific ones. I'm not against responsible evolutionary psychology, either, but I meant to caution the OP, who is a novice to the field, to tread lightly and to be aware there is controversy and inconsistency of quality.

Probably a cultural effect
In many tribes, people are naked. Also, the naturist movement is very popular in the western culture and they don't feel shame. In northern Europe, it is common to be naked in spas.
I would guess it is mainly a cultural effect and there is little heritability for this trait. I doubt you'll find a study on this particular question, so the best one can do is just to formulate a guess here.
If you don't quite understand why I talk about heritability here, then you should have a look at Why is a heritability coefficient not an index of how “genetic” something is?. In layman terms and in vague terms, I meant that there is probably little role of genes to explain why we feel naked.
Yes, but let's assume it was selected for...
If we were to assume that feeling of shameful in front of nakedness had been selected for, one may hypothesize that it could be due to sexual selection, where rich and wealthy wear clothes. It could also be due the social presssure of showing off what you are worth as sexual body parts are likely under strong sexual selection as well.

I'd say the ability to feel shame is physically (genetically) determined. The object/issue of shame may be culturally determined (what we learn what is to be shamed off). In that sense its likely like disgust. Specifically on nakedness I remember from lectures of "Eibl-Eibesfeld, Human Ethology" that there are almost no ethnic groups really completely naked. He mentioned one (Amazonian?) tribe who only wore a single small string around their waist, but fell terribly ashame when someone saw them without that string. So maybe the shame object nakedness itself is even genetically determined?


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How do animals avoid the problem of inbreeding?
In humans, there are various cultural rules to avoid inbreeding (to the level of paternal cousins, nieces/nephews and uncles/aunts etc)
How do animals such as dogs avoid the problem of inbreeding? They do not have a record of their relatives and there seem to be many siblings in each batch for some animals. How does it work in the wild or among stray animals? Is their DNA somewhat resilient to these genetic disorders?
Likewise, how do birds handle this issue?
EDIT: I am not trying to breed animals, want to understand how it works in the uncontrolled wild when the young leave home early and are scattered.

Is it even a problem?  Especially when you consider the Darwinian effects.  That is, most animals produce far more offspring than needed to keep a stable population, so only the fittest survive to reproduce.  ("Fittest" here being a rather circular definition, as an individual that survives is fit.)  So if an instance of inbreeding produces unfit individuals, they don't survive.  And at the extreme, with a limited population some inbreeding might be necessary for species survival.

@jamesqf yes, I want to know if there is such a case observed in practice. It is known that cheetahs suffer from an inbreeding problem and the genetic makeup of any pair of cheetahs is currently too similar. How about other creatures?

@jamesqf Of course it's a problem. The very definition of "fitness" is based on progeny survival. Progeny represent a large energy investment, so there's should be (and is) strong selection to prevent individuals from generating large numbers of unfit offspring.  As the answer shows, there are in fact multiple mechanisms to prevent inbreeding, so observation supports theory.

@user1952500 There are widespread claims that cheetahs suffer from inbreeding problems but they're not well supported. It's clear that cheetahs are inbred, but very little evidence that it affects their reproductive efficiency. There are well-understood mechanisms by which inbreeding effects can be minimized (flushing of deleterious alleles) and it's likely that cheetahs went through those.

@iayork: That was my point, that there does not seem to be any significant adverse effects from occasional inbreeding.  Based on my (admittedly limited & unscientific) observation of animals & humans, I'm not entirely convinced that there really are effective prevention mechanisms other than dispersal, which of course has more obvious benefits.  Certainly among humans, avoidance of inbreeding seems to be more cultural than biological.  There are examples of cultures, like ancient Egypt, where it seems to have been common, at least among royalty.

Why not ask the question "Are there significant adverse effects from inbreeding"? The answer is "Yes, there are." On the other hand, many people seem to think that inbreeding is an instant guarantee of death, and they're wrong too.  As for prevention mechanisms, many have been put forward in @John's answer; there are far more than dispersal. Also, your claim of widespread inbreeding in Egypt is flat wrong. None of this is appropriate for comments, so ask a question (and read the answers) if you want your misconceptions to be corrected.

The question is interesting. However, it will be impossible to answer accurately for all birds as the mechanisms actually used vary from species to species. So I will give you some information in the general sense.
Recurrent inbreeding reduces inbreeding depression
Inbreeding depression is caused by both

Recessive deleterious alleles that are brought to homozygosity
Some epistatic interaction

In any case, in a population where inbreeding is common, those recessive deleterious alleles and alleles involves in these deleterious epistatic combinations will be washed out (or at least brought to lower frequency) of the population via selection and the population will end up suffering less from inbreeding than a typical outbreeding population. In the extreme, a population of exclusively selfer individuals, such deleterious recessive alleles are brought to extremely low frequency within lineages.
How to avoid inbreeding?
Now, sure animals and plants typically don't have a big book that allow them to tell how related they are to another individual. However, there are other mechanisms of kin detection
Self-incompatibility
For example, in plants self-incompatibility is thought to be relatively uncommon. There exist many mechanism, so I-ll just consider a simple example. Consider a self-incompatibility locus as a specific loci for which if the same allele is shared by both the pollen and the ovule, then no fertilization occurs. This prevents selfing and prevents mating with many of the closely related mechanisms.
Body odour and sexual attraction
Also, there are mechanism that can mediate sexual attraction toward individuals that differ. The classical example is Major histocompatibility complex (MHC) and sexual attraction (vertebrates), where individuals tend to be attracted to individuals that have a different MHC.

I was just curious about dogs because I have seen stray dogs in large numbers in some countries and wondered how they would handle it. I have not seen that many stray cats or other animals. There have been many wild birds as well, hence asked about them. They could apply to any animal in general.

I didn't downvote, but would encourage you not to use the terrible, terrible "research" that claims to show MHC compatibility effects in humans -- the so-called experiments are an embarrassment that showcase virtually every bad research practice there is.

@iayork I did not read that paper. I only went to the conclusion. I did not know, their experimental design was considered so bad. I removed the reference (and the associated claim) and will read the paper to make my own opinion on it. Thanks

The term you are looking for is Kin Detection. which is the methods of recognizing related organisms, important both for avoiding inbreeding and aiding relatives.
There are several known mechanisms.
First they can avoid it the same way humans, they don't want to mate with anyone they were raised with. Humans don't need an understanding of genealogical to avoid mating with kin. Humans have an aversion to to romance with anyone they shared meals with frequently as a child. It is called the Westermarck effect or sometimes reverse imprinting and is part of humans in built kin detection system. It can work with many method just by building a brain that sees those who were around when you were a child as likely kin and thus unattractive to downright sexually repulsive. It is not perfect, it can be confused by adoption or separation, but works fairly well in the natural human setting. in effect their "record" is simply their memory.
Smell is another known method, in animals with better senses of smell than humans can detect certain factors that would indicate relatedness, like genetically controlled urinary proteins or simply smells of familiar and thus likely related individuals. This can work hand in hand with the Westermarck effect. There is even some very preliminary evidence humans may use this method to some extent.
Basic dispersal patterns can also do this by behaviorally programming one sex to travel far from where they are born and the other to not do this, it decreases the chance they will end up mating with a relative.
Now the formalized study of inbreeding avoidance is relatively new, mostly due to the technology making detecting kin for the scientists easier being new, so more and more research will almost certainly find other methods as well.


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Examples of heterologous expression in human cell beside viral expression
Usually, people are interested in expressing human proteins in fast-growing organisms like bacteria to yield a maximum of protein within a short time lapse. Codon usage harmonization/optimization have been used to increase the protein production. The role of codon usage have been studied in the context of viral protein expression, but outside this viral context, is there any example of using human cell lines for heterologous expression?

Are you asking for examples of human cell lines being used for preparaive protein production?

That should say "preparative".

Besides research (as mentioned by mxwsn), there are a lot of actual protein based medicines and vaccines produced in human cell lines. One of the first mass cultures of a human cell line was in the monkey free production of a polio vaccine
   (source). Almost every researcher working in a molecular lab has grown HeLa cells at one point during their career!

Expressing GFP in human cell lines for research purposes is an extremely common example of heterologous protein expression.
For research purposes, it's usually unnecessary to optimize codons for increased expression, especially since using more efficient enhancers and promoters produces a far greater improvement in expression levels than codon optimization which is non-trivial and species-specific.


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computing relative synonymous codon usage from a coding sequence alignment while accounting for phylogenetic inertia?
I would like to compute the relative synonymous codon usage (RSCU) from coding sequence alignments. But since the coding sequences from an alignment are not independent realization, the statistics (RSCU) need to account for the phylogenetics autocorrelation present in the data. How can I do that?

It looks like you want to test a very specific hypothesis. Wether a sequence accumulates more non-synonymous changes than expected given its phylogenetic backgroun. The programme CODEML, included in the package PAML was designed specifically for this:
http://evomics.org/learning/phylogenetics/paml/


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How many allele for one gene are found inside our cell?
I know it depends on phase. So i am talking of -
1) in human (diploid organism) with cells before prophase (before replication, when 23 pair of homologous chromosomes are present ). I think answer is 2 if we not consider male XY sex chromosome because they are not homologous in which case the answer should be 1. But then i get confuse why genotype is shown like Tt (doesnt this means two alleles per chromosome).
2) in gamete cell. I think the answer should be 1.
Please tell if i'm correct.

In short. Yes.
Each diploid cell has 23 pairs of chromosomes (22 of which autosomal)
In relation to the genotype part of the question. The "Tt" refers to each allele on the chromosome and wether it is dominant or recessive. Take for instance, hair colour. On one chromosome, there would be an allele from one parent and on the other an allele from the other parent. This is why two letters are needed, to show the allele given by each parent.
You can think of dominant and recessive in terms of how powerful the copy of the gene(allele) is. An allele that is able to overpower and mask traits is called dominant, one that is not strong and cannot mask traits is called recessive. This is why you need two recessive alleles for recessive disorders, otherwise the dominant allele would cover it up.
As this is a homework question I have tried to explain this in simple terms which you should understand. Hope this helps.

Your use of the term sister chromatid is incorrect. I think you mean homologous chromosome.

Apologies. I deleted half of a paragraph before posting and joined the wrong sentences together.


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Is there a data base, tool or method I can use to find out which of my genes code for cytokine receptors?
I have a list of over 600 differentially expressed genes from my single cell RNA seq data analyses. I want to proceed to find out which of my genes code for cytokine receptors so that I can show on a heat map how their expression varies across clusters. Can any one give me a hint on which tool or method I can use to find out which of my genes code for cytokine receptors?
Thanks in advance.

So you're saying you want to convert the gene IDs to gene symbols such as IL15RA? R script typically works

As pointed out by @CKM, this is a simple case of finding the gene name corresponding to the ids used in the sequencing analysis. It's quite straightforward if you have a table of gene ids and corresponding names. You can do it manually for a small set of genes or use a simple script in your favorite programming language for parsing the names.

I'm sure there are many ways to go about this (including literature research via PubMed), but for a start, I searched the GO term data base which, for the search term "cytokine receptor activity" returned this, which includes a number of genes which I can download as an excel file and match them with my gene set using R.

You stole this answer from someone who answered you on Biostars.  https://www.biostars.org/p/365294/  Are you going to give yourself the best answer points now?

@swbarnes2: I asked the question on both fora and I want to share what I learned from another forum on this forum. This is because the answers I got on this forum did not directly meet my needs but I do appreciate the responses I got here. Is it a crime? By the way I slightly modified the response suggested to suit my needs.