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Is PCR a DNA cloning technique?
According to Genomes
PCR is

A technique that results in exponential amplification of a selected region of a DNA molecule [in test tube].

DNA cloning is

Insertion of a fragment of DNA into a cloning vector, and subsequent propagation of the recombinant DNA molecule in a host organism.

While, Molecular Biology of the Cell, Sixth Edition says in a summary:

DNA cloning (through the use of either cloning vectors or the polymerase chain reaction) in which portion of a genome (often an individual gene) is purified away from the remainder of the genome by repeatedly copying to generate many billions of identical molecules.

Here DNA cloning has been used to mean DNA replication in general.
Question: Which author's view is correct, or at least provides the most accepted definitions?

Short answer
The Oxford English Dictionary is quite clear on this. For the verb clone there are two meanings:
Biology To propagate (an organism or cell) as a clone.
Molecular Biology To make copies of (a DNA sequence or gene).
The latter definition clearly encompasses PCR.
History lesson
Most of the information below is taken from the Oxford English Dictionary.
The term clone has a long history, first as a noun and more recently as a verb. The evolution of the meaning and use of the word suggests that we shouldn't be too precious about this.

When I use a word,” Humpty Dumpty said, in rather a scornful tone, “it means just what I choose it to mean—neither more nor less.” “The question is,” said Alice, “whether you can make words mean so many different things.” “The question is,” said Humpty Dumpty, “which is to be master—that’s all.

The word is based on  a Greek word for twig and was originally used as a noun in the form clon.

1903 H. J. Webber in Science 16 Oct. 502/2 Clons..are groups of plants that are propagated by the use of any form of vegetative parts.

It soon gained the final e.

1905 C. L. Pollard in Science 21 July 88/1 I therefore suggest clone (plural clones) as the correct form of the word.

By 1930 it had become a verb...

1930 Jrnl. Ecol. 18 357 This is probably a record for the number of ‘individuals’ obtained at one time by cloning a herbaceous plant

...and, presumably because bacteria were considered to be plants at that time, it was used in microbiology too.

1929 Bibliographia Genetica 5 234 In Bacillus coli communis...a biotype was also found having lower motility than the remainder of the clone from which it came.

By the early 1960s it was extended to animals, probably as a direct result of Gurdon's experiments with Xenopus

1963 J. B. S. Haldane in G. Wolstenholme Man & his Future 352   Perhaps the first step will be the production of a clone from a single fertilized egg, as in Brave New World.

And finally the meaning  was extended to encompass DNA molecules, thus molecular cloning.

1974 Proc. National Acad. Sci. U.S.A. 71 3459/1 ColE1 has been shown to serve as an effective molecular vehicle for cloning and amplifying specific regions of unrelated DNA.

(Extra points if you have read this far AND you know what ColE1 is.)
This final quotation seems to me to show that the confusion over what molecular biologists mean by cloning arose very early. If cloning means “to make copies of”  then why is the word amplifying there? From the outset I think that molecular cloning carried the sense of purifying (by cutting and ligating). Or that's what I thought when I did it for the first time in 1980.
Update
Despite my reliance on dictionary definitions above, and prompted by Tyto alba's discovery of a contradictory definition in a different OUP publication (see comment) here's what I really think:
Anyone who has ever obtained a bacterial colony containing a plasmid with the inserted fragment that they wanted announced "I have cloned the gene!" and meant that they had made a recombinant plasmid AND got it into cells. On the other hand, if they started with a PCR amplification then ran a gel to check before ligating and saw a fragment of the expected size they did not say "I have cloned the gene!" And finally, the successful cloner, when streaking out their transformant colony, will rarely have referred to this step as cloning.

I found in 'A dictionary of genetics' (published by Oxford again) say it means creating genetically identical copies of recombinant cells, excluding the in vitro part (pg-182)?! Should OED be considered more precise when we are looking at words as this?

Short answer
All of your sources are correct as they are not mutually exclusive. PCR is used to isolate and amplify DNA to yield small quantities of pure target product. Gene cloning can subsequently be applied to scale the production of the fragment up. PCR thus can be part of the DNA cloning process.
Background
Cloning in general simply means duplicating. Cloning in Biology refers to

[Making] an exact copy of an animal or plant created in a laboratory from the
  animal’s or plant’s DNA

source: McMillan Dictionary
Gene cloning, as far as I understand refers specifically to the isolation of one single gene and inserting it into cells to amplify it:

The production of a lineage of cells all of which contain one kind of DNA fragment of interest derived from a population of many kinds of DNA fragments.

source: Northwestern University
PCR is a technique to amplify a specific strand of DNA that can be used to subsequently clone DNA into host cells (source: New England Biolabs). The cloning is done to upscale the quantity of DNA. PCR uses primers and can be used to isolate and amplify the DNA up to the scale it is easily clonable.

You may tell so.  DNA amplification is a more generalized term for what you are indicating. Gene cloning with help of bacteria;  popularly known as only Gene-cloning or Molecular cloning; is mainly used for gene or DNA amplification in vivo; and also PCR method (the most basic type) is also for DNA amplification, but in vitro, cell-free conditions.
But practically it may create some confusion; since the term "gene-cloning"/ "molecular cloning" popularly refer to that one done in living bacteria. (though the purpose or application is very same).
Reference: Wikipedia


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What are Expressed Sequence Tags (EST)?
I read in an article that ESTs are partial or sub-sequences of cDNA. What are ESTs exactly? Which part of cDNA is cut in order to make ESTs? Why are they so instrumental in genomic research?

The question does not cite the source of the poster’s information, but it might well be the Wikipedia article on ESTs. I suspect the reason that does not answer the first question (“What are ESTs”) is the confusion in how ESTs are generated from cDNAs implicit in the second question “Which part of cDNA is cut…”. I therefore start by dealing with the source of the confusion.
Clarification 1: A Sequence need not have been Sequenced
One source of confusion lies in the word ‘sequence’. One meaning of this (noun only) is “a specific linear contiguous fragment or region of nucleic acid”. When used in this way there is no implication that even the length of this is accurately known, never mind the identity and linear arrangement of the nucleotides. The second use of the word sequence (noun) is the identity and order of nucleotides in a (linear) nucleic acid, with the corresponding verb meaning to determine this. Because today it is so cheap and quick to determine the sequence of a nucleic acid fragment, the student may not realize what a relatively slow and expensive undertaking it was in the last century. I shall use DNA fragment or region instead of the first use of ‘sequence’ in the rest of this answer.
Clarification 2: There are cDNAs and then there are cDNA clones
The second source of confusion seems to be with the cDNA clones. The question does not use the word ‘clone’, but asks “which part of cDNA is cut…”. This implies the poster is thinking in terms of individual cDNA clones in which the inserted cDNA fragment has been characterized — restriction mapped, perhaps sequenced and the protein product even identified. This is the approach adopted when the scientific problem is to identify the mRNA or gene encoding a particular protein — actin, beta-globin, etc. This is not the case with ESTs. Here the only characterization performed on a cDNA clone is a single DNA sequence determined (historically by the Sanger method) from a primer position in the cloning vector. This is because the focus is on producing a bulk library of DNA sequences.
So, what are ESTs and how are they generated?
As an alternative to the standard definition, one might say:

An EST is a single DNA sequence read derived from only part of a mRNA. Despite its uncharacterized nature, possible redundancy, limited size (perhaps 100-200 nt) and likelihood of errors it is useful in combination with many others from the same tissue as providing a reference to genes that are expressed in that tissue.

So, to reiterate, the answer to “what part of the cDNA is cut…” is “none”. One (presumably) just isolated total DNA from the recombinants in the M13 plaques and ran a single sequence determination from the primer site. And this was because one did not know which EST would be useful, but a collection or library of ESTs would likely contain some that would be useful.
The word ‘tag’ expresses the fact that they act as a handle or reference to the gene or mRNA, rather than being complete in themselves.
Why are/were ESTs important/useful?
The words the poster used originally were “Why are they so instrumental in genomic research?”, but I think that certainly exaggerates their current — if not their past — utility, so I have rephrased the question. Examples of the use of ESTs are given in the Wikipedia article already quoted, so I shall quote from Peter Goodfellow, writing in Nature in 1995.

Only 3 per cent of the human genome codes for proteins… the most important
  part of the genome is the protein coding genes and that sequencing these
  will give the largest return of biological information…

After pointing out his own scepticism towards the approach he briefly mentioned one important historical issue:

Given these disincentives, why have tens of millions
  of dollars been spent on ESTs? After a brief exploratory phase… a major driving force was the hope and the fear that ESTs could be used to patent any gene that had been tagged. Attempts to patent genes via ESTs raised the spectre of an international trade war and the echoes are still reverberating around courts in the United States.

No longer, I hope. Goodfellow then turned to the science:

It was hoped that large-scale EST projects would define the broad limits
  on the number of genes and the types of genes in the genome and provide a
  snapshot of their expression patterns. It was also expected that enough sequence
  information would be generated to be able to recognize new members of gene
  families of biological and commercial interest.

Coda: Yesterday and Today
Currently the method most used to investigate expression of genes as mRNA is, of course, RNAseq, which is faster, cheaper and, unlike ESTs, comprehensive.

source: Stack Exchange

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Is a haploid essentially half of a homologous pair?
Is a haploid essentially half of a homologous pair? I understand that a haploid consists of only one set of each chromosome, so does that mean that if that chromosome was replicated the cell would become diploid and have homologous pairs?

Yes, you seem to have understood it correctly. On top of haploid and diploids, there are also cases of triploids, hexaploids, octoploids and others.
For example, some species of strawberries are decaploid (10 copies) (Hummer 2012). Then, there are the extremes. In Entamoeba populations, there can be variation in ploidy level among individuals ranging from diploid (2 copies) to tetracontaploid (40 copies) (Mukherjee et al. 2008)!

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Is there any technique can quickly expand one set of cell chromosomes?
Assume a cell type is very scarce while isolated out and hard to expand in vitro, and I wanna have more of its chromosomes, is there any technique , in vivo or in vitro or ex vitro, any would count, that allows me to quickly expand the amount of those chromosomes?
I know it sounds weird but just some curiosity~
Thanks


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Can viruses survive super-saturated salt solution?
There is little evidence of biological activity in the Dead Sea (a salt-water lake). In addition, human blood cells do not survive in too much salt water as they shrink and die.
So I wondered whether viruses survive in super-saturated salt water. If they survive what allows them to survive and tolerate the high salt concentration? If they do not survive, what is the mechanism of their destruction?

since viruses may contain no water and are not undergoing metabolic process why do you think salt would affect them?

This issue was studied in Virus inactivation by salt (NaCl) and phosphate supplemented salt in a 3D collagen matrix model for natural sausage casings International Journal of Food Microbiology Volume 148, Pages 128–134.
Saturated NaCl was tested on 4 types of virus, foot-and-mouth-disease virus (FMDV), classical swine fever virus (CSFV), swine vesicular disease virus (SVDV) and African swine fever virus (ASFV) at four different temperatures:4, 12, 20 and 25 °C for a period of 30 days.
For ASFV, but not the other 3 viruses, saturated NaCl had a significant effect of inactivating the virus, on a days timescale.

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Drinking water after eating banana
Why elders advice not to drink water after eating banana? Is there any science behind or is it a myth?
Found a website supporting this (so called?) myth.

Welcome to Bio. If this is a persistent and widely known myth please give a few sources.

@AliceD I found this on internet

That is some random comment on a random site. We run a scientific stack and discussions of rumors are off topic.

@AliceD disbelieve are accepted in stackexchange

here I have also heard elder people say we shouldn't drink water after eating melon or peach, but that is probably some myth that grew after someone got unwell after doing so

Added a link. Replace it if you find a better one.

Related: http://skeptics.stackexchange.com/questions/4134/drinking-after-eating-fruits-causing-belly-ache

Seems to be a cultural thing, like some religions not mixing meat & milk at a meal.  AFAIK the belief is unknown (or at least not common enough for it to have come to my attention) in the US or Europe.


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Excess protein consumption effect on kidney
How does excess protein consumption through food as well as through supplements affect body especially kidneys?
Why it is advice to consume low protein diet during summer ?

Have you done any research? A quick search on google scholar for "protein intake kidney" gives several articles describing possible connections to increased phosphate and urea levels on high protein diets, which could affect kidney function.

@Roland I have and while some say that it affects kidney negatively while other says it has no effect. moreover why not consume protein rich food in summer. aren't our kidney made to this work to excrete urea and phosphate, i drink more water and kidney remove poison, shouldnt kidney adapt to new levels

Great question... I have heard several nephrologists mention that there is very little hard evidence that would suggest that protein consumption should be decreased in renal failure (sounds like mostly animal studies with exceedingly high protein diets - nothing that would be done clinically). I hope this question get some attention... it would be interesting to see the state of this question.

Short answer
The ammonia resultant from the protein metabolism is toxic to the body and specially kidney. (William V. et al.)
Long answer
Protein is a poly-peptide composed by amino acids. Each amino acid has an amine group (-NH2) in its composition. In the metabolism of the amino acids, this amine group is taken, and if it isn't needed is released the to blood vessels to be transported to the liver and be turned to urea.
Needless to say since the kidney filters the blood when there is excess of ammonia in the blood vessels the kidney is the first to suffer.
I've found some papers about the effect of ammonia in the kidney but none of them where about humans. (I may try to fetch some of them later.)
Why summer?
During summer water is lost through perspiration so there's less available for the excretion of urea.
I hope it helps.
References.
1.William V. McDermott, Jr., M.D. ,Metabolism and Toxicity of Ammonia

In the why summer part, may be u intended to write perspiration instead of transpiration. I think now u will be eligible to vote, just need to reach 150

@Mesentery Thanks for the correction! English isn't my main language and sometimes I make some strange mistakes! And I'll be very happy to be able to participate and vote =D

so if one drinks plenty of water, kidney will do its job just fine, and rest of body will heal quickly with more protein?

I would assume so if the consume of protein isn't extremely excessive. I don't know where you live but  there has been deaths for protein only diets. Of course that includes eating only proteins day in and day out. If your interested i would suggest this link. https://en.wikipedia.org/wiki/Protein_poisoning


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Questions regarding PCR
Background:
From Genomes:
The temperature of a PCR mixture is first set at 94 °C so that denaturation of DNA can happen. Then it is reduced to 50–60 °C, which results in some rejoining of the single strands of the target DNA, but also allows the primers to attach to their annealing positions. After this DNA synthesis begins as the temperature is raised to 72 °C, the optimum for Taq polymerase.

In this first stage of the PCR, a set of ‘long products’ is synthesized from each strand of the target DNA. These polynucleotides have identical 5′ ends but random 3′ ends, the latter representing positions where DNA synthesis terminates by chance.
  [Subsequent cycles give] rise to ‘short products’ whose 5′ and 3′ ends are both set by the primer annealing positions.

Now Wikipedia says:

[...] Final elongation: This single step is optional, but is performed at a temperature of 70–74 °C (158–165 °F) (the temperature range required for optimal activity of most polymerases used in PCR) for 5–15 minutes after the last PCR cycle to ensure that any remaining single-stranded DNA is fully elongated.

Questions:

I’m wondering that if the shortening of the length of new DNA is purely by chance. From Wikipedia it appears that the length of the DNA synthesised can be controlled by the temperature of the mixture?

To carry out a PCR experiment, the target DNA is mixed with Taq DNA polymerase, a pair of oligonucleotide primers, and [...]

A pair of primer cannot support the increasing number of PCR cycles, are primers added later/ throughout the process?

Besides it seems to me that the temperature of the mixture has to be changed according to the phases of the cycle. Is it changed? How is it determined that which phase of the cycle the DNAs are in?

P.S. I'm not sure if this post should be broken down into two posts or more. Suggest if you feel that's necessary.

Ideally amplification happens between the two primer pairs and results in one product. However, complicated secondary structures, the depletion of some of the reagents may cause pauses and fall off of the polymerase. This happens often later in the reaction and results in shorter products. This final amplification step is introduced to finish all these shorter products.
A pair means the combination of a forward and a backward primer (see the image below from here). Bothg primers are added in a concentration high enough that both are not depleted and enable long PCR runs. No primers (or other reagents) are added during a standard PCR reaction.

The temperature of the PCR reaction is changed through 1 reaction cycle: First you start with the denaturation of the DNA at 94°C, then cool down to anneal the primers (typically between 50 and 60°C, depending on the primers), followed by the amplification step at 72°C (it'S length depends on the length of the amplified DNA piece, Taq polymerase processes about 1kb/min) (see figure below from here). This is one cycle and you know where you are, because the PCR machine counts this cycles.


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How to interpret dual luciferase assay result (RLU)?
I performed a dual luciferase assay using pGL3 firefly luc as experimental reporter and pRL-TK renilla luc as internal control (Promega assay kit). I used a manual luminometer to analyze my sample. After that, I got following result:
Sample        RLU (LARII)                   RLU (stop & glo)
A               1978                               902
B               1702                               1101
C               1952                               980
As I am doing it for the first time, I cannot understand the result. I want to know, how can I interpret this result? There is no unit. RLU stands for relative luminescence unit; but what it actually means? What is the method to compare the results of different samples? How can I understand expression efficiency? I have read some papers but unfortunately my concept is not being clear.
Where can I find useful information and guidance about it?

Relative luminometer units (RLU) have no unit. They are the result of the luciferase reaction and proportional to the expression of the luciferase gene, meaning the higher the numbers are, the higher the expression is.
To analyze these numbers, you usually use a control, to which your samples are then relative to. So expression from your luciferase vector is 10x higher in the treated sample compared to the control for example.
As the RLU has no unit, it is hard to compare measurements directly. To overcome this problem, you can use a second luciferase reaction (the renilla luciferase) to be able to normalize between samples and to correct for transfection efficiency, but still, your values are only relative.
They are influenced but the kit you use for the measurement, the machine you use (so always use the same machine) and so on.
To normalize the values, you divide each firefly luciferase value by the value for the renilla in the same well. Ideally alls renilla measurements are the same (as you transfected the same amount of plasmid in each well, have the same number of cells etc., but if not, this corrects exactly this problem). You cannot calculate the transfection efficiency from this control.
To calculate the relative expression ratios between your sample B and the respective control A, you set the control to 1 by dividing A/A=1 (for example: A=10, 10/10=1) The relative expression of B is then B/A= relative expression (for example: B=5, relative expression: B/A= 5/10=0.5). In the example the relative expression of sample B would be half the one of the control.

Thank you for your answere. It is helpful; although I am not completely clear. I have used renilla luc here to normalize the expression which is indicated here as RLU (stop & glo) values. And sample A indicates the control. Now, how can I compare my results? Can you give me one example please? Will I have to make a ratio of the two values (firefly RLU: renilla RLU)? And what does the ratio mean? How can I calculate the transfection efficiency? Please help me to know this. @Chris

@MRahman Is this clearer now?


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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 spinal cord play its roles in human beings sex?
I know most people can't enjoy sex if their spinal cord injured.
How spinal cord play its roles in human beings sex?

can you add some background information or references germane to the question?

Assuming that the basis of your question is correct, maybe because ejaculation is controlled by parasympathetic nervous system.

One of the major functions of the spinal cord is to serve as a "highway" for signals to travel between the brain and the sensory (and motor) organs. Thus, sensory the signals that are generated on the body during sex must travel up through the spinal cord in order to get to the brain, where it will be processed into a pleasurable sensation. If the spinal cord is damaged, the signals will not be able to reach the brain and thus there will be no generation of pleasurable sensations.
Here's an image that shows the general sensory pathways. You can see they travel from the sensory organ to the spinal cord, and up it to the brain.

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Are neurons roughly a magnetic dipole?
I would like to make a simulation (concerning genetic evolution) and I want to use a very simplistic model of neurons.
I don't really care there are different kinds of neurons, I don't care much that the extracellular field is different at axons-dendrites and initially, I don't even care that the spike is transferred through the axon. What I really want to know, is whether I can approximate (very roughly) the field with a magnetic dipole pointing at the direction of the axon. Or are the directions of the MF and the axon unrelated?
I have looked around for some image depicting such a relation, but I didn't find any. Is there any resource of some kind available?

Have a look at the cable model. It models neurons as electrical cables. Modelling them as dipoles would be super excessively simplistic and very far from reality. In fact, such a reduction would not even be useful in any context.

in my research, i am trying to see if magnetic fields have any effect in some aspects of the evolution of the brain. If i was to use the cable model to deduce the magnetic fields, i would have to use a "cylindrical" cable model in order to be precise at a fields level. That of course would be really expensive at a computational level especially for a genetic algorithm. I will though try to simulate a cylindrical cable model to see what comes out. thanks.

They surely are not magnetic dipoles, but they can be modelled as magnetic dipoles (more or less accurately). I believe your question would have been received even better (at least by me) if you had asked it this way: "How accurately can neurons be modelled as magnetic dipoles?" But maybe I'm just a penny pincher.

Yes, neurons can be modeled as magnetic dipoles.  In fact, that is the basis of MEG.  Here is an example of a paper that instantiates a computational model of magnetic dipoles in order to explain MEG data Neural mechanisms of transient neocortical beta rhythms: Converging evidence from humans, computational modeling, monkeys, and mice.

ok, so i see i have to use current dipoles instead on magnetic ones. After some thought i guess it makes more sense...


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Question regarding circulatory system of the body
Does the highlighted part in the picture mean that if you take a single blood cell, it traverses through all the veins in the circulatory system ? (Including all the organs)

No.  An individual blood cell will complete the whole loop but can take any route through the circulatory system to do this.  For example, a blood cell leaving the left ventricle may immediately pass throughout the coronary arteries to supply the musculature of the heart or alternatively could carry on down the aorta.  Another cell could be swept down the subclavian artery to the arms and back through the corresponding veins, whilst another could follow a route through the external iliac arteries to the legs and back through those veins.
That being said, all blood cells will pass through the central elements of the pump every cycle.  These are the right atrium, right ventricle, pulmonary trunk (common part of the pulmonary artery), the left atrium and the left ventricle.
Other than these locations, the movement of blood cells will be random.

I agree.                          :-P :-)


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Why do female humans invest more in parental care than male humans, from an evolutionary standpoint?
As the question title suggests, why do female humans invest more in parental care than male humans, from an evolutionary standpoint?
My guess is that the crux of this that males and females have different reproductive biology, but this by itself would not a very satisfying answer, due it not being very comprehensive.

Have you investigated closely related species? Do you know Bateman's principle and the theory of parental investment?

Do you have a source that they do invest more? I have not seen research showing an non-cultural variation.

I am voting to close as unclear until the OP adresses the questions in comments.

"too broad"??? That's a GREAT QUESTION!! How can you erase it? Leave those inexpensive few kB for us to use our brains!

That's a BIOLOGY site. Most evolutionary questions are broad. How can we think biology, how can we think evolution, if "broad thinking" is not allowed? Biology is so close to philosophy, yet you keep pulling them apart!

@BiologyStudent: in Mammals, in general, the long pregnant state, plus the breastfeed, etc causes females usually displaying much more parental care than the males, because they already invested so much. In other animals, like some fish and birds, where the males build and ornament the nest, the reverse is expected.

@anongoodnurse was that too broad for you?

@AliceD was that too broad for you?

@Remi.b was that too broad for you?

@kmm was that too broad for you?

@David was that too broad for you?

And really? All this should need not even 1kB!


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What's the percentage similarity between human individuals (and other primates) when comparing only exons?
In popular science books and articles, I often see it stated that humans are >99 % similar to each other (wikipedia has it a 99.5 %, referencing Craig Venter and this PLOS Biology article) and ~96-99 % similar to chimpanzees or bonobos (Smithsonian Institute, National geographic). I have previously thought that this referred to the entire genome, but the wording on the Smithsonian Institute page I linked, makes it appear that it might refer to genes only, which also seems to be the case according to the answers to this post Do apes and humans share 99% of DNA or 99% of genes? What is the difference?.
How big are these percentages when comparing only the coding regions (exons) instead of entire genes, both within our species and compared to other species, such as primates? And, not as importantly, what are these numbers when including the entire genome with all non-coding DNA?

One of the references to the chimpanzee genome paper linked by Maximillian is Inferring Nonneutral Evolution from Human-Chimp-Mouse Orthologous Gene Trios, where the authors seems to have focused on exons only:

Here we apply evolutionary tests to identify genes and pathways from a new collection of more than 200,000 chimpanzee exonic sequences that show patterns of divergence consistent with natural selection along the human and chimpanzee lineages.

They conclude that:

Perhaps the best way to understand the relation between DNA sequence divergence and the differences between human and chimpanzee physiology and morphology is to compare these differences to the variability among humans. Human-chimp DNA sequence divergence is roughly 10 times the divergence between random pairs of humans.

Unfortunately, they didn't compare this to the fold-difference of non-exonic DNA, so the comparative quantification between coding vs non-coding regions remains to be determined.
However, this does directly answer the question of how big the genomic differences are between individuals of the same species vs those of other species, when comparing only coding regions. I also found it useful to quantify the differences in these relative terms in addition to the previously stated percentages.

This paper seems to have relevant estimates for human-ape divergences. Note again that it isn't using the entire genome, but selected regions of exons, introns, pseudogenes, etc. The chimpanzee genome paper has a nice bullet-point list towards the beginning of relevant statistics for you for that species specifically, that is on the order of 1% overall. The section on "gene evolution" has some specific numbers for coding sequences.
For among-human variation, there is a bionumbers page on that subject based on 1000 genomes project numbers, that comes out at 0.1% divergence among humans.

Correct me if I missed something (didn't read the entire paper), but doesn't the first paper you linked specifically not use coding regions? From the abstract: "...we selected 53 autosomal intergenic nonrepetitive DNA segments..."

The chimpanzee genome paper states: "When CpG and non-CpG sites are considered separately, we find that both CpG sites and non-CpG sites show markedly lower divergence in exonic synonymous sites than in introns (~50% and ~30% lower, respectively)." To me this indicates that the interspecies differences within exonic regions would be smaller than within intronic regions...

...My understanding is that this is due to the survival constraints put on exonic regions, i.e. some exonic mutations kills the organism and will not be passed on to the offspring, while mutations in non-exonic regions don't impact survival to the same extent. This is not my area of expertise though, so I am happy to hear if I have misinterpreted something.

First comment: note that Table 5 of the first paper compares coding region distances. Again, probably not the best example because it's only selected regions; but in my experience these estimates tend not to change that dramatically with sample size.

Comments 2+3: You are correct that the mechanism for the lower rate of divergence in exons is due to selection. Indeed, the inference of functionally important chunks of sequence by comparative analysis depends on this; see for instance http://compgen.cshl.edu/~acs/phylohmm.pdf. But that didn't seem to be part of the original question. There is a very large literature on this subject, but for a concise review by a well-known author you could look at http://www.sciencedirect.com/science/article/pii/S0959437X02003489. Note that among-site variation in divergence is also important in proteins.


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Major groups of photosynthetic prokaryotes
According to Stryer there are four major groups of photosynthetic prokaryotes, i.e. Table 19.1
Bacteria Photosynthetic electron donor $\ce{O2}$ use.
Green sulfur $\ce{H2}$, $\ce{H2S}$, $\ce{S}$ Anoxygenic.
Green nonsulfur Variety of amino acids and organic acids Anoxygenic.
Purple sulfur $\ce{H2}$, $\ce{H2S}$, $\ce{S}$ Anoxygenic.
Purple nonsulfur Usually organic molecules Anoxygenic.
Cyanobacteria $\ce{H2O}$ Oxygenic.
Do each groups belong to a different genus?

To answer your question, yes they are all in a different genus, but that’s really specific.  If you are wondering about their fundamental differences, they fall into a few different groups.
Green sulfur bacteria usually falls into the phylum Chlorobi
Green non-sulfur bacteria falls into the phylum Chloroflexi (Part of the terrabacteria superphylum)
Cyanobacteria is a phylum in itself but also falls into the terrabacteria superphylum.
Both, Purple sulfur/non-sulfur bacteria are all proteobacteria.
Now, pay attention here, as linking these could be somewhat confusing sometimes.  But now we can link together their relationships.
Green sulfur bacteria (Chlorobi) falls into the FCB superphylum, meaning that it is a gracilicute.
Purple sulfur/non-sulfur bacteria (Proteobacteria) are also gracilicutes.
Green non-sulfur bacteria (Chloroflexi) is part of the terrabacteria superphylum.  Terrabacteria are not gracilicutes.
Cyanobacteria is also in the terrabacteria superphylum. (Again, not a gracilicute.)
Now that we know this, we can reasonably assume that both purple sulfur/non-sulfur bacteria are related to green sulfur bacteria, as they are both gracilicutes.  Also, we can conclude that the non-gracilicute green non-sulfur bacteria and Cyanobacteria are more closely related to each other than they are to the latter mentioned bacteria.
Here’s another cool fact, some Deinococcus-Thermus bacteria (members of the terrabacteria superphylum along with Cyanobacteria and Chloroflexi) have been found to carry the bacteriophytochrome photoreceptor (BphP) which absorbs red light.  Interestingly, Deinococcus-Thermus are non-photosynthetic, but these photoreceptors are found in photosynthetic Chloroflexi as well. This indicates that the deinococcus bacteria likely diverged from chloroflexi at some point but still retained the BphP.
Hope this helped!

Genus is the classification one more general up from species.  Two species in the same genus will be pretty similar - for example wolves and coyotes.  Two things with radically different energy metabolism systems will not be in the same genus.  In fact these different modes of metabolism mean that the creatures using them are so different from each other that they are categorized in different phyla (phylum being the second division after kingdom). Humans are in phylum Chordata with frogs and fish.  Prokaryotes using such different modes of energy metabolism will not be closely related at all.

phyla! so high? need to go to so high level so that they are together?

Is there a website or something that I can determine from the name to know whether does two species are together?

Sure.  Wikipedia has them all.  For example the (super cool!) green sulfur bacteria.  https://en.wikipedia.org/wiki/Green_sulfur_bacteria


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Why are we (humans) more likely to help people genetically related to us than people who are not?

Question. Why are we (humans) more likely to help people genetically related to us than people who are not?

My understanding of this question as follows:
Because the reproduction of people genetically related to us can help us spread our genes. People genetically related to us are also more likely to help ourselves to reproduce.
Is this correct? What am I missing?
I was wondering if anybody had anything, especially intuition or some finer nuances, to add to what I have to say.

Do you have any sources to back up your claim?

Is it a homework question?

Why was this question closed? The idea that humans tend to be altruistic toward genetically related individuals is not outlandish.

This question seems to fall under the field of sociobiology, and more specifically I think kin selection. It's a controversial topic.  If sociobiology is a subfield of biology then it shouldn't have been closed. On the other hand if sociobiology is more of a social science, then I guess it should be asked somewhere else.  Still, it's a very interesting question.

I heard something like this before. E.g. it's important that children look like their parents because if they don't the mother probably cheated on the father. Promiscuous partners increase the chance of catching a disease, and so evolution made monogamous couples more prone to procreating which also helps to root the behaviour. Furthermore humans are social beings and like other primates, we strive together, so our relationships are very important. So much so that we even developed language.

I don't have time to search articles and I was just summing up related anthropological information I came across at some point. But I find your thesis very plausible. Like I said primates are social beings and of course we'll spend more time with family through out our lives, thereby building stronger bonds with genetically related individuals that help us survive as a group. Lots of other species of mammals do that too to some extent: lions and wolves.

It's also a no-brainer that the parents of any living offspring that take better care of their offspring will end up delivering offspring that will survive and succeed more often which is pretty much what you said. More advantages can be drawn from extending this model to less genetically related individuals such as cousins, the culmination of it all being an Italian mafia. :P


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Can I dry digested protein sample over weekend in a vacuum concentrator?
I have digested with trypsin the tissue protein extract for mass spectrometry, and forgot to transfer the sample from the SpeedVac to the -80C freezer. As I did this on Friday, I can transfer the samples only on Monday. Will this temper with my sample and subsequent protein identification?

I doubt there is any quality literature on this question, so the only way to find out is to try it. I suspect it would be fine but you should do some kind of risk analysis to determine whether you should just start again (ie the hassle of preparing a new sample versus the hassle of failed mass spec).

If your sample dried in the speed-vac then it should not cause to much damage to the sample. But if Speed Vac stopped and there was some liquid left, then incubation at room temperature would result in hydrolysis and sample degradation ( also depends on the pH, neutral would be slower). Also you would have modifications to the amino acid side chains like oxidation and deamidation


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Left-handedness and Right-handedness - Are they genetic?
I have a biology book that states that whether a person will be left-handed or right-handed is determined by the genetic constitutional makeup.
Is this true? As far as I knew, these traits depend on how a person is trained as a child: every child has a tendency to use the left hand first when he starts to write, but if the parents teach him, then it will change to the right hand.
What is the truth?

Not true about the writing.  If a normally left-handed person is forced to write with their right hand (as many were in my youth) the result will be a clumsy kid.

Handedness has, like many traits, a non zero heritability. You now should read the post Why is a heritability coefficient not an index of how “genetic” something is? to understanding what heritability mean.
In short, yes part of the variance in handedness seen in the human population is due to genetic variance.
You will note that footedness is highly correlated with handedness (wiki > footedness).
Note also that today, in the western world at least, it is generally considered unhealthy for the kid to force him/her to use its other hand (as the catholic church used to do). I am not sure what are the evidence for that but it is a totally different question.
References

McManus et al. 2013
Brandler and Parachini 2013
Harmour et al. 2014


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What is the difference between transverse section and longitudinal section?
Can anyone explain the difference between transverse and longitudinal section?
Or are they the same?

One passes through long axis of the body while other is perpendicular to it.

For an animal with bilateral symmetry, a longitudinal section is parallel to the anterior-posterior axis (labelled central axis in the image below). Sections through or parallel to either the sagittal or coronal (also called frontal) plane are longitudinal. A transverse section is perpendicular to the anterior-posterior axis and is also called a cross section.

image source


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Is C. elegans always observed with precisely 302 neurons? Are there ever individual viable exceptions?
This answer mentions that the C. elegans hermaphrodite has exactly 302 distinct neurons. This has made it a very effective model for a variety of types of biological research, including neurology and cell differentiation. It is also currently the only organism with a completely mapped connectome.
But the word "always" made me wonder - has a viable specimen ever been verified to naturally have a number of neurons other than 302? Not as a result of an experiment, just naturally?

tag suggestions?

Well, at the most trivial level, males have 385 neurons compared to the 302 in hermaphrodites but I don't think that's what you mean.

@JackAidley Thanks - I've made an edit to reflect that. Assistance always appreciated!

Your comment to an answer made your question confusing. Are you asking whether wild-type C. elegans can develop with more or less neurons or whether natural mutants have been observed that have more or less neurons?

@canadianer The question is worded as intended, and doesn't try to pre-specify how or why it might happen beyond "(n)ot as a result of an experiment, just naturally." I'll add a comment below the one you've mentioned to make sure it doesn't affect interpretation of the question. Thanks for pointing it out!

The mutation studied in this paper prevents apoptosis and leads to mature worms with extra neurons. However, the mutation was induced chemically. https://www.ncbi.nlm.nih.gov/m/pubmed/3955651/

According to the highly respected WORMATLAS: A Database of Behavioral and Structural Anatomy of Caenorhabditis elegans, the number is invariable in this animal, one of the most studied in the world.

There are 302 neurons in the nervous system of C. elegans; this number is invariant between animals. Each neuron has a unique combination of properties, such as morphology, connectivity and position, so that every neuron may be given a unique label. Groups of neurons that differ from each other only in position have been assigned to classes. There are 118 classes that have been made using these criteria, the class sizes ranging from 1 to 13. Thus C. elegans has a rich variety of neuron types in spite of having only a small total complement of neurons. (Emphasis mine)

From the above, you might guess that the number of synapses are not, however.

The full list of synapses for hermaphrodite (including larval stages) and adult male are currently being reviewed and revised for the Wormwiring Project. All data comes from re/analysis of the sections for the hermaphrodite N2U, N2T, N2W and JSE animals, and male N2Y and n930 animals. The total counts of both electrical and chemical synapses are likely to be substantially higher than what was reported in the Mind of a Worm.

Would I be surprised if someone found a different number in a particular  specimen? No more so than when people are born with four kidneys, a parasitized twin, etc.
Edited to Add:
An article, Mutations that affect neural cell lineages and cell fates during the development of the nematode Caenorhabditis elegans has identified mutations with more or fewer neurons:

Specifically, unc-83 and unc-84 mutations affect certain precursor cells that generate both neural and nonneural descendants; lin-22 and lin-26 mutants lead to the generation of supernumerary neural cells with a concomitant loss of nonneural cells; lin-4, lin-14, lin-28, and lin-29 mutants perturb global aspects of developmental timing, altering the time of appearance (or preventing the appearance) of both neural and nonneural cells...

However, access to the paper is restricted, and I don't know if these mutations were induced (most likely were.)
HT to @canadianer for the link that led to my link.

Thanks, this is helpful, and the issue of synapse number and its variation is very interesting. But "I wouldn't be surprised" is not really a satisfying answer to my yes or no question.

That's because people like "yes or no" questions. But the truth is that there is very little in life that can be answered by "yes or no". An oft-quoted maxim in English is, "Nothing is certain but death and taxes." However, even that can't be relied upon. Will you die? Yes. Will you have to pay taxes? It depends.

Have you rarely given yes or no answers in stackexchange?

That is irrelevant to your question.

Rats! I started counting them - you have several high-fliers with very explicit yeses and nos, and was going to create an incredibly eloquent comment pointing them out, but then you brought in logic, and my flow is lost. Hopefully along the way, someone has published an account of a wild-type with an other-than-302 neuron number. I say hopefully because its a lot harder to defend a no in this case, but a yes just needs one example. I saw a four leaf clover once, that's all it took to know they can happen.

The comment above shouldn't have used the term wild type as it speaks too specifically to genetics. The point there is that a yes would require a single example, but a no would be more challenging to support, thus the four-leaf clover example.

@uhoh - Ha! I hope you see the irony of the above edit. It satisfies both of us. ;)

I'll come back again after having sufficient coffee firing neuron number, and see if I can.

Not only is the exact number of cells in C.elegans known but the lineages of each and every cell are known and traced back to the fertilized egg. Neuron map http://www.wormbook.org/chapters/www_specnervsys.2/neurogenesis_fig2.jpg
They are an easy model organism to work with. You can perform RNAi experiments by feeding the worms bacteria transformed with the construct for your RNA. They are transparent, making live imaging easier. Hermaphrodites will produce exact clones of themselves. Plus, if you feel like going home or taking the weekend off, you can freeze the plates and pick it up later.

@anongoodnurse my goodness that's a lot of mutations, and even a lot of mutation-naming citations! I see your point now - it would be surprising not to find an occasional individual hermaphrodite with a neuron number other than 302 if one looked hard enough. That may not be as rewarding as finding a four-leaf clover, so won't be doing any searching very soon. Thanks! - I've now asked the four leaf clover question.

Male C. elegans have 385 neurons http://www.wormatlas.org/male/neuronalsupport/Neuroframeset.html

Many Nematodes do not use traditional hox genes instead the have a strange set up which controls cell placement directly. This means individual adults of many nematode species have the exact same number of cells, it can even be used to identify species. So having the exact same number of neurons is what one should expect in nematodes. https://www.ncbi.nlm.nih.gov/books/NBK26861/
Although they may have two different but none the less exact cell counts due to gender, for instance you often see it written that C. elegans as about ~1000 somatic cells, what they actually mean is males have 959 somatic cells and hermaphrodites (there are no females)have exactly 1031 somatic cells. They count this by number of nuclei since the cell size can vary.
Note that this is also in ADULT specimens newly hatched specimens have only 558 cells, so you could look at newly hatched ones for a smaller neuron count.


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COPI/COPII proteins and kinesins/dyneins
I am considering the transport of protein from ER to Golgi, and have read that this involves the COPII protein coat. I have also read that this is a form of anterograde transport, and elsewhere that kinesins are responsible for anterograde transport as they move from the negative to positive  (outside) poles of the microtubules.
Thus it seemed to me that the kjnesins carry the COPII vesicles carrying proteins from ER to Golgi.
However a Google search of the terms 'kinesins' and 'COPII' together did not seem to yield anything about kinesins carrying COPII.
On the other hand in this article it links COPII with dynsctjn, which I have not heard of before.
Does someone know the link between COPI and COPII transport, and/or retrograde and anterograde transport, with the microtubule motor proteins kinesin and dynein? Where do dynectins come into this? Do they bind the vesicle to the dynein or are they a different type of motor protein? If it is the first case, then why is this transport termed anterograde if it does not use kinesins? Are the terms anterograde and retrograde not directly related to kinesin/dyneins use?

The link in your question doesn't point to any article.

@canadianer Apologies . It seems I did not copy the end of the url link.  I have corrected this now. Thank you for letting me know@

Interesting question. The term anterograde refers to movement in the forward direction. In the context of vesicular trafficking, anterograde refers to (1) movement from the site of protein synthesis in the rough endoplasmic reticulum (RER) towards the Golgi and then (2) movement from the Golgi towards the final destination in the cell.
Both processes rely on microtubules for transport. Microtubules are polar and radiate from the microtubule organizing center (MTOC) with their (+) ends directed towards the periphery of the cell:

There are two broad classes of molecular motors that facilitate directed movement along microtubules. Kinesins are generally (+)-end directed motors whereas dyneins are (-)-end directed:

These images should already give you a hint. Your question may have arisen due to the assumption that the ER is centrally located near the MTOC with the Golgi somewhat peripheral. This is incorrect. In reality, the Golgi complex is actively clustered near the MTOC by movement on microtubules. Furthermore, the ER extends along the microtubule network towards the (+)-end periphery. Taken together, it is evident that microtubule (-)-ends are located near the Golgi and transport to it from any part of the cell, including the RER, requires the (-)-end directed motor dynein. Subsequent anterograde transport from the Golgi to a specific destination in the cell, or through the secretory pathway, requires the (+)-end directed motor kinesin. Retrograde transport from the Golgi back to the ER would also use kinesin:

The article cited in the question (which I also reference in this answer), mentions that COPII vesicles are coupled to microtubules via dynactin. Dynactin is a protein complex that is used to both activate and adapt cargo to dynein (ie COPII vesicles are coupled to microtubules via a dynein/dynactin complex):

Thank you for your reply! Just to make sure I understand correctly, for a secreted protein they would be carried by dynein from the ER to Golgi and then by kinesins from the Golgi to the cell surface membrane? Also, dynactin was entitled in the article as the way COPII bind to the microtubule. What is this third protein?

@21joanna12 Yeah that sounds right to me. I'll edit my answer shortly to address dynactin.


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Why is my blood group O -ve?
My parents have B +ve blood group in fact my brother also have B +ve blood group, then why my blood group is O -ve ?

Due to our being diploid, we have 2 genes for deciding blood type. the gene for blood type O is recessive and so is the Rh-. If your blood type is O- and your parents are B+ then your parent's genes are BO+/- for both of them. and you inherited O AND - from both of your parents.

Humans are diploid organism. So humans have two copies of every chromosome and gene.
When a person has B blood. We mean that the blood cells of that person expresses  the B antigen.
To produce the B antigen you will need at least one allele for the B antigen. Hence the B antigen phenotype can have a genotype of BB or BO.
Now if two people have the genotype of BO have children, a punnet square will show they they have a 25% of having a child with BB genotype, 50% of having a child with BO genotype and 25% of having a child with OO genotype.
Phenotypically, it means that there is 75% chance of having a child with B blood. And 25% chance of a child with O blood.
A similar system also occurs with rhesus +/- system. A person with +ve blood can have a genotype of ++ or +-. If two people with the genotype of +- have children together, there is a 25% chance that their child will have -- genotype and be rhesus -ve.
The two systems work together. So two people with genotype of BO blood type and +- rhesus antigen having children together, they can have a child with O blood and rhesus negative with a probability of 1/16 (6.25%)


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Movement of few ion during changes in membrane potential
My question is very simple: why is it sufficient for a very few ions (such as 1 in 100000 K+) to move across the membrane to generate a remarkable variation in the membrane potential (like a change of 100mV) ??
I took the examples from my university textbook, which, though, doesn't explain the reason behind this statement. Is it because during this event the permeability changes so dramatically that the number of ions doesn't have to be so big?
Can someone help me? Thank you!

See this answer: essentially, it's because when you are talking about the charge from moving ions across a membrane, 100mV is actually not that remarkable, from an electrical standpoint. You only need 1 microcoulomb of charge per sq cm of membrane to change the membrane potential by 1 VOLT and a cell has a lot less membrane than that.


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Help me identify this insect from Bangladesh
I have seen this insect flying literally everywhere in Dhaka city (Bangladesh) over the last two months. It's small -- around 1-1.5 inches long. It's not an agile flyer and can be easily grabbed by hand during flight.

woah wonderful specimen.

This is actually the flying adult of a scale insect (superfamily Coccoidea). Specifically, this appears to be some species of the genus Drosicha.
Here is a picture resembling your specimen:

 Source: John Horstman
And another from Vietnam that looks very similar:

 Source: Dan Doucette
I can only find info on a closely related species, Drosicha corpulenta, and here's a tree of related species.
Scalenet provides numerous keys and references that could be useful for positively IDing this specimen.
I will keep searching for more details, but this might be the best you get without asking a scale insect expert.

Female looks very different. https://flic.kr/p/cysZ9S


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Can hair follicle miniaturisation affect hair color?
We all know that follicle miniaturisation affects hair texture, making it look thinner(the hair shaft/root itself will be thinner), but does it affect hair color as well? So if an individual has thick mid brown hair in his/her 20s, hair follicle miniaturisation kicks in in the 40s. Does this person's hair look light brownish due to hair follicles being thinner, fewer, and they reflect light better? Is my hypothesis right? A thinner hair shaft/follicle reflects light better, ie becomes more transparent? Is this broscience on my part, or am I right? I have a hard time believing that a person's hair color doesn't look lighter/more frail if you will, after miniaturisation kicks in.


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Why do we get scars?
Feeling the hardened tissue of a scar on my head I wondered what the purpose of that scarring is, such skin scars are pretty harmless but from what I understand internal scarring can cause major problems if internal organs get damaged.
An extreme example I vaguely remember is the scarring following nerve damage, the new scar tissue can't transmit signals and so the nerve stops functioning properly.
Why does scarring occur when it seems so detrimental, why don't we rebuild the old tissue?

Scars are fibrous tissue that is left after an injury. The body does its best to fix a body part after an injury and scars are their best attempt at doing so. It would be pleasant to think we could have Wolverine type of healing capacities but we don't and the best we can do are those scars.
The ability to completely regenerate the damaged tissue depends upon the specific tissue. Also, some species are better of than others at regenerating their tissues. Such differences relate to the concept of cellular specialization.
For more information you should have a look at the wikipedia articles

Wikipedia > scars
Wikipedia > Regeneration
Wikipedia > cellular specialization

and the Biology.SE posts

Can a lizard shed a regrown tail again?
Can the regeneration mechanism of lizards be used in humans?

Thanks for the answer! But what exactly makes it so difficult to repair tissue damage for us? An amputated arm or something presents obvious problems but even relatively mild burns tend to cause scarring.

This follow-up question is hard to answer because 1) what you are asking is like asking Why is there not more (or fewer) species?. When asking such thing you should justify why you would expect something else. In other words, asking why is nature as it is? is hard to answer while why is nature not like I would expect for such reasons? is much easier to answer. 2) Because I am an evolutionary geneticists and I know very little about physiology.

I guess I would "expect" that organisms try their utmost to restore original function after damage so scarring seems a somewhat weird phenomenon when viewed this way. Surely there must be some evolutionary advantage?


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What plant is this, seen at the Allan Gardens?
I tried a couple of apps on my phone, but I could not identify this flower and plant species.  These are at the
Allen Gardens Conservatory, at the beginning of Spring in Toronto.

This is a Schizanthus "orchid" (actually not a real orchid) called Schizanthus pinnatus ("butterfly orchid" or "poor man's orchid").

It is native to Chile but the plants are also cultivated as ornamentals. It is commonly known as the "small butterfly" ("mariposita") or "small, white butterfly" ("mariposita blanca").

Description

Annual plant of 20-50 cm in height
Stem: Glandulous-pubescent
Leaves: 2.5-3 cm long; pinnatisect (divided into 6-8 pairs in oblong-linear segments, entire or separated).
Flowers: white, pink or violet, 2-3 cm diameter, arranged in panniculate inflorescences, sometimes dichotomous.


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Where can I get my exomes sequenced?
I am a private individual and I want my exomes sequenced, I don't know of any place that will keep my data confidential as I read reports of companies sharing this data with insurance companies. I tried looking into a number of university research centers but none of them sequence DNA of private individuals. Does anybody know of any university that does WES of individuals or a place which can keep my information confidential? Many thanks in advance for your replies!

There are private companies that sequence DNA; you have to pay for it. They would have legal documents in place to maintain the confidentiality of the data. Or go to your nearest university/research institute and offer to provide samples in exchange for some information (that you'll not disclose until they allow you to). That said, your question is off-topic because it is not about a biological concept.

Most companies will genotype a number of SNPs but won't do full exome sequencing. Is there any reason you'd want your exome sequenced? With SNP association studies we have, one can already tell quite a bit about health related questions. 23andMe for example does a good job on this matter.

May I ask why you want your exome sequenced? Depending on what information you'd like that may or may not be the best approach.

I will be doing my own whole genome sequencing soon. The best reputable company I've found is Veritas. For 999 dollars and at a pretty decent depth (30+ reads).  They will produce a canned report of diseases and traits similar to cheaper alternatives, but also for another $100 will provide you a complete Variant File.
My understanding is that they will only use your data after anonymization for scientific endeavors, but I still need to finish reading the fine print. See here under privacy.  Good luck!
p.s. I also would skip exome and go with WGS since the price has come down. More and more diseases and traits are being linked to variation in intergenic regions of DNA.

The two companies you are most likely looking for that perform DTC whole exome sequencing are Genos Research and Full Genomes Corporation. Both companies make a Promethease compatible file format and provide a BAM file.
Full Genomes Corporation provides full genome sequencing at various depths, exome sequencing, genome depth ancestry service, and BAM file interpretation. They don't have the most user friendly service, but I'm told they aren't too hard to work with either. I didn't see anything in their privacy policy to suggest they are sharing your data to research.
https://www.fullgenomes.com/
Genos Research is a small company that sends out your sample to be sequenced. After 9 weeks they provide a variant report, BAM file, a VCF file, and a file formatted specifically for Promethease. They don't share your information. Instead they present to you a list of research projects they hope you will volunteer your data in exchange for money. https://genos.co/
Another option you have is the Personal Genome Project. Their goal is to establish a public database of genomes and medical records. This is one were if you don't mind the privacy risk they will sequence your genome as they have funding to do so. It might take them some time to get around to your samples. They also want your medical records and other information.
Personal Genome Project is deidentified. So a person can't just google to see if someone is a member of the PGP. But it is possible to take the genetics and demographics information and search for an owner name in public databases. It is not hard to prevent such searches by making small alterations to your date of birth, broaden your area of residence, and keep your data out of DNA ancestry databases. On the other hand some people are proud to release their identity and information to the public.
http://personalgenomes.org/
Veritas Genetics. They only provide full genomes, and clinical products. My understanding is you will need your own doctor to approve the test, whereas Genos Research provides it on staff. For 999 dollars they will provide the same information that Full Genomes Corporation if you buy their full genome product. Their VCF file isn't fully compatible to Promethease, so it is of limited use on third party tools. You could hire Full Genomes Corporation to generate such a file if you wish. You have the option of volunteering your data for research. I guess they donate your information to the Personal Genome Project if you agree. They can also for an extra fee perform a clinical evaluation of specific genes.
https://www.veritasgenetics.com/mygenome
These is also Gene By Gene. They do mostly clinical evaluation and research. But they are user friendly to the person that wants to spend, in my opinion, too much to get their exome or genome sequenced. They are the company behind FamilyTreeDNA. https://www.genebygene.com/pages/research
For those whom don't know, Promethease (https://www.promethease.com/) is a third party tool for generating a health report using a genetics test and the SNPedia wiki. It was meant to be free, but since it involves heavy amounts of server usage they charge a small fee to cover the cost of service.


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Excercise and fitness in old age
I have seen so many news and study online, saying exercise keeps body healthy in old age and keeps us fit? how is this possible normal tear and wear will become more with activity hence more mutation hence more loss. Why exercise help?
Tear and wear means lots of regeneration in our body, regeneration will lead to mutations, no regeneration is perfect, hence more regeneration's, more risk of bad DNA.

Simplistically, the body repairs itself, and in reaction to the repair, often makes itself stronger.

If you decline 80% from a marathon runner you can do a 10k, if you were a coach potato now you are a vegetable.

@jamesqf - I wish that myth were put to rest where it belongs!

@anongoodnurse Specifically which myth?

@jamesqf repair means mutations

@murmansk: I really don't understand what you mean by "repair means mutations".  Do you mean accidents leading to imperfect repair?  In any case, it seems as though you're arguing from what you think SHOULD be happening, and ignoring a mountain of observational evidence that "it just ain't so".

@jamesqf - Repair does not leave things better. Healed fractured bone does not become better than unfractured bone (it's worse) unless it's fixed with titanium. A scar does not become stronger than the surrounding skin; it's weakened and less organized than normal skin. Etc. Otherwise sports injuries would never be devastating, etc. That's why studies are done on factors that improve healing.

@anongoodnurse: Yet when you stress a muscle by e.g. lifting weights to the point of exhaustion, it becomes stronger.  Likewise with aerobic exercise: stress heart & lungs, and they increase their capacity.   And (as you point out in your answer) when you stress bone, it becomes stronger.  Of course you can carry this stress/repair too far, to the point that it causes damage, but (at least to me) that seems less risky than idleness.

@jamesqf - My reaction was not to stress (I agree with that); it was to your comment, "the body repairs itself, and in reaction to the repair, often makes itself stronger."

If repair happens means there is duplication of cells and as I understand no replication is perfect, hence it will cause deleterious mutations, reason we get old and die or we get cancer

@anongoodnurse: So it seems that what we're differing about is not the process, but the language used to describe it.

@murmansk: Except for the observed evidence that a sedentary person who does not undergo that wear & tear of the stress/repair cycle is highly likely to die much earlier than one who does, and is likely to suffer from many diseases while they're still alive.  So however much you may like your theory, there is abundant evidence showing that it's flat-out wrong.

Not all "wear and tear" is bad. I will provide only one example. Trust me, I can provide many more, but I think one is sufficient to answer your question.
Exercise (against resistance, e.g. even gravity) is known to strengthen bones, for example. The stronger your bones, the less likely they will break as a result of a fall. While that sounds kinda "meh", it's incredibly important in the elderly, because once they sustain a fracture, their activity level falls dramatically for fear of sustaining another fall/fracture. Because of this, they have a decrease in muscle mass, a decrease in lung capacity, a decrease in cardiac fitness and an overall acceleration in decline of motor function, as well as a decreased quality of life.

Low-impact fractures, commonly called fragility fractures, have even higher mortality. Older patients with injuries from a fall have five times the mortality that their same age colleagues have from injuries from MVCs (motor vehicle accidents.) Five-year survival after an osteoporotic hip fracture is similar to that of patients with breast or other cancer. Almost one in 13 (7.5%) of those with fragility fractures will die within 90 days of fracture.* ...A fracture can be a devastating blow to an older adult’s health and independence, decreasing functional status and quality of life permanently. While some may recover their independence, half of older adults will require home health care in the 6 months following a fracture, and many will have long-term functional decline.

"Wear and tear" is good for muscles, bones, the heart, the lungs, balance, proprioception, and a number of other systems which help to prolong life, as well as the quality of life.
*Mortality is mainly with regards to hip fracture.
Fractures in Older Adults


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Standard Free energy of hydrolysis of phosphoenolpyruvate (PEP)
In ATP we have two anhydride bonds, each with a Standard Gibbs free energy of hydrolysis ~ -30 kJ / mol and one phosphoesterbond of ~ -20 kJ/ mol, if my notes are correct.
In phosphoenolpyruvate (PEP) we also have a phosphoester bond, but the Standard Gibbs free energy of hydrolysis is three times higher, at ~ -62 kJ / mol.
How does the double bond / enol form contribute to this high free energy of hydrolysis?

I have edited your question so that it is clear that it refers to free energy of hydrolysis. Chemical compounds do not have energy in isolation, so the term "high energy" should be avoided.

An answer to this is given in the online version of Berg et al.

Why does phosphoenolpyruvate have such a high phosphoryl-transfer potential? The phosphoryl group traps the molecule in its unstable enol form. When the phosphoryl group has been donated to ATP, the enol undergoes a conversion into the more stable ketone—namely, pyruvate.

Thus, the high phosphoryl-transfer potential of phosphoenolpyruvate arises primarily from the large driving force of the subsequent enol-ketone conversion

Note that Berg et al. use the term “high phosphoryl-transfer potential” or “high phosphoryl group-transfer potential”, as explained in sections 14.1.4 and 14.1.5. These sections are worth reading, and this terminology is worth following.

Thank you very much and also tomd for the adding comment!


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How did the felines get to America?
I don't know if the felines got originated on America or on Africa, but I do know there are species of cat in America and Africa that belong to the same family and genus (Felidae & Panthera).
How did the evolution of these animals beat the vastness of the ocean? The same way as Homo sapiens? Or did they coexisted before Pangea split?

There are species of felines native to Eurasia, so it's not as though there is a great gap, either geographically or genetically.

Short answer
It is believed that low water levels occurring several times during the last ten million years facilitated migration and divergent evolution of the felids. The North-American ocelot, lynx, puma, leopard cat, and domestic cat are believed to have evolved from a common ancestor that crossed the Bering land bridge between 5 to 9 million years ago from Eurasia. Note that Pangea broke apart 175 million years ago, way before the Age of Mammals even started, 65 million years ago.
Background
It is believed that modern felids arose in Asia with the divergence of the genus Panthera 10.8 million years ago (Mya) and the bay cat lineage 9.4 Mya. These dates correspond to the low sea levels that occurred during the late Miocene (Fig. 1). Between 8.5 to 5.6 Mya a progenitor of the caracal lineage arrived in Africa. The common ancestor to five felid lineages (ocelot, lynx, puma, leopard cat, and domestic cat) migrated across the Bering land bridge to North America, referred to as the New World migration. This period is also believed to have facilitated migrations of the Eurasian carnivores (ursid, procyonid, mustelid, and saber-toothed felids) to North America.
Additional Pliocene/Pleistocene migrations paved the way for the differentiation of the cheetah, originating from the North American puma and migrating to central Asia and Africa. Reversely, Asian Panthera species spread into America (jaguar, lion) and subsequently into Africa (lion and leopard).

Fig. 1. Global migrations of felids. source: Johnson et al., (2006)
Reference
- Johnson et al., Science (2006); 311: 73-7

I thought modern domestic cats were originally bred from wild cats of Egypt and the Middle East.


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

Hmm, interesting question. I think there are 2 aspects. 1: As the range of frequencies increases then input of signals increases which needs a better brain. 2: Since visible spectrum has wavelength in range of nm but otherwise like radio are in metres to KMS in wavelength, I think neurons( or other special cells) could not act like antenna , so there will be limit .

"...approximately 350-700nm, because that form of light is most common to our lifes." This is not correct. It just so happens that we evolved to see in this spectrum.

@anongoodnurse it is certainly no coincidence that it just happened this way. I am on my phone so I cannot link it, but there are charts that show the amount of light that reaches earth.  Most of it is light between 350-700nm. It is crucial for survival to see colour and therefore we evolved into seeing it.

There are some limits on what light can be detected biologically based on physics and chemistry. Although there are animals that can sense more UV or more infrared than humans, they are still subject to these limitations.
How Vision Works
The way most types of vision operate is by using photons to cause a conformational change in an opsin protein by influencing a chemical bond in a sensitive molecule (a chromophore, for example retinal, which changes from 11-cis to all-trans) bound to the opsin. To sense a particular wavelength of light using this mechanism, it is necessary that the energy of the light is sufficient to cause this chemical change in the opsin-chromophore, without being enough energy to destroy the molecule entirely by breaking a bond.
Sensing low-energy (long wavelength) light
Longer wavelength light ('infrared') is also known as heat. Detecting "heat" photons is difficult because they don't have much energy. Therefore, you need a molecule that is very sensitive. It turns out that the opsin-based vision strategies use chromophores that are too stable to sense long wavelength light.
Some snakes have particular sensitivity to infrared, for example the pit viper. However, these animals do not "see" infrared using their eyes: they have another specialized organ called the pit organ. The pit organ uses receptors that are much more like the heat receptors in your skin than the photoreceptors in your eye, but the pit organ uses a pinhole camera effect to organize the incoming light onto a very sensitive heat-sensitive membrane.
Humans of course are able to sense infrared, too, but the same way: through the skin rather than the eyes, and at low resolution. However, if you stand outside in the sun and close your eyes, you can probably still "see" the direction of the sun: one side of your body will feel warmer than the other! In a way, this is like a form of low-resolution "vision" if you want to define that term very broadly. The snake's infrared sensitivity is more like this sensation than eyesight.
When you get to very long wavelengths, for example radio waves, the wavelength is too long and too low-energy to even be relevant at a molecular level: these forms of light will travel right through cells, and individual photons don't carry enough energy to influence molecules in ways that can be sensed by biology.
Sensing high-energy (short wavelength) light
Very short wavelengths of light have the opposite problem: too much energy. Ionizing radiation (from the upper ultraviolet range and shorter) has enough energy to actually free electrons and create ions. This type of radiation damages biological molecules, including DNA, so organisms have a lot of good reasons to avoid these types of radiation. Exposure to short-wavelength radiation can also cause bleaching (permanent destruction) of photosensitive molecules and potentially damaging heating of tissue surrounding pigments, in addition to direct effects on other molecules in the cells.
Insects and other organisms that can see into the UV range see mostly in the near-UV range, >300nm, not too far from our own vision range (roughly corresponding to "UVA"). However, it isn't true that humans can't see these wavelengths due to some lack of sensitivity of our photoreceptors: instead, UV light is (at least partly) blocked by the cornea and lens, presumably to protect the retina from damage!
Humans and other organisms do have some sensitivity to damaging UV wavelengths, just not through vision. Instead, humans and other organisms sense UV based on the damage done within cells, which recruits repair mechanisms and apoptosis to prevent damage from leading to cancer.
Summary:
The chemical processes behind vision determine the range of potential wavelengths that can be sensed. Animals on earth are able to sample from this entire range. Mechanisms to sense wavelengths outside that range would require wholly different approaches, and maybe even a unique biochemistry. The mechanisms would have to be so different that we probably wouldn't refer to those mechanisms as "vision" (for example, even the infrared sensitivity of the pit viper isn't really though of as vision) but we would come up with a new term, such as "radio sensitivity" or "radiation sensitivity" just like we have different names for "hearing" relatively high-frequency pressure waves with the ears but we have "vibration sensitivity" for low-frequency pressure waves felt through the skin.

A very informative answer. However is it possible that some species could evolve a "sight" process not based on opsin? For example could a species evolve a structure capable of receiving AM radio? This article (https://www.seas.harvard.edu/news/2016/12/world-s-smallest-radio-receiver-has-building-blocks-size-of-two-atoms) describes a very small radio that is "biocompatible". Although using "sight" to describe this wouldn't match the current meaning of the word very well.

@Χpẘ Yeah this is exactly what I was referring to in my Summary: I think the pit viper is a great example of a place where we might colloquially say vision, but if I search Google Scholar for "pit viper infrared" the scientific literature mostly if not exclusively refers to vision only in quotes; the other terms used are "infrared detection" or "infrared imaging"; it's a stretch to call it vision because it isn't from the eyes.

@Χpẘ Also as far as biocompatibility in the article you linked, what they are referring to is that diamonds don't cause an allergic/foreign body response. No known biological mechanism can create diamonds nor substitute single carbon atoms in a diamond with nitrogen.

Yes, but that doesn't mean an evolution isn't possible. Another example, IBM has built a radio out of a carbon nanotube. Looking at the future from the point of view of earliest life, I'd venture that it wasn't predictable that human sight was in the future (setting aside for a moment the question of who would've been making predictions!). The OP says "eyes theoretically evolve" which is fairly ill-defined. "Evolution" is not even limited to earth based evolution. Second "theory" could refer to a host of disciplines, such as physics, genetics, etc. Third, meaning of "eyes" would likely change.

@Χpẘ There is "possible" in a science fiction sense and "possible" in the sense that it could happen from known biological principles. I agree that if one leaves behind known biology in favor of non-earth based life origins and completely different biological paths that a lot is "possible" but it mostly belongs on WorldBuilding.SE, not Biology.SE.

"known biological principles" doesn't include unknown biological principles. Unknown biological principles aren't SF, they are merely not known. It wasn't too long ago (75 years?) that life surviving in temperatures above 100 C would've been SF. Radioresistant organisms are a lot more common than was thought prior to Chernobyl. It's a mistake, IMO, to equate what is known to what is possible (in real sense, not SF)

@MrX In this answer I write: "Exposure to short-wavelength radiation can also cause bleaching (permanent destruction) of photosensitive molecules"; what is the intent of your comment?


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Why mushrooms have so much antibiotics?
Why they have much more antibiotics than plants for instance?

https://en.wikipedia.org/wiki/Plant_disease_resistance exists but no similar one for fungus.

The discovery of natural antibiotics seems to have been most successful in molds like the fungal species  Penicillium chrysogenum and the bacterial species Brevibacillus brevis. As @notstoreboughtdirt points out, plants have their own mechanisms. It's not quite clear what you want to know since a complete answer could be a thesis.

This isn't fully understood but one theory is that they live in soil feeding off dead things and so are in competition with bacteria and other fungi for resources including space.  The antibiotic compounds they produce have been described as a sword and shield.  Some compounds are offensive (sword) and attack other fungi and bacteria while other compounds protect a species (shield) from the compounds of other organisms seeking to do the same thing to them.  This is only half the story really, fungi also excrete compounds that look similar to antibiotics but have no known function.  Still other compounds have seemingly no effect on other organisms but when taken by humans and other mammals lower cholesterol in the blood. Strange thing for a fungus to produce.

Hi and welcome to Bio.SE. Whilst the question itself is likely to be closed, but generally, answers here should be well cited. Personally, I'd be interested to find out more about the additional excreted compounds.


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Why do certain ferns have roughened spore surface?
Ferns such as Anemia phyllitidis, Blotiella lindeniana, Ctenitis hirta, Cystopterix fragilis, Hemionitis palmata and many others have roughened splity spore surface.
I ask, why is it evolutionary so? Does it have something to do with Equisetales spores, which has long derivates to join up together to spread more effectively? Or more like a convergention with polen of Asteraceae, which is morphologically adapted to zoogamy?


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Parents that eat their own children
I am told that there are some species, like fish or rabbits, that if let, will eat their own children. If this is true, how does a species like this exist? Shouldn't the fact that they kill their own lineage make them nonviable?

Just keep the offspring away from the hungry adult.

You assume there are many chances the parents individuals can even meet their offspring. This doesn't hold true in a variable environment like the one most species in Nature normally live in. I will give you one simple example. When I was a child I had an aquarium with little tropical fishes in it. In this closed space (non-natural environment) the very parents ate their own children when they were still very yound and no child fish could get to adulthood. However, if these very same fishes were living in Nature-like in some small river or marsh or any other natural pond,

their youngsters wouldn't even had the chances of meeting their parents (and being eaten by them) because immediately after hatching the small fishes would have gone into hiding among the vegetation in this natural pond and because they re small enough to hide easily they would most likely never have met with their parents (and thus avoid being eaten by them). There are many other similar cases with other animals where the hatchlings are so small they virtually live in other environment then their parents live in.

Rabbits (at least in captivity) will only eat their young if there is a protein shortage. Obvioulsy, any aminal that eats its young doesn't eat all of them.

Yes, it is true.
Prairie dogs
Prairie dogs for example are known for frequent infanticides.

Many other species kill their babies too
But of course, such behaviour also exists in other lineages such as grey langurs, gerbilles, lions, giant water bugs and Bottlenose dolphins (just to cite a few examples).
How does that evolve
It will be impossible to provide a complete universal explanation to this behaviour because the evolutionary processes causing this behaviour varies from lineage to lineage. For examples, in lions, only males kill young of the females that are still nursing and they do so when taking over a new harem only. In prairie dogs, mothers cause infanticide preferentially on others' babies but also on their own babies.
Going into the details of how such behaviour evolves in every specific lineage would probably require writing an intro on kin selection and other fields of evolutionary biology which is way too much for a single post. You may want to have a look at the wikipedia article infanticide for a start.

Shouldn't the fact that they kill their own lineage make them nonviable?

Of course, they don't kill all the babies. Only a fraction of them!

"In prairie dogs, mothers cause infanticide preferentially other babies but only its own babies." - Could you rephrase that? I'm having trouble understanding which infants the prairie dog mothers tend to kill.

@HarrisWeinstein Thanks for noticing the typo. Fixed!