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Why do humans have eyebrows?
Why do humans have eyebrows? It seems that it isn't necessary but only humans have them, correct? So what is the use of them for humans? I hear that they protect our eyes. However, isn't that what eyelashes do? What other functions do eyelashes have?

I think apes have them,  look up chimpanzee picture.

I'm voting to close this question as off-topic because it shows no research effort

Eyebrows function to protect the eyes from perspiration and provide shade.
Eyelids function to protect the eyes from foreign objects and sunlight.
Eyelashes function to protect the eyes from foreign objects, produce sebum (a lubriant that the eyelids) and acts as protection for the eyes from tears [1].

The above seems to be backed up by health how stuff works and the anatomy of the eye from emedicinehealth.
However, note that biologist dont have any concrete reasons for the eyebrow. This is just what many of them agree on I suppose. Here is another resource from sciencefocus.

What about facial expressions?


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Are there differences in DNA between humans of today and humans from 2000 years ago?
Are there any significant differences in our genome compared to the genes of our ancestors from 1000-2000 years ago?
And if there are significant differences, do they result in significant differences in phenotypic traits?

It's a huge leap from "differences in DNA" to "differences in traits."

I don't understand the negative votes: there is some confusion in the DNA vs trait, but the question is still interesting

Exactly, I wouldn't understand down votes either. "[D]ifferences in the genome" is a legitimate question. While one may at first think of sequence changes, and some mitochondrial and Y-chromosome haplogroups may have arisen within about 2000 yrs ago, changes at the level of methylation, acetylation and other levels fits the question.

The larger differences are most likely in epigenetic marks on the DNA. The environment is a lot different today than it was 2000 years ago and those differences are stronger determinants of epigenetic change than sequence change.
2000 years is only about 40 generations and that is not very much to see great differences in DNA sequence or allele frequencies - once founder populations are removed from the analysis.
Height is highly influenced by genetics, but can be masked by environment - notably diet. Diets higher in protein content are more likely to elicit the expression of the "height alleles" but only to a point as too much protein is also unhealthy.
Added in Edit 4 Apr 2012: I should add that my response is written from the perspective of frequency of alleles or epigenetic marks across a population.

Not all enviromental influences are inheritable through epigenetic marks. Have you any evidence of epigenetic changes in human population?

I did not imply that the epigenetic changes are heritable. The environment changed over the last 2000 yrs and some of those changes are constantly acting upon the genomes of successive generations. The question asked about a comparison of a current human genome with one from 2000 yrs ago. Because the environment is different, I expect that population-wide we would see differences in epigenetic marks.

In the literature, there are examples of DNA analysis from very old specimen. For instance, look at the analysis of both nuclear and mitochondrial DNA from 62 buried humans exhumed from a Mongolian cemetery dating from 2,000 years ago, as described by Keyser-Traqui et al. 2003, Am J Hum Genet 73(2): 247–260. Despite, the publication is open-access, the DNA sequences are not available, and no comparison with current mongolian DNA has been described in the study, but for sure your question should be answerable.

It depends on what you define as significant.
The mutation rate in human that I manage to find is given as about 140bp per genome per generation
http://sandwalk.blogspot.com/2015/04/human-mutation-rates-whats-right-number.html
2000 year ago is 40 generations. So that is about 5600 bp on average in a genome of 3200 million basepairs..... 0.000175% as calculate. Next to impossible to find.
Is that significant?
Functionally... most mutation that are inheritable though multiple generations are silent mutation.. which have neither negative or positive effects. (Negative mutations are weeded out relatively fast).
So are all these mutation silent? No, some actually do things... and these are mutations are usually related to the immune system... better able to survive disease like measles, black plague, smallpox, etc.
So they these changes significant? Well.. yes... in that if you don't have those DNA changes you would likely die. Yet those changes are minor structural changes to the proteins receptors that those pathogens use to get into a cell. So extremely minor. THe proteins are still able to do their natural function but are just different enough that pathogens do not have a free pass like smallpox had with the native americans.

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Why sperm count matter for pregnancy?
In order for a woman to become pregnant, sperm is needed. Why is sperm count so important for pregnancy?
http://en.wikipedia.org/wiki/Sperm

It's more than just sperm count that matters for a pregnancy if you are considering normal methods of insemination such as intercourse or assisted methods such as artificial/intrauterine insemination or in vitro fertilization. For couples having trouble getting pregnant, most OB-GYNs and/or Reproductive Endocrinologists/Infertility physicians do a semen analysis. This involves checking several things:

Ejaculate Volume (>1.5mL)
Sperm Concentration (>15million/mL)
Motility (>40%)
Morphology (>4%)

(and a host of other factors including rapid progressive motility, pH, etc). Why? Because there is no point of there being high numbers of sperm, if their motility is poor, because they won't be able to reach the oocyte. There's no point if they can reach an oocyte, if they are poorly shaped and cannot penetrate it. There's also no point in there being a high concentration of sperm, if the ejaculate volume is so low that it thins out before reaching the cervix. All these factors matter.
Total Motile Sperm Count (TMSC) is the most common way that physicians determine what route is best to increase chances for getting their patients pregnant.
TMSC = Concentration x Ejaculate Volume x % Motile (in decimals). Thus if, the value is:

greater than 10 million = normal male factor; check anatomy, check female causes
less than 10 million = low male factor; consider intrauterine insemination (IUI)
less than 5 million = severe male factor; consider in vitro fertilization (IVF) with intracytoplasmic sperm injection (ICSI)

Sources:

Paper 1
Advanced Fertility

As sort of a generic textbook answer, there's a number of factors. The vagina tends to be acidic, much so it's within a range of intolerance for sperm. To counteract this, seminal fluid is often alkaline in nature (1). The cervix also tends to be covered in a mucus that sperm must penetrate to enter the uterus. On top of factors like sperm lifespan, tolerance to vaginal environment, etc. the necessary numbers to actually achieve fertilization is important.

authors: Алексей Павлов

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Mammal vs Placental Mammal
So for Google Earth Day's quiz I ended up being a "Pangolin." Turns out I had no idea what it was so I looked into it and honestly it reminded me a lot of an Armadillo. So I decided to find out the difference between the two, and I stumbled across this site.
It was all making sense until I got to the "bullet points" at the bottom where I saw this

Pangolin is a mammal while armadillo is a placental mammal.

And I'm now very confused. I thought placental mammal was just a subset of mammals. And I look up Pangolin's taxonomy and now I'm seeing all kinds of stuff I have no idea how to interpret. Back in my day, it was "Kings Play Cards On Fat Green Stools" for "Kingdom Phylum Class Order Family Genus Species". And now I'm seeing things like clade, infraclass, subcohort, superorder and all kinds of things I just don't get.
So I guess I have many questions, but I'm going to boil it down to "If the Pangolin isn't considered a placental mammal, then what kind of mammal is it, and where does it diverge in taxonomy from the Armadillo?"
Oh, and if someone could point me to a primer on the changes to taxonomy in the last 20 years, that'd be cool too.

Both are placental mammals.

Although the Kingdom Phylum Class Order Family Genus Species version of taxonomy is still being taught, it's mostly for convenience's sake. The truth is all higher named clades (like Genera or Orders) are chosen somewhat arbitrarily. So, if people want to talk about a clade that, say contains all of the organisms of several genera but not all of the organisms in the family, they might talk about it as being a subfamily. In short, I would say don't waste your time worrying about the difference between an infraclass and superorder and focus more on comparisons between clades

From the Tree of Life page for Mammalia:

All of these groups of animals are mammals, including extinct triconodonts and multituberculates. Among living mammals are monotremes (most notably the platypus), marsupials (kangaroos and opossums), and eutherians. Eutherians are placental mammals, so all eutherians are placental mammals, but not all mammals are eutherians.
Both armadillos and pangolins are eutherian mammals, so both are mammals and both are placentals. "Difference Between" is quite incorrect.


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MHC restricted peptide
What is an MHC restricted peptide?
I got this definition from wikipaedia, but cannot exactly extract what the phrase MHC restricted peptide means.

MHC-restricted antigen recognition, or MHC restriction, refers to the fact that a given T cell will recognize a peptide antigen only when it is bound to a host body's own MHC molecule. Normally, as T cells are stimulated only in the presence of self-MHC molecules, antigen is recognized only as peptides bound to self-MHC molecules.

I have not studied biology since last 8 years and now I am going through it because I need it for my research. So if someone can describe it in simple language it would be very helpful.

First of all MHC stands for major histocompatibility complex. There are two types of MHC.
MHC type one is present on all of our cells with a nucleus. The purpose of these protein complexes is called antigen presentation. T-cells cannot recognize free antigens on their own, it has to be presented to them in the proper way. This is what these proteins do. In every cell there are lots and lots of proteins, that get digested to small polypeptides (short aminoacid sequences) by proteases during the natural recycling process. The cell takes a small portion of these polypeptides and presents them on its surface through MHC I complexes, that the immune system can read. This is like the cell saying to the immune syytem that "hey I got these proteins in me". Now if the cell is infected (by a virus most likely) then the "attacker's" proteins get digested and presented as well and its like saying " hey I'm infected and the attacker has these proteins".
MHC II serves similar function but it is only present on professional antigen presenting cells (APCs). These complexes present peptides derived from proteins consumed and digested through phagocytosis or receptor mediated endocytosis. It's like saying "hey we got a larger attacker and it has these proteins"
So, long story short T-cells cannot recognise antigens on their own it needs to be presented to them on MHC complexes and then and only then can they be activated.
Edit: A list of useful articles in the topic of antigen processing / presentation for further details:
January 14, 1998 14:59 Annual Reviews AR052-12
Annu. Rev. Immunol. 1998. 16:323–58
MECHANISMS OF MHC CLASS I–RESTRICTED ANTIGEN
PROCESSING Eric Pamer and Peter Cresswell
Cell, Vol. 76, 287-299, January 28, 1994.
MHC-Dependent Antigen Processing and Peptide Presentation: Providing
Ligands for T Lymphocyte Activation
Terry Y Nakagawa, Alexaiider Y Kudensky
The role of lysosomal proteinases in MHC class Il-mediated antigen processing
and presentation
This one may require subscription.
and the wiki page :)

I would also like to add an analogy to poka.nandor's answer that I used to explain my girlfriend (who studies law lol) MHC restriction. Imagine you have a plate and a sandwich. When the sandwich is not on the plate you do not know that it is a sandwich. When someone puts the sandwich on the plate you suddenly realise it is a sandwich. Basicly T-cells require the context of the MHC to recognise peptides.


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Chickens roosting, is it sleep or torpor?
At night when they roost, do chickens experience a state of sleep (meaning do they move from NREM1 to NREM2, NREM3 and REM) or are they in a state of torpor (reduced metabolic rate and decreased physiological activity)?

To answer the question, I assume it would require someone to have done polysomnography on a chicken. Assuming chicken EEGs look like humans. Now that is a funny picture!

When birds sleep, they do experience NREM sleep [1]. Furthermore, Kavanau (2002) concluded that NREM has evolved in warm blooded animals [2].

Birds provide a unique opportunity to evaluate current theories for the function of sleep. Like mammalian sleep, avian sleep is composed of two states, slow-wave sleep (SWS) and rapid eye-movement (REM) sleep that apparently evolved independently in mammals and birds. Despite this resemblance, however, it has been unclear whether avian SWS shows a compensatory response to sleep loss (i.e., homeostatic regulation), a fundamental aspect of mammalian sleep potentially linked to the function of SWS. Here, we prevented pigeons (Columba livia) from taking their normal naps during the last 8 h of the day. Although time spent in SWS did not change significantly following short-term sleep deprivation, electroencephalogram (EEG) slow-wave activity (SWA; i.e., 0.78-2.34 Hz power density) during SWS increased significantly during the first 3 h of the recovery night when compared with the undisturbed night, and progressively declined thereafter in a manner comparable to that observed in similarly sleep-deprived mammals. SWA was also elevated during REM sleep on the recovery night, a response that might reflect increased SWS pressure and the concomitant 'spill-over' of SWS-related EEG activity into short episodes of REM sleep. As in rodents, power density during SWS also increased in higher frequencies (9-25 Hz) in response to short-term sleep deprivation. Finally, time spent in REM sleep increased following sleep deprivation. The mammalian-like increase in EEG spectral power density across both low and high frequencies, and the increase in time spent in REM sleep following sleep deprivation suggest that some aspects of avian and mammalian sleep are regulated in a similar manner [3].

From the Abstract and reference [3] above, we see that EEGs have been taking on birds and show that birds enter REM and SWS similarly to mammals.

In response to Chris Stronks, researchers have also studied chickens see Evolution of Sleep: Phylogenetic and Functional Perspective by Patrick McNamara, Robert A. Barton, Charles L. Nunn. In the section for REM sleep in birds, the studies were conducted on pigeons and chickens see pages 204-205.

Although not directly disagreeing, I have to say: but what about chicken? The class of Aves is pretty big, and as the question was on chicken you may be over-generalizing?

@ChrisStronks understood but the other articles establish birds have rem sleep since they are warm blooded and chicken are birds. The last article was to show that researchers have measured EEGs of birds to show it is true.

@ChrisStronks studies were performed on chickens as well. See link.

@ChrisStronks not a problem.

Well done @dustin. My wife wins the bet!

@BenPlont my bad. I bet you wanted to win.


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Evolution of dominance of alleles
Can someone tell me where can I find detailed text about mechanisms of evolution of dominance? Or, if it is possible, I would be grateful if someone will tell me about them here.

Why was it downvoted? Because it is asking for both (it is a either or format actually) a book-recommendation and a review?

And do you have any particular theory in mind? YOu might want to read this  for background knowledge ( Bourguet, Denis. "The evolution of dominance." Heredity 83.1 (1999): 1-4. )

Welcome to Biology.SE!
I am not aware of any book that talks extensively about the evolution of dominance. It is a very interesting field of research. You can probably search for papers on the subject that will go much further than my below answer. For example, you may want to read Mayo and  Burger (1996), Bourguet (1999) and Billiard and Castric (2011) I hope that my answer below can provide the ground for more searching by presenting the two main (and of historical importance) hypotheses.

There are several hypotheses about the evolution of dominance. It is important first of all, to note that empirical observations show that beneficial alleles tend to be more dominant than detrimental alleles. There are a number of hypotheses and I won't be able to make a complete review. Among the two main hypotheses to explain the evolution of dominance, one has been formulated by Ronald Fisher and one by Sewall Wright (and J.B.S Haldane).
Fisher's hypothesis
According to Fisher's hypothesis, between two equally beneficial alleles, if one is more dominant than the other than it's heterozygote carrier will have higher fitness. In consequence, beneficial alleles evolve to become more dominant while detrimental alleles evolve to be recessive (so that they can hide from selection in heterozygotes). The main criticism to this model is that selection for dominance is possible only when the locus is polymorphic. This means that the strength of selection for dominance is of the level of the mutation rate, seemingly way too weak to explain the observed pattern of dominance.
Wright's hypothesis
According to Wright's hypothesis, beneficial alleles are more dominant because of the kinetic of biochemical reactions. The rate of a biochemical reaction is a function of the concentration in the substrates of interest. The function is called "Michaelis-Menten function" after the name of the authors. The Michaelis-Menten function looks like this:

Think about a knock-out mutation. Such mutation will decrease by half the concentration of protein the gene in question produce in heterozygotes. Imagine, the concentration of proteins in the wildtype homozygote was 3 (see above graph). The rate of reaction of this homozygote is therefore about 3. The heterozygote would have a concentration of 1.5 and the rate of the reaction is therefore about 2.5-2.75. Assuming that the rate of this biochemical reaction is directly related to fitness, then a the locus of interest, benefical alleles are necessarily dominant and detrimental alleles are necessarily recessive. Selection for dominance is not involved in Wirght's model.
In addition to that, if you have a series of biochemical reactions, you will likely have one reaction that is causing a bottleneck. One reaction that is the limiting factor of the speed of some biochemical pathway. Let's call this reaction process A. If a mutation occurs on a gene coding for any other reaction process B that is not the limiting factor (process A), then this mutation will have no effect on fitness as long as it is not important enough to make process B slower than process A. This may lead to pattern of dominance. I am not quite sure by how much of this has been formulated by Wright and Haldane though.
Is Fisher's or Wright's hypothesis correct?
To my understanding, current state of the art is to consider Wright's model to be correct and Fisher's model to be wrong. In reality, the truth probably lies somewhere in between these two extremes. There exists more detailed (and more mechanistic) models of the evolution of dominance that and the above dichotomy might not be very representative of the current debate on the subject. For example, I (vaguely) remember that during my undergrad, Sylvain Billiard gave a talk at my university in which he reported that some alleles actually have some domain that are directly responsible for decreasing the expression of the other allele on the sister chromosome suggesting that Fisher's hypothesis might sometime be quite a good explanation as well.

This answer was recycled from what I wrote here. But it is a much better fit to your question than to where it was originally posted.

@Hans Thanks. Fixed

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How are signalling pathways specific when secondary messengers are not?
I'm a biochemistry and physiology student and am aware that secondary messengers like cAMP and IP3 are used in specific signaling cascades.
However, they and other molecules can innervate a variety of effector molecules which makes me wonder how specificity is maintained.
For example, if GPCRa/Gsa activation leads to the activation of PkAa, why doesn't it lead to the activation of PkAb?


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Why we need a plasmid for r-DNA technology
Recently I was studying Biotechnology. When I went through the texts, I had a doubt: both plasmids and gene of interest are made of DNA stretches and bacteria directly absorb plasmids in a test tube (where reactions take place). Why is the gene of interest not directly put in the test tube instead of recombinant DNA Technology (using Edited plasmids), so that it gets absorbed by bacteria?

A plasmid has a site necessary for replication of genetic material know as the origin of replication (ori) since gene of interest (GOI) is just a segment of DNA it only posseses the sequence of interest and lacks an ori site, due to this it will not be able to replicate by itself. Replication of GOI is important for product formation in r-DNA technology (mostly protien) as when the host cells divides the GOI is duplicated and is transferred to both daughter cells. This way the number of recombinant cells will increase hence producing more of the final product.

Please add some references to your answer and maybe add some descriptions to the technical terms you have used.

Welcome to Biology.SE! This looks like the start of a good answer (note that plasmids also add stability and selectability), but answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. This is a good example of how to format references. ——— Thank you for taking the [tour], but please also consult the [help] pages for additional advice on [Answer] effectively on this site. Thank you!

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DNA Structure and Function
In a strand of DNA, why does identifying the 3' side and the 5'side matter? Or the 3' --> 5' strand and the 5' --> 3' strand? Also, what is a single strand of DNA called, is it just a helix, or is the helix just the backbone?

These are basic questions that a careful reading of a textbook can answer. If you post to this list you need to show evidence of having made an effort to find the answer to the question. I suggest you refer to Wikipedia or, better, texts available in NCBI bookshelf and then edit your question. The link is: https://www.ncbi.nlm.nih.gov/books/?term=dna+structure. Biochemistry by Berg et al., Molecular Biology of the Cell by Alberts et al., or Molecular Cell Biology by Lodish et al. are all well-written and authoratitive.

A double strand is a helix, as the basepairs move with a horizontal angle with each step to the next basepair. Identifying the sides is important for DNA-replication and RNA synthesis as the way DNA is read is from 3' to 5' so that the complementary bases can be ''glued'' together from 5' to 3' in which the phosphate groups bind to the OH groups of the other molecule by a polymerase reaction.
Disregard first answer.
There.

Well, a single strand of DNA is called a denatured chain ... Basically, it has the structure of RNA

A single strand is a helix, as the basepairs move with a horizontal angle with each step to the next basepair. Identifying the sides is important for DNA-replication and RNA synthesis as the way DNA is read is from 3' to 5' so that the complementary bases can be ''glued'' together from 5' to 3' in which the phosphate groups bind to the OH groups of the other molecule by a polymerase reaction.

Welcome to SE Biology. When you answer a question here you need to back up your assertions with references. Otherwise nobody can determine whether or not they are correct. In this case you are certanly incorrect in stating that "a single strand is a helix". There is no reason for a single strand of DNA to adopt a helical conformation and it is unlikely to do so. It certainly will not adopt the double-helical formation as that requires base-pairing between two strands.


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Finding for evolution, comparing past flower numbers with present

In a hypothetical species of butterfly, wing spots are controlled by a single locus where BB individuals have blue spots, YY individuals have yellow spots, and BY individuals have green spots. Ten years ago, a previous collector randomly collected 1000 butterflies and reported finding 90 blues, 420 greens, and 490 yellows. You collect 40 blues, 320 greens, and 640 yellows. Has there been evolution in this population? If yes, is natural selection involved?

I have had many attempts at this question I calculated the p and q frequency for each using HW model.
For 10 years ago: 90+90+420/2000=0.3   BB
490+490+420/2000=0.7 YY
For now : 40+40+320/2000=0.2 BB
640+640+320/2000= 0.8YY
But I dont think I can know if evolution happened and natural selection from this (because Y allele in yellow for instance includes heterozygotes as well).
What do I do? Do I calculate the expected number of each and put it in Chi square test but how would I get natural selection from that? Please help

You see a question like this, you should just go ahead and calculate if the population is in Hardy-Weinberg Equilibrium, because that's almost certainly what's going to be asked.

For 10 years ago: 90+90+420/2000=0.3 BB 490+490+420/2000=0.7 YY

That notation is not helping.  B = 0.3, Y = 0.7
BB = 90/1000 = 0.09
BY = 420/1000 = 0.42
YY = 490/1000 = 0.49

For now : 40+40+320/2000=0.2 B 640+640+320/2000= 0.8 Y

BB=0.04
BY=0.32
YY=0.64
The allele frequencies are changed, which by definition is evolution.  But the populations were and remain in HWE, which suggests that all the requirements for that condition, which include there being no selection at present, are occurring.

Has there been evolution in this population?
If $p$ differs in the population, then yes. If you $p_1$ and $p_{10}$ (the two different estimates at generation 1 and generation 10) are equal, then any deviation is caused by sampling error. Hence set $P_1 = P_{10}$ as the null hypothesis and performs a chi-square test.
Is natural selection involved?
For this we have to know the generation time and the population size. We can assume the generation to be of one year (10 generations). The population size $N$ could be estimated from genetic data of the sampled butterflies. The expected loss of genetic diversity per generation is $\frac{1}{2N}$ but you will need to consider any possible path by which one can go from $p_1$ to $P_{10}$ using a series of binomial distribution and sum up their probabilities. That being said, it is a little bit computationally expensive if $N$ is large but some Markov Model theory might give you some simplifications.


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Which primates can swim underwater?
I saw a documentary awhile back and they were profiling a certain species of monkey which regularly swims underwater. I can't recall which species it was but they said it was rare for primates to do this - diving under the surface, holding ones breath, and swimming completely submerged.
I'm wondering which type of monkey this was and what other primates, besides humans, are known to engage in underwater swimming? Is there a reason this behavior evolved? My guess is that it has to do with foraging for food in mangrove type environments and possibly for avoidance of predators.

The Allen's swamp monkey (Allenopithecus nigroviridis) is also know to live near water-rich areas and they sometimes dive to avoid danger.
Also, it was recently shown that the chimpanzee (Pan troglodytes) and the orangutan (Pongo) can swim, dive and even retrieve items form the bottom of a swimming pool. (source)

The proboscis monkey (Nasalis larvatus) is a species of monkey which remains underwater. They usually found near large water bodies. And can swim up to 20m (66ft).


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Are there knots in DNA?
This question may sound silly.
How does it come that the DNA molecules are not totally entangled with time in the cell ? If I take long strings in a box and shake it, that would create knots, and I wouldn't be able to easily isolate each string apart.
But during mitoses, the chromosomes are totally isolated from each others while otherwise, the DNA is freely floating in the nucleus.

Bienvenue Arnaud! ADN is french. It is DNA in english :)

thank you. That explain why I couldn't find ADN in the tags list ;)

Related (though not strictly a duplicate): Why DNA needs histones to be packaged and ordered?

There are enzymes to maintain DNA structure; one of the main ones are topoisomerases.

I think a key factor is that DNA molecules are not passive bits of string that are left to move freely (which is what causes knots in string-like things that are left alone too long).
For one thing the DNA molecule is an active part of the cell metabolism, as it is constantly being transcribed (to generate RNA and proteins) or copied or corrected and so on. And as part of its role in metabolism the DNA molecule is closely associated with RNA molecules, proteins and specifically proteins that the DNA is wrapped around called "histones". The Wikipedia page for "Chromatin" (what chromosomes are made of, basically) describes various aspects of this organization, including:

That DNA which codes genes that are actively transcribed ("turned on") is more loosely packaged and associated with RNA polymerases (referred to as euchromatin) while that DNA which codes inactive genes ("turned off") is more condensed and associated with structural proteins (heterochromatin).

So DNA is constantly being manipulated by all kinds of proteins and enzymes that affect its shape and position in space; it isn't just lying there. And insofar as it might get into knots, that would likely be part of the manipulations of the enzymes and proteins, or would fairly easily be dealt with by them. This doesn't mean DNA doesn't have knots however, in fact it appears it very much can:
DNA AND KNOT THEORY (from The Institute for Environmental Modelling at the University of Tennessee)

Conclusions: Principles of topology give cell biologists a quantitative, powerful, and invariant way to measure properties of DNA. Principles of knot theory have helped elucidate the mechanisms by which enzymes unpack DNA. Additionally, topological methods have been influential in determining the left handed winding of DNA around histones. Measuring changes in crossing number have also been instrumental in understanding the termination of DNA replication and the role of enzymes in recombination.

(note this paper looks at DNA in E.coli, which does not organize its DNA in chromatin the way Eukaryotes do).
Untangling DNA (from the Nature blog CreatureCast, 2013)
This link includes a video about topoisomerases, enzymes also referred to in the previous link that unentangle DNA.
A Monte Carlo Study of Knots in Long Double-Stranded DNA Chains (PLOS Computational Biology, 2016)
Quote from the abstract:

Even though our coarse-grained model is only based on experimental knotting probabilities of short DNA strands, it reproduces the correct persistence length of DNA. This indicates that knots are not only a fine gauge for structural properties, but a promising tool for the design of polymer models.

The active site of the SET domain is constructed on a knot (Nature Structural Biology, 200)
A knot or not a knot? SETting the record ‘straight’ on proteins (Computational Biology and Chemistry, 2003)
These papers discuss potential knots within a histone protein, not DNA, but illustrates that topology and knots can be important in macromolecules:

A knot within the SET domain helps form the methyltransferase active site, where AdoHcy binds and lysine methylation is likely to occur.
A novel knot found in the SET domain is examined in the light of five recent crystal structures and their descriptions in the literature. Using the algorithm of Taylor it was established that the backbone chain does not form a true knot.

Discovery of a predicted DNA knot substantiates a model for site-specific recombination (Science, 1985)
This link is a bit painful to read (and from 1985 so I don't know if it was superseded, but it has over 200 citations) so I will leave it at the title.
And finally this article, which I looked at last but probably should have looked at first because the first sentence of the abstract literally answers your question :
Direct observation of DNA knots using a solid-state nanopore (Nature Nanotechnology, 2016)

Long DNA molecules can self-entangle into knots. Experimental techniques for observing such DNA knots (primarily gel electrophoresis) are limited to bulk methods and circular molecules below 10 kilobase pairs in length. Here, we show that solid-state nanopores can be used to directly observe individual knots in both linear and circular single DNA molecules of arbitrary length.


text:
Example of invertebrates that are attracted to heat?
I would like to test a device that outputs heat in order to attract schistosome parasites in water. However, I would like to use a substitute, since I cannot find schistosome parasites for sale.
Are there any organisms that are attracted to heat and are easily accessible?

The tendency to be attracted toward heat is called thermotaxis.
Documented cases
Thermotaxis has been documented in

C. elegans

Ploff and Sokut 2010

Slime molds Meloidogyne incognita

Pline et al 1988

Drosophila

Rosenweig et al. 2004

Mosquito Aedes Aegypti

Patterson and Brown 2009

Lake sculpin (Cottus extensus) larvea

Wurtsbaugh and Neverman 1988

Mammalian sperm cells

Bahat et al. 2003

The best documentation is on C.elegans. There are probably many undocumented species that display thermotaxis but above are the only documented cases I could find.
Many of these species are easy to find in biology labs. Mammalian sperm cells are very easy to find if you are a male but it may take complex methodology to observe thermotaxis on cells. Bigger organisms are of greater interest. Drosophila might be the way to go.
Do you really need to test with another species?
Whether the test is a good idea was not part of your question but I thought I would comment on it anyway!
I am wondering whether testing your device on a different species is of much interest to you. Testing that your device creates a thermal gradient is sure of interest but one species may react very differently to a specific gradient than another one and it feels a priori to me that you'd be waisting your time by testing it on a different species.
I think it would be more interesting to just place thermometers (if you have access to good accurate thermometers) along space and measure temperature to ensure that a gradient exists and make sure that the temperatures and steep of gradient are within the range of what schistosome may experience in nature.
I am not involved in this research and you may have good reasons of yours of testing your device on a different species.


text:
Do men with an African ethnic background have larger penises in comparison to men of European ethnic background? If so, why?
Do men with an African ethnic background have, on average, a larger penis than their European counterparts?

That question is... not unusual. It's addressed on Wikipedia's page on human penis size (which, by the way, exists) of all things. https://en.wikipedia.org/wiki/Human_penis_size#Size_and_race

You might want to reformulate "black and white" men. This is a rather unscientific wording. Also, I find the title of your question rather amusing :) .. This is a perfectly legitimate, biological question just say what you would like to know and try not to step into the pitfalls of everyday language which unfortunately very often has a "racial/racist" bias. There is no shame in the human anatomy.

I think that 4 down votes (5 actually as there was an up vote) is a bit overreacting. Among the 4 close votes, only one states that because the post shows lack of effort (via the 'homework question' reason for closing) and 3 said the post is opinion based. I don't thin the post is opinion based. I agree that given the gigantic genetic diversity present in Africa, the category African ethnicities might be unclear though.

I am not a student. I would like to know the answer.

Quoting from Oarkwe and Ebuh 2007

The mean full-stretch penile length of the Nigerian Blacks was 13.37cm and the mean flaccid length was 9.36cm. Similar studies reported full-stretch penile lengths of 12.50cm in Italians, 12.18cm in Greeks, 9.6cm in Koreans, 13cm in British Caucasians, and 12.45cm in the American Caucasians. The penile length for Nigerian Blacks was longer than those of the other races, but the differences were only statistically different in comparison with the Koreans.


text:
Confusion over equations for population's heterozygosity vs. heterozygous individuals
On page 24 of Gillespie's Population Genetics, 2nd ed, an equation for $H$, the probability that two randomly drawn alleles are different by state, is given.
$H$ is stated to be similar to the heterozygosity of the population, which I guess is expected to be $2pq$, where $p$ and $q$ are frequencies for different alleles. $ H′=(1−1/2N)×H$
On page 23, $H_t$, the probability that an individual chosen at random from the population after $t$ generations of random mating is heterozygous, is given :
$$H_t = H_0 \times (1-\frac{1}{2N})^t$$
For a current time $t$, are $H$ and $H_t$ measurements of the same thing, or are they different ?
I interpreted them as being the same, because drawing two alleles at random is similar to drawing a diploid individual at random.

One is a recurrence equation and the other is a general solution. These are basic concepts of mathematical modelling.
Reccurence equation
A recurrent equation describes the state of a system (here, heterozygosity $H$) at the next time step given the state in the previous time step. The recurrence relation is $H' = (1-1/2N)\times H$. Given the state $H$, at a given generation, one can know the state $H'$ at the following generation (given the population size $N$).
General solution
A general solution describes the state of a system at any time step given an initial state. Not all recurrence relation have a general solution. Here there is a general solution and it is $H_t = H_0 \times (1-\frac{1}{2N})^t$. Given the initial state $H_0$, one can know the state $H_t$ after $t$ generations (given the population size $N$).
Two equations for the same model
The two equations both refer to the same model and therefore the same statistic of expected heterozygosity which, as you said, is $H = 2 p (1-p)$ (for a bi-allelic locus) by definition.
Understanding the basics of mathematical modeling in ecology and evolution
Have a look at A Biologist's Guide to Mathematical Modeling in Ecology and Evolution by S. Otto for an introduction into mathematical modeling in the field of interest.

@ghgh Please let me know if my answer helped you or if something is still unclear.


text:
Is the human lifespan still expanding?
Description
200 years ago, the human lifespan was roughly 35 to 40 years long. And it has doubled in length since then.
Question
Will the human lifespan continue to expand in length?

Is this question about maximum human lifespan, or about population lifespan as health and general living conditions improve?

@GrahamChiu it's a question about whether it's still expanding or if it's at it's maximum length.

And what does it refer to?

@GrahamChiu the human lifespan...

So, you're asking about the maximum life span any human might attain? Like a 4 minute mile.

@GrahamChiu yes.

If you mean to ask whether or not humans will be able to continue increasing their life expectancy without an upper bound, the answer is no.  If you're asking if people live longer now than in the past and whether we can expect to see further increases, I'd guess that the answer is yes for most of the developed world, with the exception of the United States.  The same is probably true for most of the developing world; it would definitely be true in the developing world if western corporations started paying them fairly for their labor or resources, but that's getting into an answer for a different stack exchange website.
I suppose I should qualify the "no" to unbounded life expectancy, because it could come down to definitions of alive.  I don't think that it is outside the realm of possibility for science to provide techniques to artificially extend life; if we can start growing organs in labs, we might be able to just go change out our heart or kidneys much like we take our cars to have the tires changed. If you could figure out a way to take care of the circulatory / nervous system, too, who knows?  As it stands, though, our cells have an upper limit on the number of times that they can reproduce because we don't have enough telomerase in somatic cells to prevent the eventual shortening of telomeres (special sequence of base pairs located at the ends of DNA molecules) to the point where they no longer protect the DNA during replication and the cell eventually dies as a consequence. Hell, if we could just figure out how to take care of that we could probably chalk on some extra time - then we can see which system would be next to fail and take us out.

And drugs to lengthen telomeres?

You will find here on the UN World Population Prospects plenty of data and visualization about change in life expectancy over time (among other things). The data also include predictions until year 2100.
For example, here is the life expectancy data and predictions over time for men in Morocco.

and here it is for women in Norway (note that x-axis range differs between the two graphs)

I picked two random countries but the general trend is very consistent among countries.

Is the human lifespan still expanding?

Yes, life expectancy is still increasing in pretty much all countries and is expected to keep increasing.

What about maximum life span?

@GrahamChiu What do you mean? Are you asking about the change in the maximum lifespan through time or maybe about whether a theoretical asymptote should exist?

@Remi.b Not sure what is motivating the comments/question here but there was a recent paper (could be 5 years old now maybe? or older, time goes fast) that made a statistical argument that maximum lifespan reached a peak some years ago and has not risen since. That is, all gains in life expectancy since then have come by delaying earlier deaths, with no effect on prolonging the longest lives, and that new supercentenarian records are only because of increasing world population and nothing more. Sorry I don't have the reference.

There were also papers in response rebutting the original argument.

It might have been this one: Dong, X., Milholland, B., & Vijg, J. (2016). Evidence for a limit to human lifespan. Nature, 538(7624), 257. I'd also add that in the US life expectancy has dropped over the last couple of years. That doesn't necessarily mean the trend is not positive, of course.

Lifespan has obviously increased so I thought the question was asking about limits to maximum life span through time.  has that remained static since the appearance of the modern human?

@BryanKrause there's also this one, which I remember citing before the Dong paper came out: ( https://link.springer.com/article/10.1007/s10522-008-9156-4 ).
When I ask questions like this to my mentors (I'm an undergraduate and have been working with aging for the last ~3 years), I usually get some variation on a long sigh. We can make other animals live a LOT longer than normal. And humans have been living longer on average, but our maximum hasn't changed much. Lifespan, especially human lifespan limits, is a really hard-to-pin-down thing.

Whilst the graphs show rising life expectancies the rate of growth appears to be slowing, ie would (were this purely a matter of statistics/mathematics) reach a peak and analysis might reveal when and how high. Of course it is not purely statistical; the underlying reasons for the rise are an accumulation of better food, living practices and medicine. Food and living practices are likely to reach a peak for extending lifespans - in places may have peaked already. Medicine remains a wild card that could deliver more, but not necessarily across the whole population.


text:
Is this an asian hornet
My mother found a hornet at home (in northern France) that is probably building a nest. Is that an asian hornet? If yes, how can I exterminate them?

I am not very good at species ID but it does not look like a Asian giant hornet to me. Asian giant hornets typically have wider dark stripes. It could be a European hornet. Where was the picture taken?

Yes, northern France to be precise

The OP is probably asking about the asian hornet (which is invasive in France) rather than the asian giant hornet (which is not), though this one looks like neither.

Yes I'm talking about the invasive asian hornet

This is not a hornet, this a wasp. See the yellow dots on the thorax ? They are typical of the Vespula genus. So is the yellow and black stripe pattern on the abdomen. Those wasps are smaller than hornets (1-2 cm for wasps, 3-4 cm for hornets). Picture from Wikipedia:

There are two common Vespula species in France  (V. vulgaris and V. germanica), but to identify yours, we would need a better view of the head and abdomen.
On the image below, you can compare it to the two hornet species you can find in France (source). The first one is a bee, the second one is a wasp (Vespula), the third one is the invasive "Asian hornet" (Vespa velutina) and the fourth one is the native "European hornet" (Vespa crabro).

So no extermination needed ;) You can find more information (in French) on how to recognize these species on the Natural History Museum website.
Sources:

Le Rucher des Plaisirs - French beekeeper website
Natural History Museum - hornet and wasp identification in France
Same source in English
Wikipedia page


text:
Controlling the pursuit path of the human eye
The human eye scans images by panning focus along a certain path. Stork et al. (2002) revealed that there is a feedback process involved in moving ocular focus along a path that produces minimum muscular stress.
This got me thinking that, possibly, I could augment a video such that I slightly blur most of the image in each frame leaving a path (with some significant width) of the unblurred image or a path of clarity, if you will, to "control" a third party's ocular pursuit path. I hypothesize that this control would be won from imposing a path of clarity , because the eye adjusts it's pursuit path to reduce stress.
Could you help me to decide if this is even remotely possible?
Thanks in advance! :)

Welcome to Biology.SE. You said I've read that [..]. Can you please to link to your source as it could be helpful.

That comment pulls from a few places, but search this: "Intentionally-evoked modulations
of smooth pursuit eye movements".  It might help.

Assuming the the article for which you give the title reported the claim you're doing, I edited the post to include this reference. Thanks +1


text:
species ID: garden bush from Bangalore, India
Please help to identify this plant. It is a garden bush growing in soil. The pictures were taken in Bangalore, India.

Please include your question where you found it, if it is wild or growing in a garden or pot, and include the photo in the question. See

The plant was found in India, near Bangalore. It is a garden growing bush.

Could be anything, if it's ornamental. However, it would appear to be some kind of Pinaceae or other evergreen conifer. Possibly a juvenile hemlock or araucaria. I know that in Northern India there is Tsuga dumosa
Maybe an Araucaria?

Those pointed, awl-shaped leaves strike me much more as a member of Cupressaceae than the other conifers mentioned (Pinaceae, Araucariaceae). If I had to guess, I'd say some kind of juniper, Juniperus, though there are many other possibilities.
Are there any other features available, like berries or cones?


text:
What is the likelihood of a single human gene to the same gene from the other human?

The human genome comprises 3,234.83 Megabases and contains ~ 19,000 genes. It has been estimated that the genomes of humans are 99.9% identical. How likely is it that any single gene might vary from one individual to another? Assume an average length for a gene of 3 kilobases.

Is it still 0.01%, the same as for the whole genome? Why then we have the number of genes in this exercise, together with an approximate length?

Assumptions
Let's assume that we can perfectly align all human genome and therefore calculate such statistics of identity.
Let's assume that the probability of identity of 99.9% is the same for neutral sequences than for coding sequences. This assumption is most likely wrong but there is no other way to answer the question with the data that are given to us.
What is the question exactly?
Your homework question is a little unclear unfortunately. I don't know what is meant exactly by

How likely is it that any single gene might vary from one individual to another?

Does it mean

You randomly sample two humans and randomly sample one gene. What is the probability of perfect identity a this gene?

or does it mean

You randomly sample one gene, what is the probability that all humans are identical for this gene?

I will assume it means the first one.
Step by step
I will go by subquestions to guide through the thought process! Try to answer the following questions one by one and you should be able to get to the final answer yourself

Randomly sample two individuals and randomly consider one nucleotide in their genome. What is the probability that this nucleotide is the same?
Randomly sample two individuals and randomly consider two nucleotides in their genome. What is the probability that these two nucleotides are the same?
Randomly sample two individuals and randomly consider n nucleotides in their genome. What is the probability that these n nucleotides are the same?
Randomly sample two individuals and randomly consider n nucleotides in their genome. What is the probability that these n nucleotides are different?
Randomly sample two individuals and randomly consider 3000 nucleotides in their genome. What is the probability that these 3000 nucleotides are different?

What answer did you get? If you got stuck somewhere, please let me know where!
Hints

No point about using a calculator, it will return Infinite or 0 at some point anyway!
Don't worry too much if you're not using all the numbers that are given to you!

Hint: a modestly advanced calculator will easily calculate this without overflowing or underflowing.

I don't know how many bytes modern calculator typically use for a number but I think (might be wrong, you'll correct me) that it takes about 4 kiloBytes to store the inverse of this number (neglecting the decimals)! I have never seen such number being used in computer science but I don't know what data type (and how much RAM) advanced calculator typically use.

Remi, apparently we have completely different calculations in mind.  It seemed to me (and your answer also suggested to me) that the answer would just require a simple exponentiation operation, and the numbers involved would be reasonable.

Too bad we can't give the answer out loud here to further this discussion! If the OP shows effort at trying to solve the issue form my hints, we can further this discussion :)

The answer: 0.25% of genes will be different
How I got the answer is by simulating two genomes using the following code:
lengthGenome=3234.83*10^6
numGenes=19000
lengthGene=3000
fracSim=0.999

trialHolder=1:100
for(trial in 1:100){
    genomeA=rep(0,lengthGenome)
    genomeB=rep(0,lengthGenome)
    genomeA[sample(1:lengthGenome,round((1-fracSim)*lengthGenome))]=1
    genomeB[sample(1:lengthGenome,round((1-fracSim)*lengthGenome))]=1
    startGenes=sample(1:lengthGenome,numGenes)
    equalGene=0
    for(i in 1:numGenes){
      equalGene=all(genomeA[startGenes[i]:(startGenes[i]+lengthGene)]==genomeB[startGenes[i]:(startGenes[i]+lengthGene)])+equalGene
    }
    trialHolder[trial]=equalGene/numGenes
}
print(mean(trialHolder))

To quickly walk through the code you make a genome of the specified length, and then change 0.01% of the genome to be a mutation, and therefore not similar to the other genome at the same position.  Then define the start points of the number of genes specified.  For each gene region, see if the genes look exactly the same (if one does not have the mutation within).  Finally just track the proportion of genes that are all equal.
I ran the code 100 times and averaged the result, it took a little while.  There is likely a more direct, probabilistic way to do this but I imagine the result would be the same.


text:
What is the probability that there are no substitution between an ancestor and a modern individual?
What is the probability that there are no differences if you compare the DNA
of the ancient sample to a single DNA sequence from a modern individual? Assuming the individual was diploid and lived T generations ago.
How would you go about finding this probability? I would assume that drift and maybe selection would change the sequence and the probability of no change over time would be extremely low.

Expected number of substitutions
Let's assume a haploid mutation rate of $\mu$ and a population of constant size $N$. For simplicity, I will assume an absence of selection because otherwise, we would need to talk about what kind of selection you want to talk about.
There are therefore $2 N \mu t$ mutations since this last ancestor. A fraction of $\frac{1}{2N}$ of them drifted to fixation. Therefore, there were $\frac{2 N \mu t}{2N} = \mu t$ mutations fixed.
If we consequence a sequence with a mutation rate of $\mu = 10^{-4}$ (about 10 kilo bases if is a human genome) and $t = 10^5$ generations. Then, there were 10 substitutions (on average).
Of course, the assumption of no selection is likely wrong and violation of this assumption could well drastically affect this estimate. However, you would need to perfectly describe what type of selection pressures (and what selection coefficient and dominance coefficient) you want to consider for more calculations.
Probability of k substitutions
As events of substitutions are independent, the probability that exactly $k$ substitutions happen given the expected number of substitutions ($\mu t$) is given by the Poisson distribution with rate $\mu t$. The probability $P(k | \mu, t)$ of $k$ substitutions had happen in $t$ generations, given the mutation rate $\mu$ is therefore
$$P(k | \mu, t) = \frac{\left(\mu t\right)^k e^{-\left(\mu t\right)} }{k!}$$
Per consequence, the probability of no mutation is obtained by replacing $k$ to zero
$$P(k=0 | \mu, t) = e^{-\left(\mu t\right)}$$
Again, if $\mu = 10^{-4}$ (about 10 kilo bases if is a human genome), then the probability that zero mutation had happen in $t = 10^5$ generations is $e^{-10^{-4} 10^5} ≈ 5\cdot 10^{-5}$

Thanks, that makes sense. So would the probability there are no changes just 1-μt? I.e. 1-the probability of mutation,

@Frankfras I only gave you the expected number of substitutions. To compute the probability of $k$ substitutions, you need the Poisson distribution. See edit for more info.


text:
Do microorganisms contain water?
This may sound a bit strange question, but I am very new to biology. I would like to ask that do microorganisms like viruses, bacteria, amoebas, etc also contain water, as every living thing contains water?

The short answer, is yes, pretty much!
Do microorganisms contain water?*
Bacteria and eukaryotic microorganism
Bacteria and eukaryotic microorganisms (including amoebas) have a membrane that separates the interior from the exterior. And yes, they have water inside, in which all chemical reactions take place.
Viruses
Viruses, on the other hand, do not really have a membrane that separates the interior from the exterior. They are really just a bunch of proteins stuck together. As such, it is hard to tell whether you would consider the water in which those proteins float part of the organism or not.
Note however, that some viruses have a viral envelope (that can be derived from a host cell membrane). In such viruses, there is more clearly an interior and an exterior, and yes, there is water in the interior too! However, there is (except very few exceptions) no metabolism inside this envelope. This, by the way, is part of the reason viruses are not considered alive.
Dehydrated living things
Note that some organisms can survive with very little water. Some seeds can survive extremely strong dehydration. For example, some tardigrades can survive with less than 1% water in their body (see this New York Times article).

I think this answer is currently wrong Remi. Amoebas have endoplasm inside them. There is water in endoplasm and biochemical reactions require the presence of water but they take place in endoplasm. The same holds for other microorganisms. To me a strict interpretation of the question Are microorganisms made of water? is No, only water is made of water.

Yes, of course. I added the sentence "Of course, no living thing is made of 100% water. I will rather consider the question as meaning Do microorganisms contain water?" to clarify this point. Is it better?

@GerardoFurtado Following your advice...

@Remi.b, Yes, that's good. I liked the original answer.

I am the guy who asked this question. When I said "made of water", what I actually meant was "every living thing constitutes water". Since there is a general consensus among scientists that every living thing has water, so essentially it cannot survive without water or it would need water at some point in its life. As far as viruses are concerned, Remi pointed out that viruses have proteins. So are these proteins also constituted of water (or any liquid)? What about capsids of virus? Do these capsids also contain water (or any liquid)? What about viroids? Kindly answer.

No, a protein is not made of water. A protein is a large molecule. It is not a complex cell structure made of several different molecules. You might want to take an intro course to biology and biochemistry.

What about capsids of viruses? What about other microorganisms like viroids? Are these viroids even considered alive, as many argue they are not.

@Ren this is an entirely different question. Please open a new post for a new question. This question has already been asked though. Have a look at Why isn't a virus “alive”?

Thanks. But could please kindly clarify that does capsids of virus contain water? Please pardon my lack of knowledge. Thanks.

I am not a virologist but I don't think there is any difference between a capsid and an envelope. As I said, in the answer, yes, there is water in an envelope (and in a capsid).


text:
Is abiogenesis possible today?
Life on earth started about 3.5 billion years ago. I would assume abiogenesis happened because the conditions were right.
Would the current earth conditions allow for new abiogenesis and completely independent (in terms of phylogeny, not ecology)?

What do you mean by "new life"? Yes, single cell organisms reproduce to form new organisms. And yes, evolution still operates to create new traits, and ultimately a new kind of organism.

@GerardoFurtado Can you explain why the statements are incorrect?

I think what @GerardoFurtado was trying to imply is, different organisms need different environments to thrive. As a result, because conditions on Earth are right, say for a human being like yourself, it might not be right for certain other organisms.

@AMD I drastically edited your post to try to improve its clarity. Feel free to roll back if you don't like it.

Highly related (eventually even duplicates): Why did abiogenesis only happen once? and How did the first self replicating organism come into existence?. You should also look at wikipedia > abiogenesis.

Theories of abiogenesis invoke a process that starts with inorganic molecules, proceeds through simple organic molecules and macromolecules, and culminates in replicators and cells. Even if there are places on the planet today that favour this process, the emerging organic molecules and macromolecules would have to escape 'predation' by existing organisms. I think this makes contemporary abiogenesis even less likely.

I agree with @AlanBoyd. So much of Earths materials interact with already existent organic life that the generation of "new life" would be extremely unlikely/improbable to the point of complete impossibility. Perhaps we could observe abiogenesis in a completely sterile environment over large expanses of time, but that seems practically impossible as well.

I will argue that yes, it is POSSIBLE. It is possible on earth like on other planets. Given enough time, matter, and energy, "something" that resembles life will emerge. The problem I see, however, is that life has already conquered our planet, so any "new living thing" will have to compete with other long-time adapted living organisms, in practice, no chance of survival. The right conditions you refer to are the ones that allowed "life as we know it" to emerge. Given other conditions (other chemicals, other energy forms, etc), something completely different will emerge.
Of course, without final proves, this is still speculation.
Some speculative links:
http://speculativeevolution.wikia.com/wiki/Alternative_biochemistry
http://www.dailygalaxy.com/my_weblog/2015/05/alien-life-habitats-nasa-brainstorms-alternatives-to-water.html
http://www.nature.com/news/2009/090513/full/news.2009.471.html

Why is this down-voted? I think the answer summarises fairly well what has been suggested in the comments. Maybe a bit to little detail and under-referenced - but still fair enough for a speculative topic like this. +1

I'd just like to add to this response that should abiogenesis be possible at all, and I think like many that it's quite likely, then under whatever differences in conditions between the original event(s) here on earth, certainly mankind is ready to "assist" nature with state-of-the art equipment. The fact that we can manufacture diamonds at fractions of the time required by natural processes attests to how our technology practices expedite natural processes.

Unlikely
Th early earth lacked oxygen which is very harsh on organic chemistry and lacked living things gobbling up all the organic molecules. precursor molecules form all the time on earth but living things gobble them very quickly. Both of those things makes abiogenesis basically impossible on the current earth. Abiogenesis is all but impossible when you have complex evolved life competing for the same resources, fortunately the early earth lacked that.


text:
What happens between two nodes in an evolutionary tree?
Hey guys can you help me with this one!?
What happens between two nodes (in an evolutionary tree) or a between a node and a tip?
A) at least one character changes
B) all organisms die
C) Nothing can happen between two nodes
D) Monophyly, Paraphyly, Polyphyly
E) None of the above
I came down to E) and C). Since B) doesnt even make sense, organisms don't die among two nodes- they evolve. D) it is irrelevant to the question asked A) I think that probably is wrong as well, since among a node and a tip, the organism stays the same and finally I thought C) could be the answer, but at the same time a new trait could be formed,

Thank you, I did remove them. And yes I did try to solve it my self before I post the question on the internet. I wasn't aware that I have to mention what are my thoughts.

The organism most definitely does not stay the same between internal node and tip(terminal node). the only way that can happen is if no evolution has occurred (ancestor and descendant identical) in which case you are not looking at an evolutionary tree.

The question does not make much sense and I think you've gone about as far as anyone can go.

A) at least one character changes

It depends what it means by character and it depends the detail semantic of the tree. In general, an evolutionary tree, usually called a phylogenetic tree attempts at representing time by the length of the edges in between two nodes. The goal is, in general, not to represent anything else.
In the comments, @John has argued that time can be consider as a character.  Personally, when I read the term "character" I think of a phenotypic character. While it will pretty much always be true that among two nodes some difference will exist in the phenotypic character, it is not a fundamental consequence of the concept of evolutionary tree. This is why I argued that A is false. @John takes the opposite stance in his answer. Note also, that sometimes (although quite rarely today) phenotypic states are used to build a tree and hence, in such case, it would be a direct consequence of the methodology that two nodes must necessarily differ by the value of at least one phenotypic character.
This disagreement between @John and I highlights that the question is poorly phrased and actually makes little sense.

B) all organisms die

Well, most likely enough time separate the two nodes that all organisms that were represented in the ancestral node are dead but of course they have reproduced, so that we actually have another node that descend from it.

C) Nothing can happen between two nodes

As you said, they evolve. So, things happen!

D) Monophyly, Paraphyly, Polyphyly

As you said, those terms make no sense here!

E) None of the above

If there is any intuitive answer to the question what has happened between two nodes is time has passed. I think the answer your teacher was expecting here is E but it is also possible (s)he was expecting A. Really that's a pretty poorly written question.

I know, all the given questions, are like that!!
Thank you so much for responding, Ecology and evolution is somewhere very far back in my undergrad education :)

@ANNA FYI, if you consider that the answer has answered your question you can click on the checkmark next to the answer (just below the downvote/upvote buttons). That being said, I would recommend waiting a little bit to see if other users seem to approve with this answer.

A) has to be true, because for there to be two nodes the two different nodes must represent some difference.

@John While it will pretty much always be true, it does not have to be. The only thing that must separate two nodes is time. It is also very much possible that the only change in between two nodes relate to synonymous mutations (and other mutations that has no effect on the phenotype), hence not causing a change in any character fo interest. I have clarified that in my answer.

@Remi.b Time is a character a character is part of data for a specimen, It can also be location. Characters do not need to be genetic the best ones are but they do not have to be. You are confusing a character with a characteristic.

I understood character as a phenotypic character. I very much suppose this is one was meant in the question. I doubt whoever wrote this question consider time a character

Also the question, considers that the potential answer will apply between a node and a tip. I still don't think that A is the answer ..

@remi, time can be a character however time also does not have to be considered at all, in paleontology reconstructive trees often ignore time because the spottyness of the fossil record makes it counter productive. On the other hand is a highly constrained, high preservation, time series sequence time may be a character because it is actually predictively useful then.  The only thing that has to be true is something needs to be different between two nodes (tips are nodes) for there to be two valid nodes.

@John Yes, we are here entering here the domain of the practical method used to build a tree vs the actual thing that we attempt the estimate. But I agree with you! I shall edit my answer.

Your answer is A. for one simple reason, two different nodes represent at least one notable/measurable difference between groups, so between any two nodes there must be at least one difference.
Look at this example, whether A and B represents Mammals and Birds or two subspecies of chimp, or two strains of virus the fact they are two separate nodes means there is some difference between them. When constructing a tree there has to be at least one character difference to have more than one node. A tree with no differences is just a dot by itself.
Also an organisms does not stay the same between a node an the tip (the tip is a node) to use the below example the starred node between A and B is the most recent common ancestor of A and B which is not the same thing as A or B.

Yes I understand that. But on occasion the node it could be a result of a population immigrating on a different location. That doesn't mean that a new characteristic arose... It does?!

New and arose are not part of the question nor the definition of a character. Answer A is"at least one character changes" A character change be a loss, a different numerical measurement or color, a different location or time almost anything.  A character is part of the data used to describe the specimens and that has to be a att least one character difference between nodes, nodes have to have a definable difference. without a difference the specimens will be grouped into the same node.


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Help! What kind of bug is this?
Please help identify this little bug and how I make them go away.

Where did you find it? Is it a pest? How many do you have? Where do you live (country, type of ecosystem)? What is the approximate size? Any other info (behaviour, what they feed on, etc..)

If you can get a clear photo showing the antennae it would help; at the moment I suspect family Anobiidae (order Coleoptera: beetles I'm sure of), but seeing the antennal segmentation (we can't with this photo) would help with my suspicions.


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What is this wasp killing insect?
I spotted these two in my garden.  What is this insect?  He had firm control over the wasp and was just hanging on by one leg.  He appeared to hold on until the wasp stopped moving and then flew away with it.
I live in Ohio (USA). The wasp was a bit less than 2cm long while the other insect was about 2.5cm long.

Nice pic +1! What country do you live in? What privince/state/bundesland/etc.. do you live in? What size do they have approximatively?

I'm the United States, Ohio.  The wasp was regular size, maybe 3/4 inch long and the other insect was slightly larger, maybe 1 inch long

Given the large eyes, the almost non-existent antennae, the humped back, elongated abdomen and the wings, I'd say it is a robber fly.

It is one of many insects known to prey on wasps.
Note the description on the linked page:

This spindly piece of nastiness is a Robber Fly in the genus Diogmites. It seems that it's members of this particular genus that are adorned with the name Hanging Thief. You may remember that this was to denote their habit of dangling from a leg or two while the other limbs held onto prey, stabbed it to death with venom and then sucked out the insides. [Emphasis mine.]

Fun fact: They perform 'extra-oral digestion', meaning they extrude digestive enzymes onto/into their prey before ingesting them.
Not so fun fact: Those enzymes burn. I had one of these land on my arm once and try to digest me. I do not recommend it.

Interesting convergence with spiders: dangling system and extra-oral digestion.

@n_b I saw your username at the end of the post and did a double-take, thinking that it was some kind of an emoticon to express the pain.

Wow, don’t know who gave a bounty, but thanks! Hope all is well.

@anongoodnurse Charles gave you this bounty!

Maybe worth adding (info about the venom):  "Robber ﬂies are capable of incapacitating large and dangerous prey quite rapidly, depending on thesite of venom injection, and they can deliver painful bites to humans . Recent studies have described over 300 venom proteins and have organized novel venoms into ﬁfteen ‘Asilidin’ protein families, using the taxa Eutolmus ruﬁbarbis,Machimus arthriticus,Dolopus genitalis, and Dasypogondiadema." ..

.. "Some of these venoms are species-speciﬁc, consistent with observations of variable venom toxicity between species demonstrated by previous authors. Toxicity assays of crudevenom or isolated components have shown paralytic and other neurotoxic eﬀects in insect and mammalian subjects. "  Source/publication:  https://www.researchgate.net/publication/347161201_Pick_Your_Poison_Molecular_Evolution_of_Venom_Proteins_in_Asilidae_Insecta_Diptera

@iLuvLogix - They asked for an ID, not a lot of information on it. I tend to answer the question. The rest is superfluous.


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Calculate signifficance of SNP in specific trinucleotides
So, I have calculated the frequency of all SNPs (single nucleotide mutations) in some samples and have also found the nucleotides on the 3' and 5' sides of the mutated nucleotide. So I have a list of 192 possible permutations like this one:
AAA -> ACA 43
AAA -> AGA 35
AAA -> AAA 134
.
.
TGA -> TAA 345
TGA -> TCA 25
TGA -> TTA 97
.
.

What is the statistical approach to show that a particular set of 4 of these mutations is significant?
I have little knowledge in statistics so I welcome a for-dummies explanation!

Please do not suggest it is a good assumption to assume you are an idiot. It is wrong and you should work on knowing it better. I edited your post.

If you are wondering about statistical significance, it means that you want to do a statistical test. In order to make a test, you need a question to test. What is your question? Is it "Is a given SNP under selection?" or "Does the SNP really exist or is it just a sequencing error?"

Hi, the stupidity I was referring to was statistics-specific :)  But, you are right. Anyway, I am trying to prove that the SNP is under selection. Specifically, that there is a higher frequency of TCA>TTA and TCT>TTT.

Cool. You should clarify in your question that you are trying to detect selection. Also, what samples do you have exactly. Do you have different species or a single species? Do you have a structured population or a panmictic population? Do you have candidate genes (or SNPs)?


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What is the difference between "genetic" and "hereditary"?
What is the difference between the adjectives "genetic" and "hereditary"?

I suppose, that "hereditary" means something that comes from your parents (captain obvious yeah), but "genetic" also means mutations, SNP's etc. that can appear occasionally. But sorry, i should tell you that homework questions are not appreciated.

We usually use the word hereditary when we refer to ones lineage and by genetic we refer to the genes, something that is carried by the genes. Hope it helps.

Genetic information/changes are heritable. Not everything that is inherited is genetic (for example the money that you inherit from your parents or even in biological context, the cellular resources and organelles). I think this is just an issue of semantics and is therefore off-topic.

Semantic is essential to any science and, when used in the scientific literature, it is the role of scientist (and not philosophers) to define them properly. Some authors have made an entire career by clarifying semantics used in some field. I think it is a good question and should not get be closed.

The only downside I can see in this question is that it is a homework question (even if it only remotely look like one) and we would then expect the OP to show its effort at answering the question.

Possible duplicate of Why is a heritability coefficient not an index of "how genetic" something is?

From dictionnary.com

Genetic:
  pertaining or according to genetics
Hereditary:
  passing, or capable of passing, naturally from parent to offspring through the genes:

Note: I selected the pieces of definitions that I found most relevant to the current discussion.
Genetic information can be passed on to offspring. As such, I understand the confusion you may have.
When the adjective "hereditary" does not apply
By its definition the adjective "genetic" can be used in multiple situations where the adjective "hereditary" could not. It is specifically obvious when the term "genetic" is used in the context of a whole population. Indeed, not all genetic patterns are inherited especially when referring to population-wide patterns. Also, the adjective "genetic" focuses on genetics and not necessarily on its characteristic of being inherited.
Example
Consider for example the concept of "Genetic signature of selection". A genetic signature of selection is any pattern in the genetics of a population that can be used to infer past selection invent. These patterns include
 - high population divergence around the specific site
 - loss of heterozygosity (and polymorphism) around the selected site
 - modification of the site-frequency spectrum
 - genetic - environment covariance
Further information
Please note that the concept of heritability might have an unexpected definition for some layman. You might want to read Why is a heritability coefficient not an index of “how genetic” something is?.
When the adjective "genetic" does not apply
There are non-genetic information that can be transmitted from parents to offspring (or even between unrelated individuals).
Examples
Niche construction inheritance or epigenetic (esp. in the broad sense) modifications are examples of non-genetic inheritance.
Further information
You will get more information about non-genetic inheritance (and its role in evolution) in this answer.


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Standard notation for dominant and recessive allele
I'm reading through some science that could come up in my GRE equivalency.
I've never been much of a biologist, more of a chemist/geologist....though it does interest me massively!
I'm just seeing this question in a textbook....
Q) Assume eye colour in humans is controlled by a pair of alleles of a gene where the allele giving brown eyes is dominant to the allele giving blue eyes. Both parents of a blue eyed man, John, were brown eyed. He married a brown eyed woman, Sara, whose father had brown eyes and mother blue eyes. Sara had a blue eyed sister. John and Sara had a brown eyed child.
Fill in the boxes and circles on the family tree below to show the genotype of each individual.

I just wanted to ask how exactly we mark out genotype in science? Do we use D's and r's?
Thanks!

Conventionally, a pair of contrasting alleles are shown with the first letter of the dominant trait as capital for dominant, and the first letter of the first letter of the dominant trait in lower case for recessive. For this case, it'll be B for brown and b for blue. Someone homozygous for blue would be bb, someone homozygous for brown would be BB and someone heterozygous (brown) would be Bb.

@MalharKhushu -- You should put that in the answer box. :) It's correct AFAIK -- Capital letters for Dominant, lower-case for Recessive, and works fine as long as it's within a Mendelian framework.

Out of curiosity, what is a GRE equivalency?

Thanks, @MCM, but that would require citations, and so on, and for such a short answer, I don't really want to hunt out articles or studies

How can I distinguish between who is homozygous and who is hetrozygous?

So am I right in suggesting that John and Sara's sister are bb?

And both of John's parents are Bb, because they are brown eyed...which is dominant, but clearly they are heterozygous because John has blue eyes.

Thanks for all of the help I've received with this one....I'll have a go!! John's parents are both Bb
John is bb
Sara is Bb
Sara's sister is bb
John and Sara's child is Bb
Sara's mum is bb
Sara's dad is Bb

[H]ow exactly we mark out genotype in science? Do we use D's and r's?

General rule
The general rule is to indicate the dominant allele with a upper-case letter and the recessive allele with a lower-case letter.
The most commonly used letter is the first letter of the alphabet. The two possible alleles are a and A and the four possible genotypes here are therefore aa, aA, Aa and AA. Only aa has blue eyes in your example. Note that it is very common to merge together Aa and aA (that is to not consider whether the A allele was inherited from the father or from the mother) and just call it Aa.
More than 2 alleles OR no clear dominance relationship
It is quite common to use A1 and A2 as well but when doing so, we don't implicitly indicate a relationship of dominance. This notation also has the advantage to be able to deal with cases where there are more than two alleles segregating in the population (A1,A2,A3). Note that in reality perfect dominance is quite rare.
More than 1 locus
When dealing with more than one locus, we generally use A/a for the first locus, B/b for the second locus, C/c for the third etc... However, in general when dealing with several loci, authors don't have identical loci ad therefore they directly name them and use appropriate letters. For example, in models of recombination under control of a modifier locus, the modifier locus can often take the values M and m, while a random linked locus under purifying selection would take the letters A and a.

Thank you, this is so incredibly helpful!!
So brown eyes are dominant over blue eyes

Just to make sure you got it: I am not stating that brown eye allele is dominant over blue eye allele (actually genetics of eye color is a little more complicated). I only described the standard notation used to designate different alleles. That was your question right?

Thanks for this, sorry silly comment by me.
Am I right in suggesting that

John's parents are both Bb
John is bb.
Sara is Bb
Sara's mum is bb
Her sister is Bb
Her dad, is harder to figure out for.....is he BB or Bb and why?
Finally, the brown eyed child is Bb.

I'm assuming that the father is Bb, because amongst his children there is one dominant allele and three recessive

It looks like there were an implicit question in your post about the genotypes of the different individuals. I thought the post was about notation. Next time make sure to make your question clear and to limit your posts to only one question. If it was a homework question you should have used the homework tag too.


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What is the shortest read length achievable using Oxford Nanopore sequencers?
Is there a lower limit, in terms of read length, one could expect from sequencing DNA on Oxford Nanopore devices?

It depends on the size of the DNA fragments you are sequencing. They use 400bp amplicon libraries for their SARS-COV-2 sequencing protocol, which is about the shortest library prep I've seen for Nanopore. If your DNA is highly fragmented, you can probably expect a lot of reads around the 500 bp range or smaller.

I've had fragments come out in the low 10's of  bases - using non-standard protocols in a non-standard way, where you can see read through of both adapters.

@bob1 low 10’s including the adaptors?

Do you know if it is mentioned in the manual or in the sequencers specs or else? I would love to have a reference.

@alec_djinn no, actual sequence. In that case the adapters were (IIRC) about 50-80 bp each, though I would need to re-visit the sequences to confirm. I guess that total sequence length of ~150 bp as minimal. Though that would be the ones that passed QC, I haven't looked at the ones that didn't.


text:
What is the status of the cfDNA ends?
I am working on a protocol to ligate cfDNA, extracted from blood, into some vector. I have looked into the literature but I cannot find any detail about the status of the ends of the cfDNA. Are they blunt or sticky? What is the enzyme responsible for cutting the genomic DNA into cfDNA?
I know I could blunt it anyway and proceed with a blunt-ligation. However, the amount of cfDNA I have is limited and I would like to avoid purification steps. So, if it tourn out that it is already blunt-ended I would save a step in the process.
Also, protocol aside, I really would like to know more about the cfDNA molecular details and which enzyme is generating it.
Any hint is very appreciated.


text:
Can you identify this mold? (Aspergillus?)
I took some macro pictures (see below) of some black mold growing on wet straw. I noticed this creature that I think to be Aspergillus niger, but looks bigger than the one depicted in many pictures (the fruiting body is visible by naked eys) and since I am not an expert mycologist, I would like to ask the following questions:

Do you think it is Aspergillus niger?
If not what it is?
Is it dangerous (toxic/poisonous/infective) to keep it growing for the sake of making pictures?

Update. I am still getting this mold infection running on some of my cultures. Eventually, I managed to add some extra pictures.

Can you post the pic of growth? Normal shot not the macro one?

@AmodBhat Those are all the pictures I got. I trashed everything since a cloud of spores would be released after any vibration and I preferred not taking any risk. The first and the last pictures represent the colonies well though.

@AmodBhat Eventually, I got an ordinary pic of it. The piece of straw is about 4cm long.

I though it might be aspergillius niger also, but since it appears to be growing somewhat like a filament i would think it could be some sort of rhizopus. Aspergillus niger can produce mycotoxins (some strains) but generally it's safe. If it is rhizopus, the only health problem can occur if you're immunocompromized, but i'd be carful not to inhale or get near eyes. Also be careful not to spread spores (shaking, etc...). Mold can be persistent and hard to get rid of. Look into Rhizopus stolonife which is black bread mold.

@m4rio I am not convinced. The pic I find about Rhizopus are all microscopic ones. The fruiting bodies of this mold are visible with naked eye. Can you back up your conclusion with some pics?


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Which DNA polymerase can use a nick as priming site?
Which DNA polymerase (commercially available) can initiate polymerization at nicks, without a standard primer?
My goal is to perform rolling circle amplification starting at a nick.

It sounds like you are looking for a DNA polymerase that can perform nick translation. NEB maintains a chart listing the properties of their polymerases, including nick translation and extension from nick.  Without additional details, it looks like Taq would work for your purpose.

Thanks for the answer. I was looking for something with strand displacement activity rather than 5’ removal. My goal is to perform rolling circle amplification starting at a nicking site.


text:
How to engineer chromosomal duplications?
Specific genetic engineering of chromosomal aberrations like deletions, inversions and translocations are doable by using the CRISPR/Cas system or the other programmable nuclease systems. Insertions are also possible but mostly limited by the size of the insert.
Here two papers on the topic:
http://www.nature.com/nrg/journal/v15/n5/full/nrg3686.html
http://www.nature.com/ncomms/2014/140424/ncomms4728/full/ncomms4728.html
However these methods appear to be inadequate in case you want to insert a long DNA piece (>1Mb) into a chromosome (in case you want to engineer a duplication).
As far I have understood, problems arise when 1) you want to make such long DNA in the first place and 2) --suppose you have the DNA-- you need to transfect it into the cell...
Does anyone know how to tackle the genetic engineering of a large  chromosomal duplications? Is there any way to induce it without the need of supplementing the extra DNA?


text:
Identifying a weird Texas tree
I recently saw this tree in Texas, with many bees on it. I think it attracts   bees. However it didn't have any specific smell, so I don't know why there were so many bees (they were bee for sure). I tried to identify the leaves but couldn't. Dear experts: could you please identify this tree?

Yes. Thank you. It was in Mt Pleasant, TX 75455

an in-focus picture of the fruit/nut will help as will a picture of the whole tree. just from this it could be hickory or one of the  walnuts.

almost certainly not a hickory, walnut or other member of the juglandaceae family. No compound leaves for starters...

That looks like a live oak covered with oak galls

Welcome to Biology.SE! Your answer seems reasonable, but you are more likely to get a positive response if you explain why your identification is correct and specify the genus and species since "live oak" can refer to many species. Specifically, please edit your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion. ——— You may also wish to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!


text:
Did I understand the definition of "gross primary production" correctly?
According to wikipedia

Gross primary production (GPP) is the amount of chemical energy as biomass that primary producers create in a given amount of time.

So if a plant creates 6g of biomass in 1 second for example, then the amount of chemical energy stored in the 6g increase in weight is the GPP?

Yes, you more or less got it!
If you have only 3 primary producers (say 3 plants) in a given ecosystem.

Plant A produces 2g of organic carbon per second
Plant B produces 5g of organic carbon per second
Plant C produces 1g of organic carbon per second

, then the GPP is 8g per second.
This produced organic carbon can be in the form of leaves, root or whatever tissue these plants are growing.
Note: the numbers chosen are irealistic both in terms of production per second and in terms of number of plants in an ecosystem.

gC (grams of carbon assimilated) m-2 (m squared) year-1", what is meant by "grams of carbon assimilated" ?

The whole point of primary producers is to fix carbon. That is to take inorganic carbon (such as $CO_2$) and make it organic (such as $C_6H_{12}O_6$ aka glucose). This is why we are typically particularly interested in carbon and not so much in water.
For more info, you should have a look at an intro course to respiration and calvin cycle.
Note that if you remove water from an organism you are roughly speaking left with 75% of carbon, 10% of Nitrogen and the rest made of different elements.

alright thanks,,, and when we say that the GPP is measured in "gC (grams of carbon assimilated) m-2 (m squared) year-1", what is meant by "grams of carbon assimilated" ? i quoted this from my book and i dont know what they mean by that.

Okay so if a plant makes for example 100g of organic product in one second then the mass of carbon in this 100g is the GPP in gC per second , right ?

wait what did you edit yesterday ? i cant see the difference. Can you please answer my last comment ?

Yes, you were right. Note however, that when you read a paper you want to make sure that they really measure the mass of carbon and not just the dry mass or the energy freed from combustion as many authors may use proxies.


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How does the spindle fiber find the kinetochore?
I am curious if anyone knows the exact mechanism of how exactly does the spindle fiber find the kinetochore? it certainly seems like a fairly non-spontaneous reaction for a spindle fiber to reach all the way to a chromosome, how are these type of reactions carried out without producing new proteins? How Can cells execute complex "choreography" such as mitosis without making new proteins on the spot?

It's an interesting question, but don't assume that the requisite proteins are not already available or cannot be made.

But here is my confusion, we learned about the signal transduction pathway and the central dogma of molecular biology as the basis for how life exists, if DNA is bundled up into chromosomes during cell division, then how do we carry out such a complicated process ? to me its like cell division implies that gene expression isnt needed for cells to carry out complex tasks...which is crazy...You figure that  especially in the context of evolution mitosis is when a cell needs to be most responsive to problems and stimuli, you dont want your plane on "auto-pilot" when it is about to land...


text:
What is the right definition of 'Sex Linkage'?
I am confused about definition of "sex linkage". I have found different definitions but they do no match.
From P.S Verma, V.K Agarwal cell biology, genetics, molecular biology, evolution and ecology:

If the genes are situated in the same chromosome and are fairly close to each other, they tend to be inherited together. This type of coexistence of two or more gene in the same chromosome is known as linkage.

From: Anthony J.F Griffith "Introduction to genetic analysis

In general, genes in the differential regions are said to show inheritance patterns called sex linkage.

From: Wikipedia

Sex linkage is phenotypic expression of an allele related to the allosome (sex chromosome) of the individual.

Related post.

This question is being bumped often(4 times from your post history). If any of the entries below have answered your question, please consider accepting an answer or asking a follow up question instead. Bumping of a post that has a good but unupvoted answer removes a post that deserves attention off the main page.

Linkage is the tendency of two genes present on the same chromosome to be inherited together. The degree of linkage depends on the distance between the two genes, i.e two genes that are physically close are less likely to be separated onto two different chromosomes during recombination/crossover.
So this is what your first definition trying to convey.
Sex linkage simply means that a gene is to be found on the differential region of a sex chromosome (and not an autosome). See it as (gene) Linked to sex chromosome.
Note: Linkage and sex linkage are not the same.
An Introduction to Genetic Analysis, 7th edition makes it a bit easier:

Sex linkage is the location of a gene on a sex chromosome.

So to sum up the definition:

Sex linkage is the location of a gene on the differential region of a sex chromosome. (this is applicable to human beings because we have PARs)

For animals in general having sex chromosomes the definition from Genetic analysis is alright.
Note: Sex chromosomes are chromosomes that have genes that have roles in determining the sex of an individual of a species.

Good answer. +1. Why are is the PAR important in order to be allowed to talk about sex linkage? Note your answer make it feel like only animals have sexual chromosomes which would be wrong. Also, I am not sure that a sex chromosome is solely defined by the presence of loci explaining variance for sex. If I am not mistaken, there are GSD species that are not considered to have sex chromosomes (typically when sex is a polygenic trait).

The first definition is a definition of linkage as in "linkage disequilibrium" - that one has nothing to do with sex linkage.
Sex linked means that the gene or genes involved in a trait are inherited on one of the sex chromosomes (X or Y) and that, as a result, the disease may occur at different rates in different sexes. A good example of this is color blindness caused by a recessive genetic variant found on the X chromosome. Men only have one X chromosome, so if they inherit the variant, they will be colorblind. Women have two X chromosomes, so they will not be colorblind unless both of their X chromosomes have this problem.
In addition to saying "sex-linked", you can also be more specific and say that color-blindness is "X-linked". There are also Y-linked disorders, although they are much rarer since they usually cause infertility and don't get passed on. The term "sex-linked" seems to be gradually dying off as people adopt these more specific terms.
There are also some other terms you may come across, which sound similar but mean different things:
Sex-limited trait: This has nothing to do with genetics and instead refers to whether a person is biologically capable of manifesting a disease. For example, prostate cancer would be sex-limited because only men have prostates.
Sex-influenced trait: A genetically-influenced trait where, although the genes influencing the trait are not on a sex chromosome, a person's sex may still influence whether/how a trait manifests. An example of this would be breast cancer - certain variations in the BRCA genes increase risk of breast cancer in both women and men, but women with a BRCA mutation are still much more likely to get breast cancer then men with a BRCA mutation are.
Unfortunately, some people use the term "sex-linked" to refer to sex-limited or sex-influenced traits, which can make things very confusing.
To read more about these three categories, see: http://www.eplantscience.com/index/genetics/sex_linked_sex_influenced_and_sex_limited_traits/sex_linked_sex_influenced_and_sex_limited_traits.php

can you add some references so others can read about your answer, etc?

The first definition is a definition of "linkage (physical linkage)", not "linkage disequilibrium"