What factors make a sequence evolve non-randomly? On the wikipedia page about Fay and Wu's H, it talks about a non-randomly evolving sequence may be due to some selection acting or a selective sweep or population expanding/contracting. My questions about these factors that affect non-random sequence evolution are:

Does negative selection differ from a selective sweep because a sweep is a form of positive selection?
After a selective sweep, any rare mutations you see must have come after the selective sweep. Is it because they can't have come during it else they'd 'be diluted' by the positively selected alleles?
Population contraction can create a bottleneck, which makes all individuals come from a common ancestor. But how does population expansion make a sequence evolve non-randomly?

Fay and Wu test is a test that compare expected sequences under a standard coalescent theory model, that is a single panmictic population with non-overlapping generation of constant size $N$ and effective population $Ne=N$, that is the variance in allele frequency at any following generation is $\frac{p(1-p)}{2N}$, where $p$ is the frequency of a given allele. As such Fay and Wu (as well as Tajima's D and other tests) are not only test of selective neutrality but also tests of demographic neutrality as underlined in Nielsen 2001.

It may be hard to make good predictions about the extend and direction at which a given selective or demographic event will affect a given statistic such as Fay and Wu's H. Therefore, in answering the following questions, I am not specific to Fay and Wu's H. Also, answering the questions fully would require making an introduction to coalescent theory which is subject to a whole book rather than a simple post. To fully understand such test, you will need to follow an introduction to coalescent theory. You can have a look at the books recommended in the paragraph General Entry Books to Population Genetics of this answer.

  Does negative selection differ from a selective sweep because a sweep is a form of positive selection?

Let's first clarify the terms just in case. Reduction in polymorphism at linked loci due to positive selection is called "selective sweep" while when due to negative selection it is called "background selection".

Generally speaking, selective sweep is much stronger than background selection. Also, selective sweep has a higher impact on Tajima's D, then background selection.

To my knowledge, methods trying to disentangle the two processes of selective sweep and background selection mainly use inter-species comparisons to infer what types of sequences are concerned. If The loss of polymorphism is adjacent to a highly conserved sequences and is found in related species, then it is probably background selection at play. If there is a fixed mutation that isn't found in related species and loss of polymorphism isn't found in these related species, then it is probably selective sweep.

  After a selective sweep, any rare mutations you see must have come after the selective sweep. Is it because they can't have come during it else they'd 'be diluted' by the positively selected alleles?

A selective sweep indeed modifies the Site Frequency Spectrum (SFS, distribution of allele frequencies) to create an excess of high frequency variants (or a relative lack of low frequency variants). See wikipedia > Tajima's D

  Population contraction can create a bottleneck, which makes all individuals come from a common ancestor. But how does population expansion make a sequence evolve non-randomly?

Population expansion yield to longer coalescent times and therefore lack of rare alleles. See the introduction of Excoffier et al. 2009 for nice explanation and figure.


Doubts regarding definition of upstream/downstream genes and cognate protein With respect to the research paper, there are a few things I didn't understand:
1. What is upstream and downstream gene
2. This paper identifies proteins that help in secretion, but does not identify the originally secreted protein. Am I correct?
3. Does cognate protein here mean homologous protein(from common parents)?

Upstream means towards 5' direction from the reference point (conversely for downstream). Reference point can be a single position such as transcription start site (TSS) or a bigger segment such as a gene. When we say upstream of a gene, it means some region of DNA that is towards 5' direction from the TSS of the reference gene. Downstream of a gene refers to the region 3' to the transcription termination site of the reference gene.

Similar terminology is applicable to RNA but obviously, in this case your reference cannot be a gene (it can be an exon, for instance). I have not seen this terminology used in case of proteins.

This paper is about identification of the proteins that aid in secretion (TEC) of certain proteins (effectors). They identified both the proteins that help in secretion and the proteins that are secreted

  Here, we report a class of T6SS effector chaperone (TEC) proteins that
  are required for effector delivery through binding to VgrG and
  effector proteins. The TEC proteins share a highly conserved domain
  (DUF4123) and are genetically encoded upstream of their cognate
  effector genes.  [....]
  We validated this approach by verifying a predicted effector TseC in
  Aeromonas hydrophila. We show that TseC is a T6SS-secreted antibacterial effector and that the downstream gene tsiC encodes the
  cognate immunity protein. Further, we demonstrate that TseC secretion
  requires its cognate TEC protein and an associated VgrG protein.

Cognate refers to the correct binding partner which will result in a functional complex. It basically refers to biomolecular partners with a known and validated relationship. This relationship need not be synergistic. For example:

  RNA interference (RNAi) is an evolutionarily conserved process through
  which double-stranded RNA (dsRNA) induces the silencing of cognate
  genes. (Source)


Effect of single nucleotide deletion or insertion on primer annealing How is primer annealing, and, consequently, PCR amplification affected by single nucleotide deletion or insertion inside the primer ?

Imagine a primer like this:  GCGTCATAAAGGGGACGTG (primer)   and the corresponding part of template DNA has one G missing, so it looks like this:  GCGTCATAAAGGGACGTG (template).

The possible pairing could be
GCGTCATAAAGGGGACGTG primer
GCGTCATAAA_GGGACGTG template
or
GCGTCATAAAGGGGACGTG primer
GCGTCATAAAGGG_ACGTG template
 or anything in between.

Is it possible that amplification with such primer would be completely disrupted in normal real time PCR at 60°C annealing? Could this completely disrupt the amplification?

If the mismatch was substitution-like, I would be pretty confident, the primer would be still functional and amplification would occur. In the extreme case, it would be at least residual amplification at late Ct. There are a lot of data, how substitution mismatches affect primers and I also have a lot of personal experience with that.

Unfortunately, the deletion mismatches are less studied plus googleproof. The only indication I have found is this work:
Lipsky RH, Mazzanti CM, Rudolph JG, Xu K, Vyas G, Bozak D, et al. DNA melting analysis for detection of single nucleotide polymorphisms. Clin Chem. 2001;47:635-44.
In that work, single nucleotide deletion had similar or lower affect on melting temperature than substitution mismatch. But it was about longer oligos.  Examples:
Effect of deletion:
133 bp fragment, 67 % GC, deletion SNP at position 43, delta Tm (homo-hetero duplex) = 1.2°C
Effects of substitutions:
152 bp fragment, 43 % GC, substitution T to C at position 68, delta Tm (homo-hetero duplex) = 0.9°C
100 bp fragment, 41 % GC, substitution T to C at position 42, delta Tm (homo-hetero duplex) = 1.4°C
163 bp fragment, 60 % GC, substitution C to T at position 86, delta Tm (homo-hetero duplex) = 2.2°C
110 bp fragment, 59 % GC, substitution G to A at position 66, delta Tm (homo-hetero duplex) = 3.8°C

Questions:
1. Can you recommend me literature about how deletion mismatches inside (not at the very end of !!!) primers affect annealing and PCR ?
2. Would You guess the primer in my example would be still functional , at least partly, or would You expect no amplification at all ?

EDIT after your inputs:
This online application " mfold.rna.albany.edu/?q=DINAMelt/Two-state-melting " thinks, deletion mismatches are more destabilising than substitutions, at least for short primers. For my own example, it calculated delta Tm (homo-hetero duplex) = 12.9°C .
If I try substitution mismatches instead, delta Tm (homo-hetero duplex) is in interval 3,8°C to 5,7°C.

New question   If you have experience as similar as possible to my case, which is 19 nt long primer with single nucleotide deletion in the comlementary template at position cca 6 - 9 from 3' primer end, annealing temperature used at 60°C, please let me know if You achieved amplification or not.  Please, give me a respective reference, if you have it, so I will quote it in my review :-) .

Also, I am still interested in general info, as long as the topic is narrow enough to be about single nucleotide deletions or insertions in primers. (Not substitution mismatches).

We used this kind of primers to generate out of frame mutations or to add additional bases. In my experience your PCR will work (probably a a lower efficiency) and you will get a product with an additional base. We used primers with bigger differences in PCR based site directed mutagenesis of plasmids, there up to 10 bases didn't match but the primers where also longer. For single nucleotide mismatches (either + or - one base) we used primers around this size.

Regarding the literature, this publications might be useful:

A guide to the design and use of mismatched and degenerate
primers
Effects of primer-template mismatches on the polymerase chain
reaction: Human immunodeficiency virus type 1 model studies
The Effects of Internal Primer-Template Mismatches on RT-PCR: HIV-1
Model Studies
Effect of primer mismatch, annealing temperature and PCR cycle number
on 16S rRNA gene-targetting bacterial community analysis

Especially the first publication contains a lot of other interestings references.


Why does the stability of YAC increase with size? From Lehninger Principles of Biochemistry :

  The stability of YAC increases with size (up to a limit). Those with
  inserts of less than 100000 are gradually lost during mitosis.

Why does this happen ? (YAC refers to yeast artificial chromosome )

This is a question which is not easy to answer, especially the 50.000bp number (which I haven't found anywhere in there literature). However, I found some evidence, partly derived from plant and mammal artificial chromosomes (references 1 and 2), partly from the original publication from Murray and colleagues (reference 3).

The problems with small chromosomes seems to be their passage through mitosis and meiosis, where smaller artificial chromosomes tend to get lost. They are also not controlled very well in their number.

Murray states that YACs of 55kB in size are relatively stable in the yeast cells are relatively stable, but have a lower stability than natural chromosomes. When you are interested in the deeper details, I recommend reading the article.

References:

Construction of mammalian artificial chromosomes: prospects for
defining an optimal centromere
Alteration of chromosome numbers by generation of minichromosomes –
Is there a lower limit of chromosome size for stable segregation?
Contruction of artificial chromosomes in yeast.


Can solitary animals show extroverts traits? So far as it is known there are solitary animals and social animals.

Does introversion exist among nonhuman primates? says that there are introverts among social animals:

  Recent studies have identified extraversion/introversion in great apes, including chimpanzees, gorillas and orangutans. Chimps exhibiting greater solitary and reserved behaviors are considered more introverted, whereas those that are more playful and interactive fall on the extraverted side of the spectrum. Extraversion/introversion behaviors, such as sociability, have also been identified in species of monkeys.

Are there extroverts among solitary animals? I mean those who seek union with others although the vast majority of animals of their species are solitary?

So solitariness vs sociality in animals is a little more complex than we usually give it credit for. For example, even in species previously thought to be largely solitary except for mating, sustained observation and tracking often shows that previously assumed to be solitary individuals actually do interact and sometimes develop lasting social relationships with conspecifics, just not at times when people are observing them. This is a particularly common finding in nocturnal animals among males who are assumed to be solitary, such as buck deer who turn out to be more social than does--just primarily at night!

That Wikipedia article you cited for 'solitary animal' is actually pretty shitty when you get down to it; the list of "solitary animals" include several generic terms for animals that include common species known to have variable social systems depending on region, such as badgers, moose, jaguars, cheetahs (in whom males, often brothers usually form lasting social relationships), red fox, and devils, who actually encounter each other quite frequently over kills and scavenging sites. (Citations are listed in this Collabedit file, because Stack Exchange is yelling at me for trying to provide actual links.)

In that context, I don't think many people have done behavioral syndrome/"animal personality" work on sociality, because it's not a particularly good thing to measure--you're really measuring something more like 'aggression threshold.' People have done work on species like social spiders where sociality varies significantly between individuals, however.


Is there a name for this phenomenon described in "Phylogenies and the Comparative Method"? The figures below are from Felsenstein's paper "Phylogenies and the Comparative Method". I was wondering if there was a specific name for this effect where there is an apparant correlation that is actually the result of the data being structured into two separate groups, where there is no correlation within groups but an apparent correlation between groups. "Phylogenetic non-independence" doesn't seem specific enough.

I've seen this termed "phylogenetic pseudoreplication", but I can't remember offhand where. I'll see if I can find it. Without a tree, the boxes and Xs essentially represent 2 data points. As Remi.b suggests, this is really just high phylogenetic signal.


How to convert bwa mem output to BAM format without saving SAM file I want to go straight from bwa mem alignment to BAM format as I don't need the SAM file and it takes up too much space. How do I achieve this?

For directly outputting a sorted bam file you can use the following:

bwa mem genome.fa reads.fastq | samtools sort -o output.bam -

Optionally using multiple threads:

bwa mem -t 8 genome.fa reads.fastq | samtools sort -@8 -o output.bam -


What are the relative roles of coding DNA versus regulatory DNA thought to be in evolution? Intuitively, once you have the idea that some DNA is responsible for turning on and off the DNA that codes for proteins, it's possible to imagine that the regulatory DNA is actually the most important part. In the ingredients list of a recipe, you might think the coding DNA gives you the list of ingredients, but the regulatory DNA gives you the amounts of each one, plus the order in which you add them to the bowl. If that's true, then different variants of regulatory DNA should be selected for and against, and evolutionary molecular biologists ought to be tracking those variants like they track alleles of genes. But evolution always is discussed as if it's just about different gene frequencies.
Is "regulatory evolution" a thing? If so, is there an understanding of how big a thing it is? Or, if not, why not?

Yes, a simple google search reveals millions of academic citations talking about "regulatory evolution".
But it's a little over-simplistic to divide coding vs. regulatory DNA. Indeed, some coding DNA is in fact also regulatory at the level of determining gene expression in cis (a well-known example of this would be codon usage).
It is moreover incorrect to think that coding DNA products don't do gene regulation. This was recognized very early on in the ideas of "structural gene" vs. "regulatory gene". These days we would call the latter transcription factors, we don't really use the structural/regulatory terminology anymore. Transcription factors do most of the actual active work of gene regulation in trans, in collaboration of course with regulatory DNA.
So in conclusion, yes it's important and there are tons of studies that you can google if you want to investigate these problems. I would suggest reading more about cis-regulatory and trans-regulatory elements. Of course, there isn't an exact mapping of coding<-->trans and noncoding<-->cis, it's just a helpful simplification.


What advantage would the initial 'donor' in horizontal gene transfer by conjugation have received? I am struggling to think why horizontal gene transfer between bacteria would have persisted during the course of evolution as surely it puts the 'donor' at a disadvantage?

For example, consider a hypothetical situation where only one species of bacteria has a gene to resist a new (almost) omnipotent antibiotic.  When growing on this medium, this species of bacteria has nil inter-specific competition for the resources it needs.  Yet if it passes on the plasmid containing the resistance gene via conjugation to individuals of a different bacterial species, they then too are able to grow on the medium and potentially out-compete the first species - thus the conjugation could possibly be extremely detrimental to the survival of the original population.

I'm obviously missing something as the feature has persisted, so what is the advantage to the donor species of conjugation?

The donor bacterium, viewed as a unit, may well gain no advantage from sharing its genes.  The genes that are shared, however, may gain a very substantial reproductive advantage from being able to spread to other strains.  If some of the genes that are capable of being shared also promote sharing, they may be selected for by evolution.

This is a good example of the basic principle of the gene-centered view of evolution, famously popularized by Richard Dawkins is his book The Selfish Gene: evolution selects for genes that are good at spreading themselves.  This may, but need not always, imply helping the organism containing the gene to survive and reproduce.


Do people often blow out the air from their lungs a lot when living in the cold condition to keep their lungs warm? Do people often blow out the air from their lungs when living in cold climatic conditions to keep their lungs warm?

I ask this question because it could connect to how people in different areas construct linguistic sounds.

For example, the Germanic families of Language (German, English,...) use a lot of air from the lungs to construct the sound?

Is that because the Europeans living in cold climate often blow out a lot of air from the lung to keep warm and as a result gradually they construct air-driven linguistic sounds?

For people living in warm climates (ex: Sino-Tibetan language like Chinese, Thai), we mostly use the tongue to construct sounds, and we use very little air from our lungs to make sound.

I posted this question to some forums & some people said it’s baloney. However, there's one thing for sure, the environment shapes how local people construct sound. People construct the sound like that because it is constrained by something. One thing can not stand alone, it must be the karma or outcome of something else.

In a cold climate, do people often blow out the air from their lungs a lot when living in the cold condition to keep their lungs warm?

No, and it wouldn't make any sense: breathing more means inhaling more cold air that needs to be warmed up, so the result is a heat loss. The more so, as cold air (< 0°C) has a low water vapor pressure, while the lung likes to have the air at body temperature and well moistened. Which means that you also loose the vaporization heat of the water.

The function of moistening and heating the cold and dry air as well as recollecting some of the heat and water when breathing out is done by the nose. So the sensible (and done) thing in cold weather is to avoid breathing by mouth and instead keep your mouth shut and breathe by nose.
Nevertheless, neither German nor English, nor any of the Scandinavian Germanic languages is spoken through the nose.

My experience is that cold air (personal minimum: -40 °C) in the mouth is very unpleasant, and makes me cough as it is still cold when it arrives in the throat, but of course breathing out by mouth is less of a problem. But breathing out by mouth and in by nose means that the nose cannot recollect the heat and moisture from the outgoing air.

In any case, the amount of breathing is linked rather to oxygen demand and $CO_2$ to be gotten rid of), and even the fastest speaking people I know do not get close to hyperventilation by speaking, not even speaking German or English.
Which means that speaking Germanic languages needs less breath to produce the sounds than what you need to breathe for physilogical reasons even at not much above base rate metabolism (sitting while talking) anyways. Which would imply that the breathing difference between Germanic and Sino-Tibetan languages would not cause an important driving force in language evolution.

A side point is that I don't agree with your concept of cold climate. Both Germany and England are counted as temperate climate. Actually, Frankfurt has higher minimum temperature all year round than Lhasa (as you mentioned Tibetan in your language family).
Also note that the Indo-Germanic language family covers a range of climates from tropic to polar just as the Sino-Tibetan covers some cold regions as well), so maybe language families that are spoken only in polar regions vs. such that are spoken only in tropic regions would be better to look at (see e.g. the Wikipedia language family map).

However, there are probably some confounding influences that need to be taken into account. In cold weather, you do not sit or stand around chatting with people as much. And in the polar climates, historically farming has hardly been possible. So you have populations where hunting has been very important for survival, and regions with very low population density. Both mean that on average, you'll be silent instead of talking. As for having a chat with someone, you'd ask them in - or the length of the chat is limited by temperature.
Which means that if cold is a driving force for the type of pronouciation that evolves, it would be a rather weak link. And in any case, speaking less will overcompensate all these breathing differences.


Why do blue jays eat my cat food? We buy some run of the mill big-box store cat food. Over the last several weeks, I've observed a blue jay landing on the cat food dish, taking a piece or two, and flying off with it. I assumed it was eating it then, and this morning I just saw it actually eat a piece.

Why would a blue jay eat cat food?

Edit:

I just looked at the ingredient list and apparently corn is the first ingredient. But there's also "poultry by-product" and a variety of other "meats." Would the jay just smell a lot of corn or something?

Like other Corvids (Jays, Crows, and Ravens), Blue Jays are omnivorous and can eat and digest both animal and plant matter. Animal matter can include insects, carrion, small birds and mammals, and the eggs of other birds. Then there is plant matter including corn, seeds, etc. Your catfood was not only convenient but contains a good source of both animal and plant matter and the opportunistic tendencies of Blue Jays allowed them to take advantage.


Some sort of Lymantriidae caterpillar? I found this larva in Sweden in July. It was about 15 mm long. It reminded me of Orgyia antiqua that I've seen before, but smaller and with a somewhat different colouration.

I think it's indeed a young, and possibly worn, specimen of Orgyia antiqua (also Rusty Tussock Moth or Vapourer, see also UKmoths). This species is relatively common in large parts of Sweden. However, the tufts and "tail" are usually more pronounced, but there is probably intra-species variation, and old, worn individuals can have sparser tufts. As you say, they are usually longer than 1.5cm but there is large variation, sexual dimorphism and younger larvae (early instars) are natually smaller.

(picture from wikipedia)

Swedish specimen:

( from http://krypinaturen.se/fjarilar-lepidoptera/nattfjarilar/tofsspinnare-lymantriidae/orgyia_antiqua_1878_20130626/)

Lymantria dispar is rather rare in Sweden and is only found in certain localities in the south (Blekinge, Småland coast) along with Öland and Gotland.


Can (or have) antiviral drugs created drug-resistant viruses? Evolution/emergence of antibiotic-resistance in bacteria is a known effect of extensive use of pharmaceutical antibiotics.

Pharmaceutical antivirals have come into extensive use in recent decades – e.g., Tamiflu for influenza; Harvoni for hepatitis C; Valtrex for herpes.  Some are even prescribed as ongoing "suppressants."

Has anything analogous to antibiotic resistance (i.e., antiviral resistance) been observed in viruses treated with pharmaceutical antivirals?  If not, are there theoretical reasons this would be unlikely (or impossible) to occur?

Resistance to antiviral therapy is a problem in the treatment of many viral illnesses.

Influenza is particularly significant given the epidemiological characteristics of the disease. This Nature Medicine article gives a good overview of oseltamivir resistant pandemic H1N1, which is a useful example, since our assumption that resistant virus would not spread very effectively was (probably predictably) not valid.

HIV is an excellent case study as well, since antiretroviral resistance is such an important issue in the treatment of that particular infection, and demonstrates the challenges of outwitting a pathogen with such a high error rate. This became apparent quite soon after introduction of (initially successful) monotherapy with AZT. In fact, preventing the emergence of resistant virus within the population of virus in a given patient is typically the primary consideration in choosing a drug regimen.

With regard to the other examples of antiviral treatment you mentioned, HCV resistance is well reviewed here. HSV resistance is reviewed here. Resistance has been observed in both examples, though it is more often considered in the normal course of treatment for HCV than HSV. I'd note that Harvoni, which you mentioned, is a combination therapy (ledipasvir-sofosbuvir). Combination therapy is one common strategy for preventing the emergence of resistance


Is there a metabolic pathway that generates methanol? I've been looking for help topics about methanol in metabolism. Specifically, I wish to know what is a common dietary component that generates methanol following metabolism and comment on its toxicity?  I cannot seem to find any relevant data and i'm seeking to know if anyone here has any experience and knowledge of this.

This is an old question by now, but I found it interesting, so here's my two cents :)

Methanol has long been known to normally occur in humans; one study from 1963 demonstrates its presence in breath.

One major source for methanol in humans is breakdown of pectin by bacteria in the gut. Pectin is a complex carbohydrate found in many fruits and other non-woody parts of plants. Pectin is not well metabolized by humans, and so has low nutritional value and counts as dietary fiber. Still, some species of bacteria in the gut are able to degrade pectin, and this process produces methanol.

This article reports measurements of methanol levels in the breath of subjects consuming pectin. Here, 10--15 grams of pectin (equivalent to ~1 kg of apples) was estimate to yield about 0.4--1.4 grams of methanol. The authors also state that there is a basal production of methanol in humans as well, of about 0.3 grams per day; the origin of this methanol seems unclear.

There are also pathways in human cells capable of forming methanol. This study demonstrates this fact by showing that infusion of ethanol (bypassing the gut) leads to a rise in methanol levels.

A recent review of metanol metabolism in humans can be found here.


Making a hole in a tree is okay? Or does it damages the tree? I am watching a TV series named "Treehouse Masters." What they do is make houses on trees or around it getting physical support from a big strong tree, like this:

But to make the support strong, they make a big hole in the trunk of a tree

Then they put a steel beam into it, like this:

In some cases, they make more than one hole. So, does this affect the tree in any way?

If anyone makes a hole that big or even bigger but doesn't fill it with any other thing(like the beam), will the tree heal itself?

I have heard that trunk is the most important part of a tree. So I am curious to know if this act is cruel towards the trees or not.

It can have a negative effect if parasites are able to take advantage of the holes in the tree.The bark is the first line of defense against parasites and making holes without covering them tend to have a negative effect.Furthermore, the bark also protects the plants against adverse weather conditions.


How do gory images lead to nausea? How do gory images lead to nausea?

Yesterday my friend visited shock sites (a website). He said that he got nauseous sensation within seconds after viewing the gory images. However, I don't understand how seeing such sights can lead to nausea? Eyes are present at the top of the head and the digestive tract is present below the mouth. They aren't physically connected.

The connection between eyes and food pipe had to do nothing with the motion sickness because the visual inputs and outputs to these sensory information are processed in the brain itself, So there is not need for eyes and food pipe to be connected together in order to cause nausea.

  Vasovagal response or vasovagal response or vasovagal attack (also called neurocardiogenic syncope) is a malaise mediated by the vagus nerve. When it leads to syncope or "fainting", it is called a vasovagal syncope, which is the most common type of fainting.

(from http://en.wikipedia.org/wiki/Vasovagal_response)

This case is most commonly seen in adults and adolescents. There are several syndromes which comes under the vasovagal syncope which consists of symptoms like loss of consiusness,lightheadness,nausea,sweating,tinnitus,confusion,altered heart rate,fuzzy thoughts,cloud like spots in vision etc.

  Vasovagal syncope occurs in response to a trigger, with a corresponding malfunction in the parts of the nervous system that regulate heart rate and blood pressure. When heart rate slows, blood pressure drops, and the resulting lack of blood to the brain causes fainting and confusion.

(from http://en.wikipedia.org/wiki/Vasovagal_response)

Several pshychiatric disorders can cause vasovagal response like,

Agoraphobia
Obsessive–compulsive disorder
Social anxiety disorder
Blood-injury phobia
Hemophobia
Traumatophobia
Trypanophobia

http://www.nwocc.com/Pt%20Education/neuro_syncope.pdf http://en.wikipedia.org/wiki/Vasovagal_response

  When it comes to seeing red, the faint feelings could be tied to a phenomenon called blood-injury phobia. According to WebMD, this condition evolved as a way for humans to cope with threats:

  "The idea is that back in time, when someone was coming at someone else with a sharp stick or rock, a kind of genetic variation allowed certain people to faint in response," explains Tyler C. Ralston, PsyD, a clinical psychologist in Honolulu, who treats people with blood-injury phobias. Warriors who fainted looked dead and were passed over during battle. The blood pressure drop also might have helped those who were wounded avoid bleeding to death. Survivors then passed on the "fainting" gene.

(from: http://www.popsugar.com/fitness/Why-Sight-Blood-Makes-You-Feel-Faint-3061135)

"Overcoming Obstacles in CBT" written by Yvonne Tone and Michael McDonough states a condition about a patient having similar psychological problem described in the question. Here the patient's panic is associated with "gory images" of injury or illness, and his responses included intense nausea, pale skin, sweat and sometime fainting. He also reports avoiding gory scenes on TV/filim and medical programmes. The problem is identified as co-morbid panic/agoraphobia and blood injury phobia.

http://books.google.co.in/books?id=1uIYqkKgKRYC&pg=PA44&dq=nausea+and+gory+images&hl=en&sa=X&ei=qLZ2VJPMJ420uAS8qoHIBA&ved=0CB0Q6AEwAA#v=onepage&q=nausea%20and%20gory%20images&f=false


The source of ABA for inducing stomatal closure in the detached leaves? As you may know, when leaves detached from the whole plant close their stomata to maintain water and prevent wilting. Could you please let me know what is the mechanism of stomatal closure in the detached leaves? if it is induced by ABA, what is the source of ABA under these conditions?

Please provide me the corresponding links for your answers as I couldn't find an appropriate answer for the question.

Thanks

I think that ABA could be one of the player involved on the stomatal closure in detached leaves. In fact originally it was think that ABA is the main player on abscisic leaf but this in correct only for a small number of plants. Moreover ABA is produce in terminal buds to slow down the plants growth and prepare it for the winter (it is also produce in response to water depravation by roots). So probably ABA could also migrate in leaves and provoke the stomata closure.
This is what wikipedia suggest by looking on Abscisic acid.

ABA was originally believed to be involved in abscission. This is now known to be the case only in a small number of plants. ABA-mediated signaling also plays an important part in plant responses to environmental stress and plant pathogens [...].
Abscisic acid owes its names to its role in the abscission of plant leaves. In preparation for winter, ABA is produced in terminal buds.This slows plant growth and directs leaf primordia to develop scales to protect the dormant buds during the cold season. ABA also inhibits the division of cells in the vascular cambium, adjusting to cold conditions in the winter by suspending primary and secondary growth.

By digging more on internet I found that abscission (the shedding hence the dropping of the plant leaves) occurs after the senescence of the leaf. In fact, before the leaf falling, the plant draws resources out of leaves and degraded the chlorophyll. This will cause also the change of colour (the leaves are green thanks to the presence of chlorophylls).
Finally I think that the stomata closure is also due by the darkness and the senescence. In fact the open or close state of stomata is mediate by guard cell and their state (swollen guard cell stomata is open, shrunken guard cell stomata is closed. Those state are influenced by Temperature, Darkness, Photoperiod, pH and also ABA. Hence when the plant start to take out nutriments from leaves, on leaves there will be a rise on pH and a diminution on water contents that will provoke the closure of stomata. Those two image could maybe help 3.

Hope my answer will help.


Same 185th million grandfather? I was watching a lecture by Richard Dawkins earlier today and he mentioned that “Your 185th million grandfather was a fish.” I started wondering about the following question,

Is it true that my 185th million grandfather is the same as your 185th million grandfather?

Now, I fully recognize that there are more generations in my family tree than in yours or vice-versa so the 185 million may not match up exactly. This is not the point of the question. Do Humans share a common ancestor substantially after the origin of life?

All currently existent forms of life (and all their ancestors) are thought to be descended from a single life form known as LUCA (Last Universal Common Ancestor). Within those organisms, all organisms that share a common ancestor more recent than LUCA are said to be phylogenetically related. These organisms are (ideally - see note) grouped together by scientists into monophyletic taxa.

Therefore, ideally, each taxon represents a group of organisms that have descended from a single common ancestor, not shared by any other taxon. Taxa are defined at various levels including, but not limited to, Kingdom, Phylum, Class, Order, Family, Genus and Species, with organisms at each level having a more recent common ancestor than the ones preceding it. For example, for humans, a superficial phylogenetic classification would look somewhat like this:

Kingdom: Animalia (shares a common ancestor with all multicellular, eukaryotic, heterotrphic, motile organisms)
Phylum: Chordata (shares a common ancestor with all animals that possess a spinal cord)
Class: Mammalia (shares a common ancestor with all chordates that produce milk and are warm-blooded)
Order: Primates (shares a common ancestor with all monkey-like mammals)
Family: Hominidae (shares a common ancestor with all the great apes)
Genus: Homo (shares a common ancestor with relatively recent humanoid species)
Species: sapiens (shares a common ancestor with all humans)

As you can see, this means that all humans share a common ancestor with all other humans, but going further back, they also share a common ancestor with all primates, all mammmals and all vertebrates. Eventually, all animals share a common ancestor, and if you go as far back as LUCA, so does all life.

Note on taxonomy and phylogenetics: Many modern taxa are (to the best of our knowledge) monophyletic, meaning all organisms in a given taxon share a unique common ancestor. However, there remain several taxa that are paraphyletic, because they were described before modern genetic methods became available, or because no one has got down to reclassifying them or (in at least one case, reptiles and birds), because they are so widely used that changing the classification could (and probably would) cause a lot of confusion. So, when using taxonomic classifications to deduce phylogenetic relationships, a bit of caution must be exercised to ensure that the taxon one is talking about is indeed monophyletic.


Which blood vessel carries the most impure blood? There is a question in my Biology textbook:

  "Which blood vessel in the human body carries most impure blood after
  few hours of meal."

The answer is given as Renal artery.

But I think the answer should be Hepatic Vein, because the liver produces urea and other waste materials and then it pours it all in the right ventricle of the heart for oxygenation. And then the heart distributes the blood to various parts of the body. So the impure blood brought by the Hepatic Vein and other blood vessels gets distributed through the aorta. This will automatically imply that the Renal Artery will contain lesser impure blood than the Hepatic Vein.

Impure blood is the blood with urea, uric acid and other components of urine.

It would be good if you give your opinion and also a reason for it.

It's the renal artery because it will contain everything from the liver as you describe plus all waste accumulated on the way from the liver to the kidney. Here it gets filtered, so there cannot be a place after the kidney that is less "pure".


What makes DNA sticky-ends sticky? When restriction enzymes jaggedly cut double stranded DNA it results in so called sticky ends. What is the substance that makes the DNA sticky?

What are sticky ends.
There is no substance that is attached making the DNA ends "sticky". What has actually happened is an overhang of at least a few nucleotides. Blunt ends are another kind of cut, but have no overhanging residues.

Why are sticky ends sticky?
Restriction enzymes usually cut these ends deliberately so that a four nucleotides are overhanging on the 5' end of the double strand. These are complementary to other overhangs and because they are less stable than a bound double strand region, and are able to hydrogen bond easily with complementary bases, they are easier to attach with a ligase.

Below is an image of the base pairs interacting via H bonds.


What is the reasoning behind the Drake Equation? I've read a bunch on how the Drake Equation is constructed, but I'm not able to understand some of the reasoning behind it.

$$
N = R_* \cdot f_p \cdot n_e \cdot f_l \cdot f_i \cdot f_c \cdot L \cdot f_d
$$

Why does $f_c$ represent the fraction of intelligent life able to communicate? Isn't communication (in some form) part of what defines intelligent life itself? Or is this term included just to break the number down further?

I'm asking this here and not elsewhere because I'm wondering specifically about this term and not the entire equation.

Humanity has had roughly the same level of intelligence for tens of thousands of years, and as the Drake Equation estimates the number of civilizations capable of extrasolar communication - we only met that criteria ourselves within the last century.


It there any experimental approach to determine the electronic structure of a given aminoacid inside a protein? It there any experimental method to determine the electronic structure of a given amino acid inside a protein?

The two most often used methods used to determine protein structures are X-Ray crystallography and NMR (nuclear magnetic resonance spectroscopy). Both of these allow some deductions of electron configuration, but don't actually measure it directly (and as far as I know there is no method available that can do that, but physicists might know more about that).

X-Ray crystallography essentially detects the electron density of a protein crystal. Usually this density is 'only' used to calculate the structure of the protein, but using good controls and smart math might allow one to also detect charges or specific electron configurations (I haven't checked if anyone ever tried something like this). One general caveat of protein crystallography is that the protein structure/configuration in a crystal may not actually correspond 100% to the state of the protein in its normal environment.

NMR measures the chemical shifts and coupling (quantum) spin of atom nuclei (usually H, N & sometimes C), which is more or less directly depend on its electronic micro-environment. Since structural biology usually doesn't care about things like orbitals, protein NMR data is then used to determine the distance of specific nuclei, which allows derivation of a protein structure.
Since NMR data directly measures atomic properties of single nuclei, I think it is probably the closest to what you are looking for, but asking actual NMR experts will be necessary to figure out whether determining specific orbital configurations could be possible (and even then it would likely be a multi-year interdisciplinary research project).

Another approach, that was mentioned in the comments on the question, would be determining charges on specific amino acids, which could be done using biochemical or spectroscopy assays, if one is only looking at one (or a few) specific amino acids in a protein. These assays need to specifically designed for your protein and amino acid of interest - I can't give specific sources here, but reading up on how people (started to) figure out the chemical mechanisms of enzymes might give you some insights on possible experiments.


Why don't weak detergents lyse the nuclear membrane? A low concentration of a non-ionic detergent lyses the cell membrane, but leaves the nuclear membrane intact. Both are phospholipid bilayers, so why is only the cell membrane lysed?
Under these conditions, are the membranes of other organelles lysed?

First, an important fact   about non ionic detergents- {1}They have a hydrophilic head group that is uncharged and are preferred for their ability to break lipid-lipid and lipid-protein interactions. They have limited ability to break protein-protein interactions and are often referred to as non-denaturing detergents and are used to isolate biologically active membrane proteins.
Generally, moderate concentrations of mild (i.e., nonionic) detergents compromise the integrity of cell membranes, thereby facilitating lysis of cells and extraction of soluble protein, often in native form.
An example would be Triton X-100. {2} Non-denaturing detergents such as Triton X-100 have rigid and bulky nonpolar heads that do not penetrate into water-soluble proteins; consequently, they generally do not disrupt native interactions and structures of water-soluble proteins and do not have cooperative binding properties. The main effect of non-denaturing detergents is to associate with hydrophobic parts of membrane proteins, thereby conferring miscibility to them.
The following article is about the same protein insolubility that I have written above, but in the nuclear membrane of chicken RBC’s. {3}

Protein has been selectively extracted from isolated chicken erythrocyte nuclear envelope by (1) dilute MgCl2/Triton X-100 followed by (2) concentrated MgCl2/Triton X-100 solutions. Certain proteins appear to be selectively dissolved in the first solvent and may occur in the nuclear envelope primarily as lipoproteins. Among the proteins insoluble in the low MgCl2/Triton X-100 wash, as well as in 500 mM MgCl2 without Triton previously used in the preparation of the envelope fraction, the quantitatively major polypeptides dissolve in a combination of high MgCl2 and Triton X-100. Further, much of this dissolved protein precipitates when the MgCl2 concentration is lowered by dialysis. The insolubility of these proteins appears to result from a combination of ionic and hydrophobic interactions and may explain the resistance of nuclei to various manipulative procedures including nonionic detergent washes.

The conclusion is that the protein insolubility of these detergents is what makes the nucleus resistant. You know that the phospholipid bi-layer is common for both- the cell membrane and the nuclear membrane. But underlying the inner nuclear membrane is the nuclear lamina, a fibrous meshwork that provides structural support to the nucleus. The nuclear lamina is composed of one or more related proteins called lamins.
Coming to your last question, using the example of Triton X-100 and leukocyte cells, a paper says: {4}

Leukocyte membranes except the nuclear envelope were solubilized in a buffer that contained 1% Triton X-100.

Which means that all membranes- including mitochondrial, dissolve in the detergent because they do not have an additional protein layer in them, like the nucleus does.
1-http://www.genotech.com/protein-research/detergent-accessories.html
2-https://www.thermofisher.com/in/en/home/life-science/protein-biology/protein-biology-learning-center/protein-biology-resource-library/pierce-protein-methods/detergents-cell-lysis-protein-extraction.html
3-https://pubmed.ncbi.nlm.nih.gov/999948/
4-https://link.springer.com/article/10.1007/BF00554425


What is measured by electroencephalograms and local field potentials? In the Scholarpedia article on local field potentials (2013), I read:

  The current view is that EEG and LFPs are generated by synchronized
  synaptic currents arising on cortical neurons, possibly through the
  formation of dipoles (Niedermeyer and Lopes da Silva, 1998; Nunez and
  Srinivasan, 2005).

There are three things I do not understand:

What does "on neurons" mean? Why not "in" or "around neurons"?
I assume that what is measured is the electric potential in an electric field that is generated by charges (the ions). So only the changes of the measured potential are due to currents, the potential itself (at any given point in time) is only due to the distribution of charges. Is that view correct? Independent of the nature of the charges.
What exactly are the above mentioned dipoles? Of which are they formed and what is their size? (At least, the article says "possibly generated through the formation of dipoles".)

Does all this sum up to the picture that it is all and only about the ions that pass through the ligand-gated channels at a synapse and the electric field and potential generated by them, the contribution of all other charges being cancelled and filtered out?

[I give this as a sketchy answer being aware that it might be nonsense. So feel free to downvote in this case. I should have mentioned - thanks to Bryan for having remembered me - that this answer has been inspired by Buzsáki/Anastassiou/Koch's article on The origin of extracellular fields and currents and just tries to sketch the mental image this article evoked in me.]

I assume that what is actually measured by an EEG electrode is an effective dipole moment in the upper cortical layers underneath the electrode (which decays with $1/r^2$). The way this dipole moment is created by "brain currents" is the matter of this answer.

There seem to be some premises under which a measurable EEG signal (= a dipole) can be detected:

The presynaptic action potentials must arrive highly synchronized. (Additive superposition.).
The apic dendrites of the pyramidal neurons that give rise to the dipole must be vertically oriented (pointing to the skull, resp. the electrode). (Orientation of the dipole.)
The sodium potassium pumps trying to restore the rest potential are unevenly distributed, i.e. mainly located at the soma. (Breaking the symmetry.)

This is the situation for the neuron (gray) at rest:

The dipole then forms as follows in three steps:

Step 1: An presynaptic action potential releases neurotransmitters that open ligand-gated ion channels causing sodium ions to enter the neuron.

Step 2: The extra sodium ions wander quickly to the soma. This happens passively, i.e. driven by repulsion and diffusion. At the end of step 2, all ions inside the neuron are distributed approximately evenly (i.e. not giving rise to an inner dipole).

Step 3: At the soma sodium ions are pumped out of the neuron. During this step equidistribution of ions is maintained inside the neuron (still no dipole inside the neuron).

In the extracellular medium, we now have an observable dipole.

Summary: What is measured by an EEG are not directly "brain currents" but an effective dipole moment that results from three different currents on different time scales:

Ions passing the membrane of apic dendrites into the neuron. (Slow.)
A net flow of ions wandering from dendrite to soma (driven by repulsion and diffusion). (Fast.)
Ions leaving the soma, e.g. by sodium pottasium pumps. (Slow.)


Which requirements are needed for 2 different species to be able to have offsprings? Sometimes different species mate and they are able to have offsprings, usually with anomalies. Are there known requirements for 2 different species to produce offsprings? Why species like the lion and the tiger, which seems to have many differences are able to produce offsprings, when others which supposedly share 99% of the DNA can't?

Lets break this down like a logical problem. In reality, it involves the correct gene expressions at the correct time, place, etc. But that would be a book.

Prezygotic reproductive isolating mechanisms

Environment

A bull and a whale can't mate; they don't live in the same environment. Lions and tigers similarly do not mate in the wild due to lack of overlap in the environment. In captivity, yes.

Delivery of gametes

Sperm must be able to be delivered to the ovum for fertilization to occur. Some species just can't get this part right. Your house cat would not be a suitable donor for an elephant.* In closer species, say a chicken and a peacock, the rooster's courtship display (which is nowhere near as spectacular at the peacock's) will not be accepted by the female; no opportunity for delivery of gametes.

Some gametes can be delivered but not ova (the female isn't "in season".) Zero there as well.

Unity of gametes

If the gametes are both delivered at the correct time, can the sperm bind to the egg? Successful binding requires a receptor-ligand interaction which actually has a high degree of species specificity. So binding requires that the sperm and the egg can, say, "communicate" successfully. Dog sperm doesn't "speak" cat ovum.

If they do "speak the same language", can the sperm penetrate the ovum's protective coating (the zona pellucida)? Assuming sperm capacitation (a big hurdle right there), the sperm may not have the correct enzymes in it's 'head' to penetrate zona pellucida. Not all enzymes carry out the same function on all molecules, and if the correct enzymes are present to digest/break through the zona pellucida, is there enough? Is the sperm active enough? I'll liken this kind of communication to 'pillow talk'. We're getting much closer. Let's say the sperm has his pillow talk down, and can penetrate the layer.

Postzygotic isolating mechanisms

Viability

The hybrid embryo must be able to develop into a zygote. Hybrid inviability means there wasn't enough similarity to proceed to a blastocyst and the hybrid dies.

Say viability is achievable. The blastocyst/blastomere must "communicate" with the mother so that attachment is not only possible but can be sustained. In effect, it must "shout" to the mom, "I'm here! Pay attention to me!" (In humans, this involves secretion of large quantities of a hormone called chorionic gonadotropin, which stimulates continued secretion of progesterone, thus no shedding of the uterine lining. Not all mammalian blastocysts communicate the same way. If what we have here is a failure to communicate... as with Cool Hand Luke, the result is not good.

Hybrid sterility

The species were close enough for the conceptus to be heard by the mom. The right chromosomes with the right gene expression results in a live birth.

Success!

If the hybrid is fertile, it is by one definition not a different species. (There is much debate as to what exactly defines a species. See the references.)

If you are still left saying, "But why?", then it must be explained on a genetic/molecular level, with sentences like,

  The zona pellucida of mammalian eggs is composed mainly of three glycoproteins, all of which are produced exclusively by the growing oocyte. Two of them, ZP2 and ZP3, assemble into long filaments, while the other, ZP1, cross-links the filaments into a three-dimensional network. The protein ZP3 is crucial: female mice with an inactivated ZP3 gene produce eggs lacking a zona and are infertile.

If this is the level of explanation you seek, there's a book for you: Molecular Biology of the Cell. Alberts B, Johnson A, Lewis J, et al.

Fertilization
The Process of Speciation
Fertilization

*Note here I'm referring to morphological differences, one way used to define species.


Does the location of the double bond in chlorins yield a distinct biological function? Chlorins differ by the number of double bonds and their location. Chlorin has 20 pi electrons, whereas bacteriochlorin and isobacterichlorin have 18 pi electrons, but at different locations.

Do chlorin, bacteriochlorin and isobacteriochlorin have distinct biological function due to this double-bond difference?

I only found a hint that this might be the case in this publication by Singh et al., stating

  Porphyrins, chlorins, bacteriochlorins, and isobacteriochlorins each have unique photophysical properties that are exploited by nature and can be used for diverse applications (1, 2).

I don't have access to "The Porphyrin Handbook" (The first citation in the quote above), but I suspect it would be your best guess in finding more information.


What determines the physical location of differentiated cells in an organism? Exposition:

As a little kid, I always thought of DNA as being a description of how to build an organism. For example a human DNA would have "Add two legs and two arms", a dogs DNA would have something like "put a tail here". Now, at school, I have learned that DNA codes for proteins, for structural proteins, enzymes etc. But how does a growing fetus actually know where to put the different parts of the body?

Examples:

For example, why don't I have retinal cells growing on my feet? Why is my cerebral cortex not in my mouth? And where is the information stored that humans do not have tails, or that elephants have trunks?

Summary:

What determines where different cells should be located, and how is that information stored?

Cool question. As the other answer mentions, the process is very complex, and we are still learning the relevant mechanisms in organisms other than the fruit fly. But it is considerably well described in the fruit fly which merits a brief summary.

Since a lot of asymmetric (A-P axis, for our purposes) development occurs pretty early in embryonic growth, whatever drives this pole-specific differentiation must act early. As it happens, it begins as early as maternal ovum (Bicoid mRNA). Using cellular machinery (microtubules, motor proteins), these are concentrated towards one end of the egg and subsequently of the early embryo. Once such an asymmetry in the concentration is achieved, further development genes can take advantage of this patterning by being influenced by downstream signalling. Hence there is a cascade of gene activation downstream, which involve Gap genes, Pair-rule genes and several homeotic genes (see Hox genes) which are also differentially expressed along the A-P axis. They directly control patterns of the organs formed from there. Using a gradient of these genes, further patterning of organs can be similarly achieved (the retina gene would be activated only at a concentration of these genes which is found only at the top and so on).


How does a fetus retain a blood group different from its mother? It's a well-established fact that blood group is decided by genotype. But, when a new child starts its journey in the womb, the mother's blood (along with it's agglutinins and agglutinogens) flows into the baby's heart. So, how does a baby (having a blood group different from that of the mother) retains it's own blood group (with it's own agglutinins and agglutinogens) instead of the mother's blood group, which moves in and out of the baby through the umbilical cord.

Do both kinds of blood flow in the baby's body constantly in such a case?

Apart from that, I know of rhesus incompatibility. But there are also incompatible blood group types. How does a baby survive agglutination in those cases?

The maternal and fetal blood circulation systems are completely separate. The embryo's blood cells start developing at around week 5 gestational age (3 weeks after conception), the same way any other tissue is developed by the fetus itself. By around week 7 gestational age, a circulatory system has developed and the heart has started beating.

All nutrition goes through the placenta, which keeps the two circulatory systems separate by the so-called placental blood barrier.

Rhesus incompability is only a concern after the first birth (or miscarriage) because then the maternal and fetal blood had the opportunity to mix and lead to the mother developing antibodies.

Also, as AMR pointed out in the comments, blood group incompatibility is mediated through IgG antibodies - those don't start to be produced at all until birth and at higher levels not until six months to a year after birth. See also At what age do babies begin to synthesize their own antibodies?


Why do physicians try to match HLA complexes for organ transplant? My understanding of acute transplant rejection is that donor dendritic cells present donor antigens on MHC1 to host naive CD8+ T-cells resulting in an immune response against the graft. If you match MHC1 complexes between donor and host, wouldn't t-cell activation actually be more likely than the case where MHC1 complexes between donor and host are different?

Reasoning: I imagine in the case where MHC1 complexes between donor and host are different that the  t-cell receptor is unable to bind the MHC1 complex in the first place..making the transplant essentially invisible. In the case where MHC1 complex between donor and host are the same, the t-cell receptor would bind the MHC1 complex, and increase the likelihood of an immune response. Given that HLA mismatch is a major cause of transplant rejection, something is wrong with my reasoning. Thoughts?

Cells with low MHC1 or non-recognizable MHC1 are destroyed by NK cells, so e.g. viral infections, intracellular bacterial infections and cancer cells cannot hide with their "abnormal" proteins...


What is the biding site code recognized by the parts of the spliceosome Another question about another Youtube video. At 0:50, the splicing process begins to remove the non-coding section of the DNA (intron), so the different parts of the spliceosome attach to the borders on the intron.

My question is, what is the code found in the borders of the intron which is recognized by the parts of the spliceosome, so they attach to it ?

For example, in the transcription of the DNA, the process begins after the transcription factor "TBP" recognizes the code "TATA" in the DNA string, then attaches to it. This triggers a whole process described by this video.

Did you try googling "splice site recognition sequences"?

In general, the first two letters of the intron must be GT, the next three are often ARG.

The last three letters of the acceptor site of the intron are virtually always YAG


Effect of 260/230 values on PCR To what extent does the 260/230 value affect the efficiency of PCR reactions ? Do the constituents leading to a low 260/230 value (EDTA, guanidine salts and oligosaccharides) inhibit PCR ? I have been getting pretty low values of 260/230 (0.5-1.0) for DNA extracted using Charge Switch Protocol using Magnetic beads and the PCR has been failing. Also, is there any reason why I might be getting low 260/230 values in Charge Switch method ? (I was getting good values using Phenol-Chloroform extraction method)

EDTA carbohydrates, phenol all have absorbance near 230 nm.  TRIzol reagent is a phenolic solution which absorbs in the UV both at 230 nm and ~270 nm

Guanidine HCL used for most DNA isolations will absorb at ~230 nm also

All these things will seriously inhibit your pcr, (and lower your ratio) especially the denaturing agents like guanadine.

All these DNA kits are different spins of a pretty similar process.

If you have a good steady centrifuge stick to the phenol & ethanol. Be certain you are drying your pellet well, but don't over dry it. I'll hear my pellet at 37 for 3-4 min to get rid of ethanol. Ethanol no good in pcr. If you hate doing ethanol precipitation (which I do) cause of invisible pellets, add a high grade bit of glycogen to your aqueous phase before the precipitation. This will make your pellet visible and is completely inert.

If your cleanup isn't the problem do an annealing  and Mg gradient and up your primer quantity.

May want to give me more info like the individual absorbance, pcr conditions, template size etc

Traditionally bead purifications gives really good purity, reason I use it for microarrays. But it's expensive and not necessary for pcr.

Charge switch is just changing the charge of the bead by changing the ph.


Are there any animals that gradually approaches the predator to search for food? I was wondering if there is an animal (or insect, bird, etc.) that eventually comes close to its predator to search for food, but only does so if it couldn't find food in the environment it is in. So it first searches part of the environment farthest away from the predator, but gradually comes closer and closer to the predator as it searches for new food. That is, over time it dares more to come closer to a, lets say ambushing predator, since it has ran out of food (or perhaps for other reasons). Similar behavior is ok, but note that the key behavior that I want in the animal is that it "gradually" comes closer and closer to the predator.

Thank you.

The behaviour that you describe is common in most animal species, as part of the natural trade-off between access to food, minimizing risk, habituation and hunger. Animals usually choose to forage in high-quality habitats that has a low risk of predation, but if food sources are depleted (or competition and/or territoriality is high) they will move to other areas with lower food quality or higher risk (since they are desperate for food).

In general, the effect of predators are both direct (killing of prey) and indirect (changes in prey behavior to avoid predation). The indirect effects means that prey will often choose to feed in habitats that are suboptimal from the perspective of forage quality, which will have negative effects on their foraging efficiency. These types of indirect effects of predators are often labelled as 'The landscape of fear' or the 'ecology of fear' (see e.g. Brown et al, 1999). However, as food resources run out this will trade-off against the fear of predators (along with possible habituation effects), which will lead to the behaviour you are asking for. You might also be interested in Gamelius et al (2014), as an example of how prey behaviour can be influenced by the presence of predators (here, roe deer and lynx), but there is a large number of studies looking into these issues. The review "Fear in animals: a meta-analysis and review of risk assessment" by Stankowich & Blumstein (2005) will also give you a good background and many examples.

The use of scarecrows is a simple way to understand the 'landscape of fear'. By placing a scarecrow in a field you strengthen the "landscape of fear" (by adding an artificial 'predator'), which will modify the behaviour of perceived pest species (prey), so that they avoid the areas around the scarecrow. However, if the animals you want to scare away ("pests") run out of food they will take larger risks and venture closer to the scarecrow to forage. Over time, they will also become habituated to the scarecrow, and will discover that it doesn't seem to pose a big threat, which will decrease the effectiveness of the scarecrow.

References

Brown et al. 1999. The Ecology of Fear: Optimal Foraging, Game Theory, and Trophic Interactions. Journal of Mammalogy
Gamelius et al. 2014. Habitat Selection and Risk of Predation: Re-colonization by Lynx had Limited Impact on Habitat Selection by Roe Deer. Plos One
Stankowich & Blumstein. 2005. Fear in animals: a meta-analysis and review of risk assessment. Proceedings B


What kind of small insect is this? Found in central florida in the bath tub. Its about the size of a pencil marking, very small. What is it?

This small hexapod appears to be a species of Springtail (or Collembola).  It is similar to the one below, with slightly different markings.

From the University of Florida:

  Springtails are minute insects without wings in the Order Collembola. They occur in large numbers in moist soil and can be found in homes with high humidity, organic debris, or mold. Homeowners sometimes discover these insects occurring in large numbers in swimming pools, potted plants, or in moist soil and mulch. They feed on fungi, fungal spores, and decaying, damp vegetation, causing organic material and other nutrients to return to the soil; these nutrients are later used by plants. Occasionally, springtails attack young seedlings and may damage the roots and stems.

More information can also be found at NC State University Entomology Website:
http://www.cals.ncsu.edu/course/ent425/library/compendium/collembola.html

It is hard to say what species it could be, but it looks most similar to:

Isotomurus plumosus:

or Isotomurus tricolour from Rick Cowen:

It is hard to tell but it seems to be part of this genera, or is at least in the family Isotomidae, if not the exact species.

Their taxonomy is actually under debate, and they are in a group of hexapods that are no longer considered insects.


Biological origin of shuddering during sleep What is the biological origin of the following behavior:

Sometimes, during the early, formative phase of sleep (when you have a gradually dimming consciousness of what all is happening around), you feel some kind of a tremor of sorts - a feeling as if you are about to fall off. The body responds by twitching the limbs, so as to "balance", and you end up waking up for a second or two, where you realize that you aren't about to fall and all is fine.

Since Cerebellum is involved with maintaining equilibrium and balance, I have the intuition that this is related to some transient behavior where the Cerebellum is dimming down. When you are in deep sleep, you do not have a sense of balance, so I guess Cerebellum does dim down the sense of equilibrium.

But the apparent flaw in my reasoning is - if this was indeed the origin, one would have experienced these tremors every time one slept. That doesn't happen, it is only occasional (AFAIK).

So, biologically, what is the true origin of this behavior?

These are called hypnic jerks, also known as hypnagogic jerks or sleep starts. They are normal part of the wake-to-sleep transition. Hypic jerks consist of non-periodic myoclonic movements, generally involving an isolated limb.

The exact physiologic origin of hypic jerks is unknown. We can say that they correlate with a particular waveform on the EEG known as a K-complex:

Picture from http://en.wikipedia.org/wiki/K-complex

K-complexes are a normal part of Stage II sleep and can evoked using auditory stimuli, even if sleep is not interrupted. In the case of hypnic jerks, the K-complex is usually followed by alpha (wake) activity. To my knowledge, there is no evidence that hypnic jerks originate in or are routed through the cerebellum. K-complexes themselves are related to cross-talk between the cortex and the thalamus, a circuit that doesn’t involve the cerebellum.

In addition to the EEG findings, it has also been shown that the jerks are accompanied by autonomic activation — transiently increased heart rate and respiratory rate. There is also an (unexplained) subjective aspect. You described it as feeling "as if you are about to fall off,” which seems to be consistent with the published literature on this. As mentioned in the review cited below, some people report a sensation of "falling into the void.”1

The clinical implications, in case you were wondering, are summarized well by Vertugno et al.:

  Sleep starts are common physiological phenomenon affecting up to 70% of the adult population and their course is benign, resolving without any neurological sequel. Therefore, reassurance and counselling are all that is needed to treat the patient. Though an adequate explanation and reassurance may be sufficient, some patients may require a small dose of clonazepam (0.5–1 mg at bedtime) to ameliorate the symptoms on a short-term basis.

1. Vetrugno R, Montagna P. Sleep-to-wake transition movement disorders. Sleep Med. 2011 Dec;12 Suppl 2:S11-6.

You requested in a comment a reference to introductory material on the topic. What we know about the neuro-physiology of sleep is mostly based on the analysis of EEG (brain-wave) tracings. I therefore refer you to this introduction to sleep polysomnography if you would like to get a better handle on how scientists think about sleep.


Why do some animals have beards? Why do some animals such as some Goats, Ibex, Orangutan etc, have long well-shaped beard like men?

In humans and animals beard growth is usually restricted to males, since it's dependent on hormones (testosterone or, specifically, according to wikipedia it's dihydrotestosterone). By no surprise it starts growing during puberty.

But why?

Growing a long beard is costly concerning the necessary resources but also because of a potential handicap. Being able to afford a nice beard is showing dominance among males and attractiveness for females. It could be seen as a direct display of high testosterone levels. This is comparable to peacock feathers. They are very impractical, but have great value for showing dominance and attracting females.

I think, there are many psychological theories around to explain the attractiveness of beards. Some might also be meaningful in animals. Apart from cultural, religious or hipster beard trends, we generally consider old men with long beards as wise and knowledgeable. In animals the beard might also signal social status in groups, additionally to male dominance and sexual attraction.

Further reading:

Importance of hair in humans and hormones involved
Sexual attraction of beards in humans
Trustworthiness of bearded men
Intrasexual competition influencing sexual dimorphism (here: size)
Sexual selection
Costs and benefits of male hair (lion mane)


Non Coding DNA and its effect on evolution I had a discussion with a friend of mine; from his understanding, bacteria and other small organisms have higher amounts of "coding" DNA and, as such, are able to evolve much faster than organisms like us.  His argument was that if bacteria are able to evolve so much faster than us, then they should have become the Apex Predators on Earth instead of humans.

I argued that the 2% of the "coding" DNA is probably as long as the 90% of a bacterium (I'm guessing at this point) and that it is the bacterium's small life span that makes it evolve so fast.  Was hoping to get clarification from someone with more experience in the field.

Richard Dawkins discusses this in his book The Greatest Show on Earth: The Evidence for Evolution

Bacteria and other microorganisms, specifically Archaea, are able to exchange in a sort of 'copy and paste' genetic exchange that differs wildly from sexual reproduction.  They can even exchange genes with other distantly related species.  This, coupled with their short (compared to Humans) lifecycle, accounts for much of the difference in evolutionary rates.  Often, it makes sense to speak in terms of evolution in terms of specific genes themselves (in the case of bacteria), as opposed to evolution of the species as a whole, due to the 'copy and paste' exchange that can take place.  For Bacteria, there is something to be said for compiling a 'true' family tree for each gene separately, regardless of which kind of bacteria in which it resides.

Dawkins remarks, "The philosopher Dan Dennett has put it, 'Where the tree of life for animals is a majestically spreading oak, that for bacteria is more like a banyan.'"

Also, evolution by Natural Selection and random mutation does act on 'non-coding' DNA, just to be clear.


Is it possible to add a new sequence to a blast database without recreating it from scratch? I have a new sequence and I want to add it to a pre-constructed BLAST database containing other sequences. The makeblastdb help does not give any hint on this regard.

You can use blastdbcmd to extract FASTA sequences from the BLAST database. Then you can append your extra sequence to the newly created FASTA file, and remake the BLAST DB using makeblastdb. Assuming you have a protein BLAST database in the current working directory, and a sequence you want to add to it in new.fa:

$ blastdbcmd -db proteindb -dbtype prot -out db.fa -entry all
    $ cat new.fa >> db.fa
$ makeblastdb -in db.fa -out newproteindb -dbtype prot

(Replace prot with nucl if you have a nucleotide database)


Are wasps attracted to a sting A little backstory, I was trying to get something that was in a little wooded bit at the back of my garden and stepped on a swarm of wasps was stung 3 times and got out of there but I brought 8 wasps inside and was wondering if they know if you've been stung and are attracted to it and also out of curiosity what would happen to a wasp if it was stung by another wasp

Tackling the second part of the question first: If a wasp is stung by another wasp, that's usually super bad for the wasp in question. Wasps are pretty good about not stinging one another, but occasionally wasps from other communities come in and cause a ruckus, or even predate on other communities of wasp specifically. If a wasp gets stung by one of these, it's about to die horribly, then get eaten.

On the other hand, if it's stung by 'friendly fire', it'll just die horribly. The venoms wasp stingers carry, while merely irritating and only occasionally fatal due to allergies on our scale, are generally pretty lethal to insects, arachnids, and other tiny critters; also, having a huge hole in your exoskeleton doesn't help.

As for the attraction question, the answer is a solid and absolute 'Eh, probably not.'.

Wasps, like a lot of insects, communicate on pheromones and dancing, but on the whole their 'deal' when not hunting is to repel, not kill. They don't care if what they sting gets killed or not; so long as it gets out of their zone of control. While they do issue alarm pheromones and other calls to action, these are not associated with stings in particular, which mostly deliver poison and sharp force trauma, not orders to the swarm.

You'll probably want to clean out the stings in any case, but it's unlikely that your new house guests want anything so much as just going home. Usher them out the door, and they'll be happy as clams.


BLAST with minimum E-value cutoff It's easy to set the maximum E-value threshold in a BLAST request. I need to set the minimum E-value. Does anybody have any suggestions?

There is no such option. You can perform the alignment and filter the hits later. However, I wonder why you really need that. Lower E-value indicates lower chance of an alignment randomly picked from a database, to have a given score.


How do parents give their offspring a chromosome? Whenever an organism sexually reproduces, it gives its offspring one chromosome from each of its pairs of chromosomes. My questions are

Is this done randomly?
Is it uniformly random?
If so, what mechanism allows it to be random, considering that the laws of physics are deterministic?

(Note: I'm a little rusty on this subject, so if there are any errors in the question, feel free to correct them.)

Are the laws of physics deterministic? I think no one knows, currently.

In any event, yes, the segregation of homologous chromosomes during meiosis I is random: there is an equal probability for each chromosome of a homologous pair to segregate into a given gamete, and this is independent of other homologous pairs. This idea dates back to Mendel, who observed that the heritable “factors” (what we now know as genes) responsible for macroscopic phenotypes are inherited independently of one another (this is his Law of Independent Assortment). This isn’t actually true when considering linked genes, but is certainly true of chromosomes, as was described by Sutton in 1903:

  ...many points were discovered which strongly indicate that the position of the bivalent chromosomes in the equatorial plate of the reducing division is purely a matter of chance - that is, that any chromosome pair may lie with maternal or paternal chromatid indifferently toward either pole irrespective of the positions of other pairs...


Base pair and amino acid weights? How does a base pair weigh approx. 650 Da (which is two paired nucleotides) but an amino acid (3 nucleotides) weighs only approx. 110 Da ?

In short: base pairs are not composed of amino acids but nucleotides. Base pairs are parts of the DNA, while chains of amino acids forms proteins.
Certain parts of the DNA (called genes) are transcribed to messenger RNAs (mRNA) which are sequentially translated to amino acids and the chains become proteins. 3 bases (called a codon) code for 1 amino acid.

Please look up the Central dogma, DNA, mRNA, protein and translation for further information


What is the difference between a phosphotransferase, a phosphatase, a phosphorylase and a kinase? I've looked in several sources, but I'm still confused. This is what I have so far:

A phosphotransferase catalyzes the addition of a phosphate group.
A kinase is a type of phosphotransferase that transfers a phosphate group from ATP to a substrate.
A phosphorylase is a type of phosphotransferase that catalyzes the addition of a phosphate group from an inorganic phosphate (HPO4) to a substrate.
A hydrolase catalyzes the hydrolysis of a chemical bond.
A phosphatase is a type of hydrolase that removes a phosphate group.

Is this right?

EDIT:
Also adding to the confusion is the enzyme Phosphorylase kinase, which is the kinase that phosphorylates the enzyme Glycogen phosphorylase, which hydrolyzes glycogen.

Don't get caught in the linguistic trap of attaching too much significance to the precise meaning of any one piece of scientific jargon. Nomenclature, the system of naming things, utterly sucks in biology, and it sucks even harder for protein biology. There is no one universally accepted classification and naming system for proteins, although there have been plenty of attempts.

For example, phosphotransferases are classified as EC number 2.7. However, Glycogen Phosphorylase is classed under 2.4, which might make you think "well, clearly kinases are enzymes that transfer phosphate groups from organic substrates such as ATP and are classed as 2.7, whereas phosphorylases are enzymes that transfer from inorganic substrates and are therefore classed as 2.4". But wait! RNase PH is a phosphorylase that's classed under 2.7 and uses inorganic phosphate, so um... yeah.

In any case, don't get too hung up on the nomenclature. Unless you're working in an enzymology lab just say "kinase" and everyone will know what you're talking about.


Genotypes in diploid/haploid cells under mitotic/meotic cell divisions I am new to genetics , and am stuck with the following question at hand:

  If $2$ cells with genotypes $(A/a)$ and $(A/a,B/b)$ undergo mitotic and meotic cell divisions respectively, what will be the  genotypes/gene compositions in the resultant diploid and haploid cells with respect to the above mentioned alleles?

Can someone help me how to proceed?

Though broad, here I provide a summary in graphical way.

Mitosis:

 .

MEIOSIS: 2 successive steps : Meiosis-1 and meiosis-2

Meiosis-1

Meiosis-2

So lets see what happens with cells given at question.

1. Cell with genotype Aa

(monohybrid or one-point cross-experiments; that means we are looking to gene-pair at 1 loci; not looking to any other genes):

1. A.  Mitosis:

Possible genotypes of their offsprings: All Aa.

1. B. Meiosis:

gametes will show 2-possibilities ; A, a.

2. Cell with genotype AaBb

(dihybrid or 2-point cross-experiments; that means we are looking on genes of 2 loci; not to any other cells):

2.A. Mitosis:

all offsprings AaBb.

2.B. Meiosis:

If given condition says the loci for A (or a) and B (or b) are on same chromosome (linked genes) and no crossing-over is there;

then We will get only 2 types of gamete AB and ab.

If crossing over(s) take place between the 2 loci; then we'll get 4 types of gamete AB, Ab, aB, ab; but their ocurring frequency will deviate from Mendel's independent assortment.

If the 2 loci are not-linked; i.e. they are located in distinct chromosome; then also we'll get 4 types of gametes AB, Ab, aB, ab; but they will follow Mendel's independent assortment pattern.

  Reference:

  Concepts of Genetics, 8th Edition (EBook) By William Klug, Michael Cummings, Charlotte Spencer / Pearson; chapter 2 (mitosis and meiosis)
  The science of Genetics, 6th edition, by George Burns and Paul Bottino, Macmillan.
  Genetics/ P.K. Gupta/ Rastogi Publication Meerut


Does sociality evolved before or after the ability of motility? According to book Life Ascending: The Ten Great Inventions o Evolution.
(Lane, N.;2010),

  Motility has indeed transformed life on earth in ways that are not
  immediately apparent, from the complexity of ecosystems.

As I understand it, when animals had begun to actively use their bodies to locate resources and thus left the sedentary way of life the amount of information they received has increased exponentially. It induced the rapid evolution of additional physiological, morphological and behavioural adaptations such as specialized brain regions enabling spatial memory, vision or cognition.

Was sociality also additional adaption induced by motility?
Is sociality as a life strategy present only in mobile animal species, or they exist also a social sedentary organisms?

Working definition of sociality: Forming of animal group where information transfer enable cooperation among individuals.

I'm going to hazard that primordial sociality by this definition and this question proceeded primordal motility in cells.

Algae started to form physically attached groups like these filaments, giving them some of the advantages of higher organization.

Its easy to see how this is a relatively simple adaptation - just have proteins or carbohydrates on the cell surface that stick together.  This might also have evolved from large cells compartmentalizing since we're talking about very ancient stages of life on earth.


Does eating hard food really cause wisdom teeth to erupt properly? According to the article Bad molars? The origins of wisdom teeth, in our evolutionary history, people were eating harder food like nuts and had unimpacted wisdom teeth. Later, that article appears to have jumped to the conclusion that if you eat hard food, that can actually cause your wisdom teeth to erupt properly. I don't see any reason for that conclusion. Maybe they made that mistake because it's a reasonable mistake to make but it's actually not true. I think that in our evolutionary history, people reproduced at the age of about 14. Although at the age of 28, I started getting an infection from an impacted wisdom tooth and had to have it removed, that was probably already nearly grandparent age according to our evolutionary history and that explains why the natural selection against that type of problem at that age was weak. Maybe after we started eating soft food, we had an evolutionary advantage in having a smaller jaw but the evoluionary cost in having a smaller jaw was smaller because we could just evolve to slow down the growth of the wisdom teeth to delay the potential problems it causes to grandparent age. Just because a change in diet affected the way we evolved doesn't mean a person's actions affects the way their own body grows at the individual level. I do realize that it some cases, ones own actions affects the way their body grows.

You may be thinking "Why didn't you ask the question 'Why did we evolve to have impacted wisdom teeth when it sometimes causes a severe infection?' before asking this one? You could have used its answer to help you ask this one better." I could do that but then I would just end up explaining that I Google searched "why did we evolve to have crowded wisdom teeth if it can lead to infection" and then got the article Bad molars? The origins of wisdom teeth as the first search result. That's the very article I linked earlier in this question that I explained why I suspect is inaccurate. I don't think it would have been better to ask that question first and then explain how the first search result didn't answer my question when that search result is in fact inaccurate. If the question I have can be answered, some way of asking a sequence of questions and picking which Stack Exchange website to ask each of them on that will get me an answer to the question I have has to be accepted.

Yes

The relative size and robustness of the jaw does appear to be strongly affected by diet, significantly more so than other parts of the skull. This is not that surprising many developmental pathways interact with physical activity. Bones in particular often rely on a certain amount of stress to develop properly. It is not all that different from low scale bone atrophy.

Size of the jaw of course effects how much space there is for wisdom teeth. As for the evolutionary effect, consider we have only had access to soft processed food on any scale in the last few generation, that is not much time evolutionarily.

Source


Can animals, like monkeys, be homosexual? I heard that some monkeys can be homosexual? a friend of mine was saying that he saw a male monkey having sex with another male monkey in the zoo, I honestly didn't believe him, I think he just got confused or he made it up.

Could this be true? can monkeys become homosexuals? does homosexuality (other than human) exist in the animal kingdom?

Cases of homosexuality have been described in numerous species, including primates, and the wikipedia link posted by @shigeta lists and describes some of them.

It could be difficult to untangle the difference between an animal not being able to identify sexes very well, or, deliberately mating to anyone and those actively making a choice to engage in intercourse with a same sex individual.

I there are some species where sexes are very difficult to tell apart so they may just go around having sex with anything that looks like the right species because the mating is relatively low cost so doesn't matter if the partner was male or female. This is one such example in sea snails:

  "In a laboratory mate-choice experiment, male N. radiata preferred to
  mate with females, indicating precopulatory sex identification. They
  copulated with males, however, at the frequency of 37%, perhaps
  because of sex misidentification."

Other likely candidates are those with little sexual dimorphism and those with sneaker males that mimic females.

I have also heard theoretical discussions (oh the joys of lunchtime in an evolutionary biology department!) which suggest it may be a way of individuals (particularly males) practising or keeping up fitness relating to sex or stimulating better sperm production etc.

Once you decide what constitutes "a homosexual animal" then it is perhaps easier to examine. I would say a homosexual animal is one that mates exclusively (or highly preferentially) with same sex individuals when given the choice.

Models of genetic and epigenetic inheritance have been used to suggest just how homosexuality could evolve and you can read more about it in this Biology.Stackexchange post.

So it seems that monkeys, and other animals, have been documented to exhibit homosexuality, reasons for them to do so could exist, and it could be a heritable trait which persists despite seemingly strong negative selection.


Any evolutionary explanation for human blood groups? What is the explanation of people having blood types from an evolutionary perspective?

Researchers have puzzled over the selective explanation for the ABO polymorphism at least back to the 1950s. Multiple lines of more recent evidence, including the very old age of the ABO polymorphism and (perhaps) multiple convergent evolution events, suggest that the ABO polymorphism is maintained by balancing selection (E.g. Saitou and Yamamoto 1997, Segurel et al 2012). As best as I know, is no general consensus on what is driving balancing selection, though some researchers have argued that the selective agent is Plasmodium falciparum (e.g. Cserti and Dzik 2007).


Why do pigeons kill their chicks when touched by a human? I used to have many pigeons around the house. If by chance one of the chicks fell out of the nest, we used to put it back using gloves.

Usually, if we would touch the chicks with our bare hands, however, the other pigeons would usually kill the chick. I want to know why they do that?

This is a story I have been told as well when I was a kid. Usually this is related to the foreign smell that the humans leave on the chick. However, this seems to be an urban legend, as birds have not a great sense of smell.

Snopes says about this:

  However, Mother birds will not reject their babies because they smell
  human scent on them, nor will they refuse to set on eggs that have
  been handled by a person. Many birds have a limited sense of smell and
  cannot detect human scent, or if they can detect it, do not react to
  it.

What can happen is that the birds returning to their nest which find the nest disturbed compared to the situation when they left might cause them to temporarily or permanently abondon their nest.

You can find this and more urban legends about birds here and here.


Why does IUCN classify pistachio as a "Near Threatened" species? When reading the Wikipedia entry on pistachio, I noticed that IUCN has classified the plant under "Near Threatened". On looking up its entry at IUCN, I see that its population is trending downwards, and it is "threatened by fruit collection, livestock grazing and cutting". The treat seems to have nothing to do with the often reported fungus. Looking up the yearly yields at Administrative Committee for Pistachios, I see that 2010 and 2012 were bumper years, but otherwise, I see no real trend of a decrease. Quite the contrary, I get the impression that the yearly yield is increasing. It's not as if the tree is difficult to grow, and we rely on trees growing in the wild; these trees are grown in orchards.

So, what's going on? Why would IUCN say that pistachio is Near Threatened?

Short answer: They were talking about the wild species.
Using the presentation by a Farm Advisor and a Pomologist, Pistachio Cultivars as a rough indication of the state of the species, we see that the commercial crop does not have much diversity.

Probably 97% or more of the pistachio acreage in California is planted to the Pistacia vera female cultivar called ‘Kerman’ and a P. vera male called
‘Peters’.

The presentation mentions that other geographic regions prefer other cultivars. But generally, the the entire commercial population of pistachio seems to be limited to a few tens of cultivars.
The IUCN Red List that I cited in the question is rather poor on the details. However, the publication, Geneflow '06, included a report on Uzbekistan's pistachio:

Saving Central Asia’s pistachio diversity
For three millennia, pistachio trees were used in metallurgy and mining in Central Asia due to their accessibility and the highly calorific charcoal they produce. The result was a major depopulation of wild pistachio in the region. During the Stone Age, pistachio trees in Central Asia covered approximately 2 million hectares, compared with only 300 000 hectares today.
The loss of wild pistachio diversity in Central Asia has major implications for pistachio growers in the region and beyond. Most of the pistachio gene pool is to be found here, where it is needed to underpin the continued availability of the tasty nut.

All the reasons they cited as factors for threatening the species likely refers to the wild trees.


What are artifacts in microbiology? What kind of objects can be qualified as artifacts? How do we distinguish such objects?

An artifact in biology usually refers to experimental error or other spurious results. In the context of microbiology, you will get artifacts if, for example,  you sneeze on the plate you are growing a colony on.

The term is generally used for any result that is not actually true but stems from bad analysis or experimental procedures. Take, for example, this definition from biology-online.com:

  Something artificial, a distortion that does not reflect normal anatomy or pathology, not usually found in the body. For example: in radiology, the appearance on an x-ray of a surgical metal clip that obscures the clear view of an anatomical structure.


Are the Fastq files content is truly random I'm building a system to generate fastq files as they are being output from HiSeq 3000 and HiSeq 4000. This will serve us to test our internal systems with some gold standards.

As we are working with microbiome a standard sample may contain around 1500 different species, is there a a bias in the output regarding how 'close' each assembly record appear next to each other or is it truly random?

If record 1,1 is from assembly 2913, what are the odds that record 1,2 is of that assembly as well (assuming 1500 species with the same strain length) ?

I couldn't find any paper on that so any help from experience would be great.

Thank,
Eden

In my experience, the distribution of reads on the flow-cell is pretty much random, but the sequencing errors are not necessarily randomly distributed.  In all Illumina instruments I have seen, it is common to see edge-effects, or other localities on the flow cell where the error profile differs from the rest of the cell, and QC pipelines generally test for this problem.

A particular issue with the HiSeq3000/4000 patterned flow-cells is that, in situations of under-clustered runs, it would be typical to find the same sequence repeated multiple times in nearby 'clusters' - in other words, a clustering of clusters all containing replicates of the same underlying molecule.  Even for runs where there is no severe under-clustering, it might be expected that duplicates would be found in adjacent cells.  qcfail.com has an outline of this phenomenon: https://sequencing.qcfail.com/technologies/hiseq/