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Why can't there be fructification of mycelium in submerged culture?
I am very new at this. I am wondering why fed batch cultures produce a lot of mycelia but no fruit. I thought the more mycelia you had, the greater chance of it forming a fruit body.
I am refering to this paper http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3768415/ but there are many others with the same methodology. It seems to oppose fruit  body production to submerged cultures.
It seems to be submerged in water and in sugar.
It also seems you can have fruit bodies with a single mating type :
- Coprinus sterquilinus (The Fungi by Sharma)
- A bisporus and V volvacea (Chang Chiu)

Can you provide some more background to your question? What species are you working with, for what purpose, and exactly what do you mean with "submerged culture" (grown in water?)? In general, fungi produce fruit bodies (Sporocarps) after hapliod hyphae of different mating types have fused, and environmental conditions are also important. If your culture only  includes one mating type/batch culture, this could be a reason why you do not see any fruit bodies.

Do you have a reference on what those environmental conditions are ?

Can be all sorts of things, and depends completely on the species. Note that many species produce fruit bodies during a particular time of the year (in seasonal environments), which can give you some clue. Can you back up your last statement (fruit body from a single mating type)?

I think it's a paper by Ohta but let me check

Great. It might occur, but should be an exception from what I know. Sex in fungi is complicated though, and not my area at all.


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Why aren't green eyes more prevalent?
Why aren't green eyes more prevalent, given that the green allele is dominant over the blue one?
My understanding is that human eye colour is determined by two genes:
1) HERC2, with alleles Bx, BB or xx,
2) gey, with alleles GG, Gb or bb,
where

B means brown
x means not brown (this is less confusing than using b for blue here, because having no B allele in HERC2 doesn't necessarily give someone blue eyes; their eyes will be either blue or green depending on the gey gene)
G means green
b means blue.

Capital letters stand for alleles that are dominant; lower case, ones that are recessive.
So the 'algorithm' goes:

1) look at HERC2; if it's anything other than xx, you've got BROWN eyes
2) if HERC2 is xx, look at gey; if it's anything other than bb, you've got GREEN eyes
3) still here? then you've got BLUE eyes

My question is this: why is it that green eyes are so rare if the green allele is dominant over the blue one? When a blue-eyed person and a green-eyed person interbreed, their offspring will either be equally likely to have green eyes as blue (if the green-eyed parent is Gb) or always have green (if that parent is GG).
But many more people have blue eyes than green eyes, despite blue being recessive to green.
The obvious answer is that people with blue eyes (xx bb) and people with green eyes (other xx-ers) have tended to avoid breeding with each other to a large extent. Is any other explanation in the ring? Perhaps the greens are catching up?

The gene which is important for the eye color is actually OCA2. In HERC2 is a regulatory region located which regulates the OCA2 expression. And there is a polymorphism which affects this.

Thanks @Chris. Will the question I'm trying to ask be more accurate if I (or you) amend HERC2 to OCA2? (That said, if HERC2 regulates the OCA2 expression, then HERC2 must be important for eye colour.)

No, it's not HERC2 that regulates OCA2, it is a regulatory region which is located inside the HERC2 gene.

@Chris - Part of HERC2, then? If the question needs correcting, please do correct it.

It's not correct that human eye colour is determined by two genes. Eye color is a polygenic trait. See for example (Sulem,..., Stefansson, 2007).

A gene being dominant does not necessarily imply the gene is also common.
An easy counterexample is Huntington's disease. The gene is dominant, and only one mutant allele of huntingtin would result in development of the disease. However, the allele prevalence of the mutant is low in the general population.
In the absence of a selective advantage of green eyes over blue eyes, the two alleles of the gey gene should remain in genetic equilibrium, and therefore the number of people with green eyes will not increase. In fact, a similar misunderstanding applies to the disappearance of blondes/redheads. In both cases, the allele frequencies will remain unchanged in the absence of selection pressure.
The initial imbalance in the allele frequency could be due to many reasons. Population bottlenecks, genetic drift, and historical selection pressure could all be valid answers.

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Neural correlates of the function of the cardiovascular system?
Are there any known neural correlates of the function of the cardiovascular system? I'm looking for research results that use standard brain imaging techniques (e.g. electroencephalography, magnetoencephalography, or functional magnetic resonance imaging), and compare the brain signals to respiratory and/or electrocardiographic signals.
Actually, ECG is frequently seen in EEG and MEG recordings. It is considered as an artefact, and typically removed in an early phase. Only the QRS complex is usually visible (or the R wave). If the ECG was recorded from the chest/limbs, proper signals would be gained. It would be interesting to compare the heart rate variability etc. to brain signals but has this for example been already done?
I don't have much background to respiratory signals, so I'm particularly interested about that.

Welcome to Stack Exchange. Here at Biology.SE we tend to like specific, solid questions. I would recommend you to do a first search on e.g. Google Scholar with the keywords "electrocardyogram electroencephaolgram" or "ECG EEG", or "ECG fMRI" etc etc. Try to pin down your question and specify it. As of now, it is too broad. If the question is put on hold it is likely for this or a related reason. You can always edit it and try to re-open it after that. Some cool questions have gone through this cycle. Interesting question though! Good luck.

I added some more text to the post.

Great addition. +1 and I retracted my close vote.

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How exactly are genes swapped during the process of recombination?
I am studying recombination in Meiosis and the idea of crossing over doesn't make sense. My understanding is that 46 chromosomes in our germ-cell (23 from mom + 23 from dad) line up next to each other and recombine (swap areas of DNA). My confusion is that, since, for example, Chromosome 1 from mom is same as Chromosome 1 from dad, how is swapping areas of DNA going to exchange any information. Brown eye gene from dad would just be swapped with brown eye gene from mom. How will have any affect on the offspring? OR is it that if mom has brown eyes, the brown eye color gene in mom has something attached to it?
OR is my understanding of genes incorrect and not every nucleus has all possible genes? (except the difference of X and Y chromosome.)?

The chromosomes are not equal. Read about alleles first before you start reading about recombination.

And please change your title since it bears no relation to your actual question.

@adjan thank you for your suggestion! So, one person has a form of a gene and not ALL forms of all genes. This clarifies a lot.

There is quite a few misunderstanding in your question. So, I'll shortly give you some (simplified) definitions and then point you to another post.
Definitions and Basic Concepts
A locus (plur. loci) is a position along a chromosome. A some loci, there are  genes. To make things easy a gene is any sequence which is transcribed into RNA and translated into proteins.
Now at any locus, you might see different individuals having different variants. For example an individual may have the sequence ATTCT while another individual may have the sequence ATTGT. Those different variants are called alleles. It is key to understand that there is genetic variation in populations. This genetic variation is a big part of the reason why people around you look different and why you ressemble more your siblings (if you have any) than a random person in the population.
How does recombination have any impact?
To understand the effect of recombination you necessarily have to picture a several loci model. As you now understand the above definitions you will find your answer at this post: Why do we need two markers to measure a recombination rate?
Further readings
The following posts will also be of interest to you:

Do only one or both pairs of homologous chromatids exchange genetic material during the process of crossing over?
Chromosome and chromatid numbers during cell cycle phases

Thank you. My main misunderstanding was that same chromosomes in all individuals is exactly the same. I now understand that there can be different forms of a gene (allele). Not all people have all forms of a gene.

Cool. There is indeed genetic variation in the population. This is a big reason for why we look different. Note that have understanding the existence of genetic variation and its maintenance in populations is key to have a basic understanding of evolutionary processes. If you think I answered your question you can check the checkmark to the left of my answer.

My question now is, "Do all genes get transcribed then?" I remember reading that only a percentage of DNA is transcribed. When I read that, I thought maybe if you have blue eyes, only blue eye gene would be transcribed and genes for all other eye color would be "trash DNA". But since you only have one gene for eye color, and same with all characteristics, what part of DNA does not transcribe? I hope my question is not too confusing.

We typically define a gene as a sequence that gets transcribed. So, by definition, yes all genes get transcribed. But most of DNA is not made of genes. There are regulatory sequences and introns (~24%), there are pseudogenes, there's loads of transposons and retrostransposons (~60%) such as the ALU sequences. "Junk DNA" is some kind of an undefined term that encompass all the non-coding DNA (~ 98.5%) but the term "Junk" has been very misleading to the large public. Of course all of this is not so specific to humans. Plants typically often have very large genome with loads of transposons.

Anyway, your follow-up question is very broad. You should just follow an intro genetic class or read some wikipedia articles and try to come back with a more narrow and accurate question. Good luck exploring this fascinating field of knowledge!

That was actually a perfect answer to my question! Thank you so much.

Let us continue this discussion in chat.


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Is Chargaff's rule really applicable?

Chargaff's rules states that DNA from any cell of all organisms should have a 1:1 ratio (base Pair Rule) of pyrimidine and purine bases and, more specifically, that the amount of guanine is equal to cytosine and the amount of adenine is equal to thymine.

As in the table $A \ne T$ and $C \ne G$.
So I was wondering if Chargaff's rule is really applicable?

BTW did you try reading Chargaff's papers? This was way before the discovery of DNA structure. Even their method (at that time) of DNA extraction and analysis was not as refined as the ones that we have now. You may not find Chargaff's paper that easily but have a look at one of my answers in Chemistry.SE.

In addition to Remi.b's answer, it should be noted that the phage Phi X 174 is the only organism in your list which significantly deviates from Chargaff's Rule (by more than 1-2 percentage points for the A-T pair). While sampling errors are indeed more likely in organisms with small genomes, there is in fact another factor in play here.
This is because Chargaff's Rule only applies to double-stranded DNA, due to the complementary base pairing that occurs between A-T and C-G. Since Phi X 174 is in fact a single-stranded + sense bacteriophage, Chargaff's Rule is inapplicable to it, since it does not obey the standard Watson-Crick base pairing that is the molecular basis of Chargaff's Rule. In fact, the Wikipedia article from which you obtained the chart states this as well:

The following table is a representative sample of Erwin Chargaff's 1952 data, listing the base composition of DNA from various organisms and support both of Chargaff's rules. An organism such as φX174 with significant variation from A/T and G/C equal to one, is indicative of single stranded DNA.

Oh... how did I miss that?! Very good point! +1

@Remi.b because OP should have read about dsDNA

Does Chargaff's rule hold true on these data?
From the table:

Ratios A/T and G/C are close to 1 with an extreme at 0.77 and 1.05.
Ratios A/G and T/C are quite far away from 1, with several extremes around 2 or 0.5.

So, yes Chargaff's rule seems to apply quite nicely.
Why isn't the ratio A/T exactly 1?
The question of why the ratios A/T and G/C are not closer to 1 is interesting though. To fully answer this question I would need to go back into the primary literature who produced those numbers.
It appears that the three species of the list that have the smallest genome size ($\phi X174$, E. coli and yeast) are also the three species that show the greatest deviation from unity. The two species that have the largest genome size (maize and wheat) have the smallest deviation from unity. Overall, this suggests that this deviation is only a consequence of sampling error.
Did you say Sampling error?
This is just a small stat reminder
From Wikipedia

In statistics, sampling error is incurred when the statistical characteristics of a population are estimated from a subset, or sample, of that population. Since the sample does not include all members of the population, statistics on the sample, such as means and quantiles, generally differ from statistics on the entire population

Sampling error is not an error that a researcher does but an intrinsic property of the sampling process. Expected deviation from the true value is decreasing as the sample size increases, i.e. small sample size will show greater deviations (on average) from the true value than the larger sample size.

I would put it down to straightforward experimental error rather than sampling error. The methods used to obtain the numbers are relatively crude chemical methods.

Not sure if you mean "measurement error" or "bias" when talking about "experimental error". In any case, I am personally not be able to give my opinion on this matter as I haven't read these papers.

Preamble
My original answer to this question has recently fallen into the third circle of hell because of a contrast I made between physics and biology which seems to have offended some biologists. I shall let that rest, but provide a new answer to make one point that I feel some biology students need to absorb.
Answer
The use of the word ‘rule’ should be regarded with great caution in biology. There may be some rules or laws in biology that justify the name (e.g. those that apply to classical genetics), but in many cases, the term is misused.
I maintain that the word ‘rule’ was misapplied by Chargaff to what was actually an observation. In science what is important about observations is how their interpretation can lead to an understanding of fundamental processes — in this case, the base-pairing in the double-helical model for the structure of DNA in many chromosomes.
This is what the modern student should focus on — the understanding of the fundamentals — so that when faced with observations about a particular chromosome that are inconsistent with the double-helical model he considers whether the fundamental model of the chromosome might be different in this case, rather than frets about some incomprehensible ‘rule’.
In the case of 174 this leads to the answer provided by @MarchHo, that the chromosome is single-stranded. Another possibility one might have considered would be that there were other bases than ATG and C that had not been detected (we now are aware of chemically modified bases in genomes). The fact that this would have been incorrect in this case is irrelevant — it would be the way one would want a student to approach observations.
Footnote: History and Science Education
I am not against making students aware of the experimental basis of our current views of molecular biology, and (given my age) have been in a position to do that for a number of posts. In general, it is a difficult task because so much is known. However, I feel that the teaching of ‘Chargaff’s rules’ (and Crick’s wobble ‘rules’) is often done without due reflection because they have a certain scientific celebrity. As a teacher one needs to have the courage of one’s own convictions. I feel it helps students if one always refers to ‘Chargaff’s observations (his so-called rule)’ and ‘Crick’s wobble predictions (his so-called rules)’.
And it seems that I’m not the only one. In the 5th edition of Biochemistry by Berg et al. we have no mention of Chargaff’s ‘rules’. Instead we have:

“In 1950, Erwin Chargaff reported that the ratios of adenine to
  thymine and of guanine to cytosine were nearly the same in all species
  studied. Note in Table 5.1 that all the adenine:thymine and
  guanine:cytosine ratios are close to 1, whereas the adenine-to-guanine
  ratio varies considerably. The meaning of these equivalences was not
  evident until the Watson-Crick model was proposed, when it became
  clear that they represent an essential facet of DNA structure.”

Seems that there are some people who still need the security blanket of rules (and rulers?).

March Ho's answer is correct. However the important thing to learn from this is that biology is not physics, and there are no rules — only observations and explanations. What Chargaff made was an observation for which he had no explanation. It was only when Crick and Watson postulated AT,GC base-pairing in double-stranded DNA that the observation was rationalized. More important, those DNAs that were exceptions to the 'rule' could be rationalized as differing from the Crick/Watson model. In the case of phiX 174 it was because it had a single-stranded genomic DNA, but one can envisage other (incorrect as it turns out) explanations in terms of modified bases that were not detected in the assay. Biology is a science of exceptions rather than rules.

While the answer is otherwise good, I don't understand what you mean by "biology is not physics and there are no rules". As far as I know, rules are violated rather often (relativity vs Newtonian mechanics for example) in physics as well.

Rules (indeed Laws) in physics tend to involve equations based on a conceptual framework. Deviations of observations from equations (one can stick to Newtonian mechanics and look at deviations from Boyle's Law, I seem to remember) lead to modified equations based on additional assumptions rather than fudge factors. I don't see any equations or theory in biology, except at the very basic chemical level. It seems to me more that Nature finds one solution to a problem, we observe it, but it isn't a rule as somewhere else she solves the problem with a black swan.

Did you just say I don't see any equations or theory in biology?? You should read some primary literature then. I am a theoretician working in the field of population genetics (subfield of evolutionary biology) btw.

Well I'm molecular biologist turned bioinformatician with a first degree in chemistry. Sure there's a role for maths and theory in your sort of biology, but it doesn't underpin the subject like it does physics. And my answer was intended to help the questioner in a wider sense. Namely that she should not be looking to learn or lean on apparent rules, but to look for the pattern behind observations and prepare herself for Nature's variety of patterns. Shine and Dalgarno, won't prepare her for Kozak, and Kozak won't prepare her for internal initiation. Nor Mendel's 'laws' for McClintock.

@David biology has not been classically employing mathematics which the field of physics has been since ages ago. This is changing as more and more mathematicians (and even physicists) are applying mathematical models to explain biological systems. The issue is that biological systems are way more complex than a bouncing ball (or even space rockets). People like Remi and me and many others are working in this interfacial area where mathematical principles are combined with biological observations.

Fair enough. But there is a difference between mathematical modelling of complex systems and blindly learning 'rules', which the questioner seems in danger of doing. In this respect she is not unlike many very non-mathematical biology students of my experience, and my reply was an attempt to get such students to think about principles rather than parrot stuff from Wikipedia. The negative votes my answer has attracted seem to reflect the antagonism this guidance usually receives (unless it comes from people who think biology is physics). There's none so blind...


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What physiological processes within a muscle cause the latent period in a muscle fiber?
This is a lab question I cant find the answer in the lab manual or in the text book.
What physiological processes in a muscle cause the latent period in a muscle fiber?
Please help.
Edit:
The latent period is the short delay between the muscle action potential and the beginning of muscle tension development. This is what I'm talking about. I'm sorry I didn't make that clear.

The action potential causes Ca2+ ions to be released in the cells, that is needed for muscle fiber contraction. There is a small time delay from the arrival of the action-potential until the Ca-ions are released and reach the required concentration in the cell for contraction. On the molecular level there is a protein called troponin (this is bacically located on the actin filament along with tropomyosin and obscures the myosin binding site(s)), that bind calcium and then undergoes conformational change - this also adds up to the delay. After this - the conformational change of troponin - myosin and actin can bind together and contraction can occur through conformational changes. All these binding and conformation changes take a small time to be completed, and thus causes a small delay. Below is a picture about the molecular mechanism ofof muscle contraction taken from this wiki page. The linked wiki page has real good detailed information.

I found this article and where they exactly measured things. To clarify my answer (taken from the linked article):

Electromechanical delay (EMD) was described as a time elapse between the onset of muscle electrical activation and onset of force production, reflecting both electrochemical processes [i.e., synaptic transmission, propagation of the action potential, excitation-contraction (EC) coupling] and mechanical processes [i.e., force transmission along the active and passive parts of the series elastic components (SECs)]

So as for the whole muscle, not for just one cell the delay is caused by the things listed in the above quote - although excitation-contraction (EC) coupling and force transmission (things I have described earlier) take place in every single muscle cell that is in a specific muscle fiber.
Edit 2: I found a good and simple ppt/pdf about AP propagation and muscle contraction here.

I think this pretty much sums up the steps necessary from neuro-muscular junction until contraction, but what is the rate-limiting step? Your answer is basically a summing up of events, and not a dedicated answer to the question from m y understanding of PO's intentions. I mean, a chemical synapse is pretty much a 10-ms event if I am not mistaken, so that's not the bottleneck. What is?

The Latent period is caused by:

Time taken for the stimulus to travel along the nerve to the neuromuscular junction
Time taken for the impulse to cross the neuromuscular junction and to stimulate the muscle
Time taken for the excitation-contraction coupling to occur
Time taken by the lever to overcome the inertia of rest
Time taken to overcome the vicous resistance of the muscle.

The latent period is usually about 10 ms.

Taken from Textbook of Practical Physiology Edition 2, by GK Pal & Pravati Pal


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Why is marginal reconstruction "more correct" than joint reconstruction in some cases?
When reconstructing the ancestral states on a phylogenetic tree given the states at the tips, there are a number of methods for performing the reconstruction. This question is about marginal and joint maximum likelihood reconstruction.
To quote the wiki, marginal reconstrucion "is akin to a greedy algorithm that makes the locally optimal choice at each stage of the optimization problem", while joint reconstruction "find(s) the joint combination of ancestral character states throughout the tree which jointly maximizes the likelihood of the data"
Pupko et al. (2000) describe an algorithm for performing joint reconstruction.
I have a question about a paragraph in the discussion of this paper, where they discuss the differences in the results between the joint and marginal reconstructions.

Deciding which is ‘‘ more  correct ’’ depends  on  the  question
  asked.  For instance, if one wishes to count the number of threonine-
  to-methionine replacements over the entire tree, then the joint
  reconstruction should be used to obtain this number (2,  in  our
  case,  on  the  branch  connecting  node  24  to node 3 and the branch
  connecting node 32 to node 33). However,  if  one  wishes  to
  synthesize  the  hypothetical cytochrome b sequence  of  the  ancestor
  of  Cetartiodactyla,  then  one  should  use  the  marginal
  reconstruction approach. We emphasize that both methods compute op-
  timal reconstructions by using all of the available data.
  Discrepancies originate not from misuse of information, but from the
  difference in the nature of the probabilistic questions asked

I don't understand why you would use marginal reconstruction for estimating the ancestral state at one node, or how the question you ask affects which method you should use. There is only one true ancestral state, I would think that the correct method for any question is the one that most accurately estimates the true ancestral state. Can someone shed some light on why the marginal reconstruction method is preferable in this situation?

I know this is too late, but since this is something I'm struggling with too I thought I'd post here in case others also find there way here. I don't have an answer but, here are some quotes that might help (I found them at least partially helpful).
Yang (2004): "Marginal reconstruction is more suitable when one wants the sequence at a particular node, as in the molecular restoration studies. Joint reconstruction is more suitable when one counts changes at each site."
http://aracnologia.macn.gov.ar/st/biblio/Yang%202006%20Computational%20Molecular%20Evolution.pdf
Revell (2014):
"Joint reconstruction is finding the set of character states at all
nodes that (jointly) maximizes the likelihood."
"Marginal reconstruction is finding the state at the current
node that maximizes the likelihood integrating over all other
states at all nodes, in proportion to their probability"
http://www.phytools.org/eqg/Lecture_5.1/Revell.ancestral-state-reconstruction.pdf
Joint reconstruction is "not (necessarily) equivalent to picking the state at each node with the highest probability" (Revell 2014), but is the method of picking the tree with the overall highest MLE.

This is just a comment to warn people about the options in the R-package ape for the function ace. Contrary to expectation, "marginal = F" for discrete traits DOES marginal reconstruction (and vice versa). So, keep that in mind.
More here:
http://blog.phytools.org/2015/05/about-how-acemarginaltrue-does-not.html


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Are Young Girls Stronger than Young Boys?
According to "common wisdom" the average man has, as a proportion of his body weight, 50% more muscle mass than the average woman. This is in addition to how the average man is several inches taller than the average woman and thus has a larger body mass to take that proportion out of.
Notice the above is phrased in terms of men and women as opposed to boys and girls. I am interested in how strength compares at a younger age. If we took the average ten-year-old boy and the average ten-year-old girl $-$ before the first growth spurt of puberty $-$ and compared their proportional muscle masses, how would they compare? Have any studies been carried out?
Looking for information online about this nets me a hundred accounts from men who remember how, as children, they lost every fight with their older sister. The problem here is that in any contest between siblings (twins excluded), the older sibling most likely has a height and mass advantage. So it's hard to say much about proportional muscle masses.
My guess is that if we took twins Bill and Roberta then they would have similar muscle-mass proportions up until about age 10. From then Roberta would have a growth spurt and increase proportional (as well as absolute) muscle mass due to extra testosterone (in addition to extra estrogen). A few years later Bill would have a growth spurt and increase proportional muscle mass to exceed Roberta's. But she would still be stronger than him, until he caught in terms of height.

Why is this VTCed as opinion based? It is clearly possible to do studies like this, similarly to other types of studies on the average development rates in children (as well as sex-differences), and I assume that there are data out there that could answer this question.

Here's a study comparing performance in swimming. Before age 8, there's no difference; from age 11-12, there's some small difference, after age 13, there's a large difference.
https://www.eurekalert.org/pub_releases/2012-05/iu-wsg052512.php


text:
Is there a name for the evolutionary loss of vestigial structures?
Consider a biological structure which no longer benefits an organism, such as the eyes of an organism whose population now lives in total darkness.  I can think of three reasons why such a structure might disappear:
0) Random changes to the structure over time wouldn't be corrected by selection favoring the functional version of the structure, leading to a wider variation where most versions of the structure no longer effectively function.
1) The resources the structure demands could be better spent on structures which are actually being used; e.g. human eyes require a lot of blood that could be used elsewhere.
2) Perhaps the existence of a very complex structure leads to biological problems which would no longer be an issue if the structure were not present; e.g. human breasts plus breast hormones frequently leads to cancer.
Are these three examples reasonable means by which a feature would disappear?  Are there any other possible reasons?
Is there a general name for the phenomenon of evolutionary removal of vestigial features due to those features no longer being useful to a population?

Natural selection?

I'm referring specifically to the loss of unused structures, because I've heard some biology students claim "it doesn't happen" which is overly broad.  It would be useful if there were a name for when "it actually does happen".

Your examples are fine, but in general you should try to avoid "just-so" stories when considering evolutionary events. The truth is always a combination of the kinds of reasons you listed. The most you can say for sure are post-hoc phenomenological observations, ie "The fitness of the population which lost its tails increased relative to the fitness of the population which retained them".

I didn't mean to imply that those reasons were in any way mutually exclusive.

This phenomenon can be (and has been) described as regressive evolution (the loss of a phenotypic trait). There are several reasons why this occurs:

Neutral mutations which become fixed through genetic drift.
Positive selection of regressive mutations that are beneficial.
Pleiotropic antagonism: positive selection for one trait may have the consequence of disrupting another trait which isn't strongly selected for.

The eye degeneration example you chose is a good one because it is well studied in cavefish (which evolved from sighted surface fish and have degenerate eyes). Normal eye development is under the control of the Pax6 transcription factor. Expression of another transcription factor, Shh, reduces Pax6 expression. Shh expression along the embryonic midline is responsible for splitting the eye field bilaterally. Overexpression of Shh in surface fish leads to eye degeneration and, indeed, it was found that cavefish have an expanded Shh expression pattern.
Cavefish have also undergone a behavioural shift to bottom feeding and have become less aggressive to focus more on finding food. As it happens, the expanded Shh expression also causes a widening of the jaw and amplification of taste buds, both of which aid in scooping and sampling the river bottom. Furthermore, increased Shh expression during brain development influences a decrease in aggressiveness and a shift to foraging behaviour.
This is an example of pleiotropic antagonism: positive selection for jaw enhancements and behavioural changes via expanded Shh expression, which increase fitness in cave environments, can explain why the eye degenerated.

Thank you so much for your detailed answer.  By describing the terminology and addressing the subject around it, I think you've helped me understand the underlying concept itself much better.

@TrixieWolf You're welcome

So-called "vestigial" features are defined in a post-hoc fashion as features which do not have a positive correlation with a population's fitness under its current living conditions. There are no special names for the evolutionary processes that lead to their loss, since they are exactly the same evolutionary processes that act upon any feature that has a neutral/negative effect on fitness.


text:
Are there any examples of how to apply evolutionary models?
Apologies if this question it too open-ended; evolutionary biology is not my primary field.
I have been reading a lot about the use of statistical mechanics in analyzing evolutionary dynamics. As an example, consider this paper: http://www.pnas.org/content/102/27/9541.short.
The ideas are pretty straightforward. There is some genotype-fitness landscape and selection drives populations towards maximal fitness. However, genetic drift can pull these populations away from maximal fitness. These two concepts are analogous to minimization of internal energy and maximization of entropy in thermodynamics.
However, most of the papers that develop these models never properly explain how to apply them to observable phenomena. Is it because there is some disconnect between the parameters in the models and nature? For example, many of these models use the effective population size, which is unknown for most species.
I guess my main question is this: are there any demonstrations on how to use these toy models to predict something in nature, or are they simply for theoretical purposes.

The paper you mention basically describes an approach to modelling evolution — so it may be of theoretical interest. Most models are built with an intention of predicting something or explaining some phenomenon in mathematical terms. You can find many studies that do predictions.

You may take a look at this software, aimed at estimate conservation status for declining populations: http://www.cbsg.org/download-vortex

Hypothesis testing in evolutionary biology
Pretty much any paper of empirical evolutionary biology tests hypothesis. If you go on google scholar and look for any empirical paper in the field of evolutionary biology such as "does sexual selection has antagonist effect to natural selection", "evolution of range limits", "evolution of mutational robustness" or "sensory drive speciation" you will find tons of papers that test hypotheses. Many of these hypotheses have been developed either in pure theory papers on in papers that mix some level of theory (no necessary need of complicated modelling) and empirical work. There is nothing in evolutionary biology that is different from the other field of biology or the other fields of science in our ability to test hypotheses.
A tiny bit of history
In the first half of the century most work in evolutionary biology was theoretic. Many hypotheses were left untested. Today, we perform lots of tests and the technics of molecular genetics (sequencing and stuff) help a lot to test hypotheses. Some papers, indeed uses metrics that are very hard to estimate, eventually too hard (too expensive) to be estimated today, it is true and it is an issue, an issue that all sciences know of. We sometimes have to wait for technical advancements before being able to test a hypothesis.
Concerning the paper you mention
From your description of the work they performed in the paper you linked (I haven't read this paper) it sounds like they are describing the concept of shifting balance theory, a process that has been first hypothesize by S. Wrigth in 1932. As said on the wiki article, there is little empirical evidence for shifting balance theory (but you may want to read this and that). The reason is that shifting balance theory is link to the concept of adaptive landscape. Adaptive landscape is what we call the relationship between fitness and phenotype or fitness and genotype. We have descriptions of fitness-phenotype relationship but we are only starting to offer good and complete descriptions fitness-phenotype-genotype relationship. Understanding the link between genotype and fitness is essential for testing shifting balance theory. Shifting balance theory is a logical consequence of the process of drift and selection, both of which are very well known (and well tested). Most of the issue is in the description of how rough is the fitness landscape to know whether shifting balance theory is indeed a thing that occurs in nature or whether it is very unlikely of such process to ever occur.


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Short dated spontaneous ringing in ear
What causes very high pitched sound in one's ear?

Someone mind telling me how is this a "personal medical question" which is just something experienced by everyone?

Spontaneous ringing is caused by When the outer hair cells put energy back into the vibration, which is known as positive feedback. The process is meant to amplify very quiet sounds more so than loud ones. Normally this works, and you would not notice the sound. But occasionally, the amplification level of one or more outer hair cells will go awry and as a result, the whole system will erupt into spontaneous oscillation.

When this occurs, it becomes audible to us. We perceive it as a ringing in the ear, or “sudden-onset ringing tinnitus see here”. As with most of our biological systems, there are quite a few homestatic control mechanisms (negative feedback) which exist to correct the problem and get rid of the oscillation. It takes about 30 seconds for this mechanism to begin, and then sends messages which suppress the ringing. After the message is sent and received, the tinnitus percept begins to fade away.  You can tell when this reaction has taken place as its often accompanied by a slight reduction in hearing sensitivity (like background or ambient noise we hear suddenly getting quieter), followed by a feeling of fullness in the ear. It usually takes about a minute for this process to fully complete.
Sources:

Wikipedia. Wikimedia Foundation. Web. 30 Jan. 2016 (https://en.wikipedia.org/wiki/Tinnitus)
"What Causes Spontaneous Ringing In Our Ears?" Zidbits. Web. 30 Jan. 2016.
"What Causes That Spontaneous Ringing in Your Ears?" Sciencedump. 2015. Web. 30 Jan. 2016.
"Tinnitus." [NIDCD]. Web. 30 Jan. 2016. (http://www.nidcd.nih.gov/health/hearing/pages/tinnitus.aspx)

When you add sources to an answer, please link to them. It's great you used Wikipedia - which freaking page? I'd also stay away from "popular science" Buzzfeed-type websites and look for actual medical literature. Maybe google "tinnitus" or use PubMed instead.

@MattDMo apologies for that – I edited my sources


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Why don't half of us have situs inversus?
I don't see any possible evolutionary disadvantage in situs inversus(the condition where major organs are mirrored from their normal positions) when people with situs inversus can have a normal healthy life.

Can you expand this question by adding a definition of situs inversus and maybe some material that backs up your claim of no adverse effects?

if there is no evolutionary advantage or disadvantage then its frequency is only the result of genetic drift, given that it is a recessive trait (according to wiki) then it is not surprising it presents rarely.

downvoting because you give no reasonable justification for you assumption that a neutral trait should be present in half of the population. Also, some health issues appear to be tentatively (accroding to wiki) linked to situs inversus.

I'm voting to close this question as off-topic because it is based on a faulty presuppositions (that situs inversus is completely benign, and that even neutral phenotypes should be evenly distributed throughout a population.)

During development, cilia in the node are responsible for defining the left-right axis and subsequent asymmetry. Situs invertus is often caused by ciliary defects, which disrupts this process. These defects can also cause lung defects and male infertility. It would also be reasonable to expect that whatever other molecular defects cause situs invertus would also effect other developmenal programs.

@canadianer - while situs inversus is found in diseases caused by ciliary defects (e.g. in patients with PCD, 50% aslo have situs inversus), not all ciliary defects cause situs inversus. Do you have a particular reason for saying "situs invertus is often caused by ciliary defects"? Just curious. I read a ton about this and never saw this statement.

@anongoodnurse Perhaps often was the wrong word. Situs invertus can be caused by ciliary defects. I was trying to make the point that, while situs invertus itself may or may not be detrimental, what ever is causing it can affect other processes and decrease individual fitness.

@canadianer - that, I agree with completely.

The condition is autosomal recessive so not only is there only a 1 in 4 chance that offspring to two carriers will be affected, it also requires two people with the genotype (heterozygous, unaffected carriers or homozygous, affected) to mate, and that makes the chances less likely. Also there may be many more carriers in the population, so the allele(s) responsible may be in the population at a much higher level that we are aware of... As even then 75% of the Heterozygous/Heterozygous offspring will have the phenotypically-dominant trait.

The homozygous genotype is not always benign. Your assertion that because the phenotype isn't in the population that the allele isn't in the gene pool isn't necessarily the case as carriers are phenotypically dominant, so the alleles could very well be prevalent. It is also a mutation that isn't always identified if the person does not have health issues, so its prevalence could be underreported. Finally, body plan genes are very powerful and as heterozygotes are phenotypically dominant it shows that there is no dosage dependence when there are functional copies of the gene present during dev.

Theoretically, a perfect mirrored body should be indistinguishable from the normal state and therefore there should be no effects whatsoever. And if there was no preference for left--right during development, half of us should indeed be "mirrored", as the title suggests. But this theoretical model is getting confused with the real condition situs invertus, which I guess is debilitating because the mirroring is in fact not perfect, so "conflicts" arise somehow. So it comes down to how the developing embryo can distinguish left from right, and how this goes wrong in the situs invertus.

In the Wikipedia article linked to in the question, one will note that there are several medical conditions associated with situs inversus, including congenital heart disease, primary ciliary dyskinesia, and Kartagener Syndrome. These can easily lead to reduced fitness for reproduction, especially PCD/Kartagener Syndrome, as one effect is male infertility due to lack of functional cilia on sperm.
Therefore, there likely is a negative pressure on the alleles responsible for this condition, explaining why it is so rare.

When I was a post-doc my mentor used experimental manipulation to create the equivalent of situs inversus in C. elegans embryos. The embryos hatched and grew into "left-handed" or "anti-worms." He published that as a single-author letter to Nature in 1990, and had a series of grad students working on isolating mutations in handedness. It turns out that the main way humans with situs inversus are identified is at fertility clinics. Sperm motility is cilia-based, and functional Fallopian tubes have cilia that move the just-released ovum down to the uterus.

If a polymorphism is neutral and has no effect on reproduction, it will not necessarily present itself to the population in a 1:1 ratio. For instance, for a single-gene polymorphism with two alleles in the absence of evolutionary forces like selection and gene flow, the trait will be at Hardy-Weinberg equilibrium, meaning the two different alleles will be present in some ratio (not necessarily 1:1) and will stay in that ratio from generation to generation. Of course, I'm not an expert on animal physiology and I don't know the genetic basis for situs inversus, but either way two equally fit traits may still be present in the population at very different ratios as there is no force pushing them to be present at equal ratios.
Traits undergoing density-dependent selection, on the other hand, such as sex, are under selective pressure to exist in a 1:1 ratio. There are unlikely to be any such forces acting on situs inversus vs situs solitus

I am an eighty year old woman with Kartageners Syndrome.  This means, I have bronchiectasis which was diagnosed in 1948. The disease was isolated in my left bottom lobe. I also have chronic sinusitis. I think cilia is lacking or if not lacking at least too short to be effective.  For most of my childhood I was unwell but after age eighteen I seemed to be quite a bit better and I have lived a healthy life.  It is only recently that I have had health problems relating to Kartageners and I tend to think my age is now contributing to lung infections and therefore the quality of my life is deteriorating.

@AliceD Sorry, but this answer is on topic. Kartageners Syndrome is a disease associated with situs inversus, and I believe that the purpose of the post was to refute the claim made by the OP that situs inversus is benign.

@AMR - you are right. Thanks. I flagged this answer to alert the mods that they should be dismissing my previous flag. Thanks again.

@AliceD No worries. While I was familiar with situs inversus, I was not familiar Kartageners, but after looking it up, I got a clearer picture of the posters intention, and how often do we actually get to hear from someone who actually has complications from a 1 in 10,000 disorder (that is aware of it). It seems that the unfortunate thing for this poster is that it was partial and not total, as it seems that total reversal has the same phenotypic behavior as the majority of the population, except in rare occasions. It is only those partially affected that tend to have health related issues.


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Are transgender people born physically different from others?
Are all children born with only either male or female body parts (other than exceptions), or is there actually a natural third gender with the physical characteristics of both genders, e.g. the child has the genitalia, or reproductive organs, of both sexes?
According to Wikipedia they are only either male or female when born. They only feel different later on in life.

@MattDMo I edited out the reference to breasts and made it more comparable (i.e. male and female genitalia)

Why all these down votes? I was being told this from a long time that they are physically born different. It is obviously noob's question.

I don't know why you've tagged me in that comment (I haven't downvoted) but it's probably because you are incorrectly trying to label Transgender and Hermaphroditism as the same thing.

@GriffinEvo I didn't tag you in that comment. You can see that. Anyway I didn't knew the correct word.

Seems you did because it flagged my inbox, it only does that if you use "@username" (it also does notifies the author of the original post when you comment)... maybe something glitched. Regardless, I'd guess that's the reason - I can imagine some might find it offensive that your question makes them out to be the same thing.

@GriffinEvo FYI, if the author of a post writes a comment but does not tag anyone and there is only one other user that has commented (note MattDMo's comment has been deleted), the system assumes it was intended to be in response to the other user, and notifies them automatically. See How do comment @replies work?

@p.s.w.g - Thanks, I'd never noticed it happening before!

The concept of transgenders has nothing to do with sexual organs at birth. Transgenders is a concept that has to do with sociology, not biology. See the wiki link.
intersex (previously called Hermaphroditism) has to do with biology. The wiki link makes a great job at defining intersex.
In short: A transgender person is born anatomically either male or female (with eventually exception of intersex who go on to become transgender) and they then identify themselves to the opposite sex (or a third sex) rather than identifying themselves to their actual anatomic sex.
Note that this post is closely related.


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Why does the sex of the parent species determines the species of a hybrid offspring
I've read a little about hybrid animals, and have been amazed by the fact that the sex of the parent species determine the species of the offspring, in some hybrids.
A male horse and a female donkey will give birth to a Hinny, while a female horse and a male donkey will give birth to a Mule.
The same goes for tigers and lions, male lion and a female tigress will give birth to a Liger, while a male tiger and a female lioness mating will result in a Tiglon
I thought that the only difference between the male and female reproductive cell's DNA code is the X-Y chromosome that determines gender, not differences that can define the phenotypical result of the offspring. Why does this happen?

Excellent question. Unfortunately, I am guessing that the answer is simply “because we defined it that way”, rather than a biological insight. Species are usually defined in terms of the possibility of interbreeding, which isn’t relevant here (hybrid offspring is usually sterile).

@KonradRudolph, but species are not defined just for the fun of it (I guess, I don't really know), they are defined because there are significant differences between two animals, and in the case of those two interbreeding, those differences are consistent with the gender of the parent species. In other cases, like the different types of Zebroids (Zebra and donkey/horse/pony hybrid) that doesn't seem to be differentiated by parent species gender. (http://en.wikipedia.org/wiki/Zebroid)

@Ilya Melamed: there is no strict definition of species... and anyway hybrids are NOT defined as separate species, but as the cross of two different ones.

@nico, maybe I'm using the word "species" wrong, I use it in its layman definition, as "different types of animals". The meaning is, as I said, that significantly different animals are born from the same parent animals, and that the change is consistent with the gender of the different parent animals. If you can think of a better term than "specie" please edit the question to bee more accurate.

I thought that the only difference between the male and female reproductive cell's DNA code is the X-Y chromosome that determines gender, not differences that can define the species of the offspring. Why does this happen?

Well that is not the only difference, there are certain characters that are only transmitted by one of the parents.
First of all you have to think that the zygote (the cell deriving from the fusion of two gametes) contains the nucleus of the egg and of the sperm but the cytoplasm of the egg only (or at least in great part).
One thing that is present in the cytoplasm are mithocondria, which contain DNA, called mtDNA. mtDNA is therefore transmitted only by the mother (at least, in most species). Therefore a hinny will have donkey mtDNA, while a mule will have horse mtDNA.
Furthermore, cytoplasm contains transcription factors and various proteins that will influence the subsequent development of the zygote into an embryo and, again, these are maternally derived.
Another thing that changes is that there are certain genes on nuclear DNA which are expressed in a single-parent manner. That is, you have 2 copies of these genes, called imprinted genes, one from the mother and one from the father but only one of these copies -that of the mother or of the father, depending on the gene- will be expressed.


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What sort of assay could be used to identify mutants with mutator phenotype?
By mutator phenotype, I mean being more prone to mutations, for example due to mutations in genes involved in DNA repair.
I was thinking about exposing the cells to agents that damage DNA (uv light, for example). Compared to normal cells, mutators would be less likely to survive, because they lack the ability to repair damages in the genetic material. To a certain extent, that's the principle of radiotherapy (cancer cells are more suscetible towards radiation).
Are there other options? Moreover, is it possible to select the mutators (instead of killing them)?

What is proner? Do you mean "more prone"? What is "danificate" ?

Most of your question is answered in this previous post of yours.

There are a number of ways to screen for mutator genes. One straightforward approach in bacteria is to take an antibiotic sensitive non-mutator strain, grow it up, and expose to different antibiotics. Cells that survive in the presence of multiple antibiotics have acquired multiple de novo resistance mutations and thus are highly enriched for mutator alleles. Here is one example: Wiegand et al (2008) AAC.


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Mechanism by which $lacI^{d}$ is a dominant mutation, impairing the function of normal copies of the Lac Repressor
Jacob-Monod model for the lac Operon was based on experiments using two strands of bacteria which constitutively expressed $\beta$-gal: $I^{c}$(mutation in the gene lacI , which encodes the repressor) and $O^{c}$(mutation in the operator, the site where the repressor binds).
$I^{c}$ mutants are usually recessive: the Lac Repressor cannot bind to the operator, however, if a wild-copy of the gene is present in a merodiploid, the inducible pattern of expression is restored, because the Lac Repressor acts in trans (that is, it will inhibit expression of both operons when lactose is not present).
However, I've read that there's a strain ($lacI^{d}$) which is dominant, so the expression is constitutive even in the presence of the normal repressor. According to the article linked, abnormal subunits may mix with normal subunits, resulting in a disfunctional tetramer, even if a wild type lacI is also present.
In terms of protein structure, why some mutations may have this effect and be dominant while other mutations do not interfere with normal copies of the protein and are recessive?

They explain in the paper you linked to that these muteins affect tetramerisation of the repressor. This means weaker binding of the repressor and no DNA looping. Does that explain it for you?

@canadianer partially. Why some mutations may lead to incorporation of abnormal subunits to normal subunits and in other mutations this doesn't happen?

The lac repressor act as a tetramere molecule and requires all 4 of the subunit to be able to bind DNA to act on the operon and repress β-galactosidase expression.
The "all 4" is the key here, if any of the 4 subunits is unable to bind DNA then the whole complex cannot attach to the operon. The lacId mutation produces a repressor subunit that cannot attach DNA, yet can tetramerize with other lac repressor subunits, therefore impeding WT subunits to bind the operon.
For your question on the protein structure. Mutations can occur at different locations in a gene and therefore impact different proteins domains. Proteins contain different type of domains, such as an active site for an enzyme or a binding sites for attaching to the DNA. A mutation might act on one of the domain while leaving others fully functional.
In your case this is exactly what happens, the mutation is in the protein region involved in binding DNA but does not affect the region involved in the protein-protein binding with other subunits.

Concerning the difference between dominant vs. recessive mutations, in general, recessive, or loss-of-function mutations, are much more frequent than dominant, or gain-of-function, mutations, because there are many different ways to "break" or inactivate a protein.  For example, not every amino acid site has the potential to mutate to a residue with dominant phenotype, but most sites can mutate to a side chain that might destabilize, disrupt, etc.
The lacId allele is a dominant loss-of-function (and so somewhat more complex than the simple explanation I just gave). It makes a so-called "poison product"

lacID is an example of a dominant-negative allele (or mutation) so the phenotype is visible in m/+ (the bacterial merodiploids are the prokaryotic version of heterozygotes), and therefore, by definition, dominant, however the phenotype (in this case constitutive expression of the lac operon) is the same as the loss-of-function phenotype (a complete knock-out, or deletion of the lac Repressor gene).
If m/+ has the same phenotype as m/m it could be dose-sensitive, or the protein could be a multimer, or the mutant protein could titrate (or sequester) an interacting protein.


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Why sigmoid curves appear in quantitative analysis of many biological phenomena?
I know two examples:
1-The binding of hemoglobin to oxygen (binding of oxygen to one site of hemoglobin induces conformational changes which increase the affinity of the other sites for oxygen - the curve could be interpreted as transition from a low affinity T sate to a high affinity R state). The plot can be seen here
2-The denaturation of DNA by temperature (when one segment of the double helix opens, base stacking is disrupted, making the denaturation of the rest of the molecule easier); Another plot
The two examples I gave were actually of positive cooperative phenomena, that is, the occurence of a first event favours the next events. There is also the titration curve, which is a sigmoid, but I don't think it's correlated.
I'm asking that because I found it amazing that the same sort of curve appeared in the study of such different subjects.
Are these examples somehow correlated, that is, for which sort of phenomena sigmoid curves are expected?

Logistic functions have a sigmoidal curve. Logistic functions are used extensively in ecological models. This question as it stands appears too broad. You can come up with lot of examples. You should narrow it down to a specific issue.

Agreed. These curves are widespread in population genetics as well.

Tons of examples in psychophysics and neuroscience...

Agreed - psychometric curves in a host of tests follow sigmoids.

can you rephrase question so that it is not encyclopedic but rather about biological principles? so far seems you can answer it extensively searching pubmed on sigmoidal curve

Dinosaur Growth Rates, neuron sensitivity to angle (auditory system) etc...

voted down for too broad scope

@aandreev I have reformulated.

seems more interesting now. can we remove hold?

I've already edited the question. Could you reconsider if it's still too broad or at least suggest other editions?

why is this question closed? i also want to know the answer/opinion. glad that there's still one person answered this.

I would suggest following: take any one-dimensional process that is described by gaussian function. If you integrate such process along variable, you will get a sigmoidal curve. For details see normal and cumulative distribution.
Now, the question is: how many biological processes are described/modeled by Gaussian distribution and dependencies? A lot!
Let's take a look at dinosaur growth from Revisiting the Estimation of Dinosaur Growth Rates

This figure describes how size of dinosaur changes with some time (model, I assume). Remember link between gaussian and sigmoidal functions? If you differentiate, that is find how fast aforementioned sigmoidal function changes, you will get gaussian bell-curve! Which tells you: dinosaur grows faster during middle age, and slower before and after that.
DNA denaturation curve is sigmoidal because efficiency of denaturation is again gaussian. At low temperatures very limited amount of molecules will denature, but at high temperature there are no more molecules to denaturate left, so the bell-curve. Anothe explanation goes like that: at low temperature additional heat doesn't change much because it is still too "cold", at higher temperature same amount of heat is just a drop in a bucket, barely noticeable.

How do you say that relationship of temperature and denaturation should be gaussian? Gaussian CDF looks sigmoidal; that doesn't mean that all sigmoidal curves have a gaussian explanation.


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How to correlate the pattern by which CAP activator from E.coli binds to DNA and its mechanism of action?
The catabolite activator protein (CAP) activates the expression of more than 100 genes involved in secondary sugar metabolism in E.coli.
Apparently, it always binds in sites that are away from -10 and -35 elements of the promoter by multiples of 10 base pairs (-70 or -60, for example). How could this be related to its mechanism of action?
I've searched about this particular activator and I found that it acts mainly by recruiting RNAP to weak promoters, although it does alter the architecture of the DNA, introducing an abrupt bend (for some CAP-dependent genes, this favours conformational changes in RNAP involved in the initialization of transcription): here's the crystallographic data.
However, I did not find anything conclusive about the pattern of binding to distances which are usually multiple of 10 base pairs (which is close to the number of base pair in a complete turn of the double helix).

The spacing between TF binding sites is often important as it directly relates to their relative orientation. If two binding sites were, say, 15 bp apart, the TFs would actually be on opposite sides of the DNA helix. This is why the spacing between -10 and -35 is so critical for efficient initiation. I don't know if this effect applies to the spacing you mentioned (60 to 70 bp); at first thought, it seems like it would be less relevant as there is greater flexibility over such a distance.

I found a great article that might help. To summarize the contents of the article, there are two classes of CAP dependent promoters/genes, and the distance of the CAP bindings site in these classes are different. Also the actions in which CAP is involved are different in the two classes of promoters. In the first class it does not overlap with the promoter region and is only involved in RNAP recruitment. In the second class it overlaps with -35 element of the core promoter and is involved in multiple interactions.
So the binding distance of the CAP is determines what interactions is it involved.
You can see the difference between the two classes on the picture below (taken from the article i linked). And I think this answers your question on why the patterns are multiples of ten - because this is the space needed for alpha-CTD to make a bridge between the protein complexes, or the CAP to interact with the RANP complex.

I only took a glance at the paper I linked and quickly extracted the info, but I hope it still helps


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Why mutations in genes involved in general processes like DNA repair increase the risk of developing specific types of cancer?
For example, mutation in MHS2, which encodes a protein involved in the repair of mismatches that occur during DNA replication, dramatically increases the risk of developing colon cancer.
(There are many other examples, like the RB gene which encodes a tumor supressor protein and is correlated to retinoblastoma, thus its name)
My question is: how a gene like MHS2 which participates in a general mechanism of DNA repair increases the risk of a specific type of cancer? Why doesn't it increase the risk of developing cancer in other tissues as well?

I can't fault @WYSIWYG for mentioning the cited Vogelstein article in providing an answer. You point to what seems like a great explanation for why certain cancers arise in some tissues but not others. However, for those who look closely this paper has some serious errors in its derivation of the model, and for good reason it has come under strong fire in the last couple of months.
See this for a really important rebuttal:
http://ameyer.me/science/2015/01/02/vogel.html
Unfortunately, the paper provides an elegantly specious explanation for, in part, the longstanding paradox of why cancers more readily arise in some tissues like the intestines and from seemingly identical mechanisms, but do not seem to arise in other tissues. My favorite example, though @El Cid you do list some good ones, are inactivating BRCA1 mutations which normally play a role in repairing double stranded DNA breaks. And yet even when mutated in the germline this only seems to increase cancer risk in the breast, and really only in one gender (females).
So the answer is still quite certainly that the field does not understand this paradox, and the cited Vogelstein paper was a total tragedy of a publication. There have been a number of officially submitted critiques of the paper and the Vogelstein lab has been trying to defend it as best they can. This is however a great example of how big name labs can seem to get anything published in Cell/Nature/Science.
Another thing to consider and @El Cid points to a good example, is the pRb mutations (in a very central tumor suppressor pathway for all cells) cause retinoblastoma and not for instance intestinal or blood cancers very readily, and the retina is not a rapidly dividing tissue. So the Vogelstein paper cannot explain this.

Retinoblastoma happens in early childhood. This is a carryover of actively dividing cells during embryonic development. pRb is involved on other cancers too.

From here.... In addition to bladder cancer, somatic mutations in the RB1 gene are associated with many other types of cancer. For example, changes in the RB1 gene have been reported in some cases of lung cancer, breast cancer, a bone cancer known as osteosarcoma, and an aggressive form of skin cancer called melanoma. Somatic RB1 mutations have also been identified in some leukemias, which are cancers of blood-forming cells. Somatic RB1 mutations in cancer cells inactivate pRB so it can no longer regulate cell division effectively.

Yes, both good points. First you are right, pRb is going to be found other cancers but why it cannot sometimes be found in every Cancer is the paradox. And about retinoblastoma occurring during early age you hit on the most widely cited criticism of the aging-Cancer theory. However, it does overlook an important difference, and that is germline versus somatic mutation. The reason we often associate retinoblastoma with childhood disease is because when they carry a germline mutation, every cell in the tissue carries this, therefore they do not need a high division rate to drive oncogenesis.

With germline mutations it is no probably more a question of overall somatic fitness. Every cell carries an oncogenes mutation, and is therefore at a functional disadvantage thereby more likely to allow for the expansion of a newly acquired secondary mutation.

Yes it is perhaps not understood why germline pRb mutation is manifested (first?) in Retinoblastoma why can't it cause some other cancer. I am not really sure if pRb's connection with retinoblastoma is anecdotal or whether it predominantly is manifested in this cancer.

Definitely not just anecdotal, we should never use anecdotes as support. http://cancer.sanger.ac.uk/cosmic/browse/tissue#in=t&sn=eye&ss=all&hn=retinoblastoma (not sure how to post a link in comments) but as you can see here pRb may not be essential to drive this Cancer, as we see in every Cancer I Can think of. But this still does not answer the original question of why certain central mutations like this are preferentially found in only a handful of cancers.

I should look at the rebuttals. The points raised in the linked one are not very strong; for e.g. plotting on log-log axis. I'll read the actual paper more carefully. Regarding "anecdotal": I meant, though most cases of disease is because of pRb mutation, the converse may not be true. That is what I was saying

Okay yeah that makes more sense. And yeah you can look around there are a few that have already been officially submitted to Nature and I think they might have been in press already? I'm not entirely sure because I read them as drafts.

I think it would make sense that I don't delete my answer until the paper is retracted. It is controversial but not yet proven wrong. At least the OP will have an idea of the entire picture.

Yeah don't ask me I'm very new to this site if I were in charge of the site I would see keep all relevant answers. Even if yours turns out to be incorrect I think it is always good to have contrarian view. It gets people to think.

You should have a look at this interesting article published earlier this year in Science.
There are two mechanisms by which cells can accumulate mutations in DNA:

Replication errors
External physicochemical agents such as UV, carcinogens etc

In the abovementioned paper, the authors classify cancers into two types:

That arise predominantly because of environmental agents (D-type)
That arise predominantly because of replicative errors (R-type)

Moreover in the same article, the authors point out that the lifetime risk of a cancer is positively correlated with the number of stem cell divisions in the associated tissue. FAP colorectal carcinoma features highest with respect to, number of stem cell divisions and consequently lifetime risk.
Since these cells divide more, they are likely to accumulate more mutations and a defective DNA repair process will worsen the situation. I cannot find a great amount of study on MHS2 gene and its connection with different types of cancers but in general, the above explanation would be applicable to most genes that are involved in DNA repair.

NOTE: As mentioned in the other answer, the abovementioned paper has received some criticism from the scientific community for making far-fetched claims which apparently fits so beautifully with the theory that it seems quite correct. The article however is not retracted. Therefore, it is important to not completely believe in this hypothesis but at the same time keep it in mind considering it as a possibility that needs further verification.


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Primers for human tissue?
If I wanted to examine human tissue samples, such as hair, blood, fingernails, etc, for their DNA, what primers would I use for the amplification of the DNA when extracted(PCR)?
edit: To look at the STR in the human genome based off of the FBI's CODIS system http://en.wikipedia.org/wiki/Combined_DNA_Index_System
from wikipedia:
"CODIS identifies genetic markers at 13 STR loci, plus Amelogenin (AMEL) to determine sex.
CSF1PO
D3S1358
D5S818
D7S820
D8S1179
D13S317
D16S539
D18S51
D21S11
FGA
THO1
TPOX
vWA

"
I read something about CODIS, but I don't know too much about it, if any one could give me some specifics that would be helpful.

The human genome is 3 billion letters long.  You aren't going to look at all of that, are you?  You have to know what you want to look at.  Are you just trying to examine the microsatillites that are used in DNA fingerprinting?

@swbarnes2      Sorry I was not thinking, I want to look at a microsatillite area, a subset i believe is called STR(single tandem repeats), since they have been used before in identification historically?

Saying that you want to look at the STR is still pretty broad.

@Chris          I guess I want to do the same type of identification that the FBI does with its CODIS system

The References and External Links sections of the Wikipedia article in your question contain a great deal of relevant information to get you started. There is a link to the FBI's CODIS and NDIS (National DNA Index System) Fact Sheet, which contains a lot of relevant information, including part numbers for validated kits from several manufacturers. DOI numbers for some journal articles are given in the Wikipedia article as well, wherein you may be able to find specific primer sequences or references for them. Finally, there is a link to the main CODIS page on FBI.gov, which contains an abundance of useful information, including the NDIS operational procedures manual.
You just need to look to find what you seek.

Extracting genomic DNA and PCR are different processes. Extracting genomic DNA means that you get all the DNA sequences from human genome. Using extracted DNA, you can amplify a specific region from the whole genomic sequence.
A primer set is usually set at the both ends of a sequence you want to amplify the sequence. In your case, you the region highlighted in yellow in the figure "CODIS markers" of the wiki would be amplified.
Different people may set primers differently even if they want to amplify the same region; however, in this case, primer sequences are already determined to get consistent results. If you would like to know the actual sequences that FBI is using, you (or someone or I) have to search to find them.

By the way, some protocols may skip the extraction process--taking several micro litters of buffer-suspension of samples or something like this. It may depend on whether  the PCR enzyme can overcome inhibitory effects of crude DNA solutions to amplify fragments.


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How long can one leave sample in lysis buffer for DNA extraction?
I am trying to do some DNA extraction for my professor, and I make a lysis buffer with proteinase K. I did not have the time to continue the procedure so the hair and the buffer have been sitting together at room temperature for about 12 days. My professor stated it would be "fine" to continue on with my DNA isolation procedure, but I have my doubts.
Should I continue my DNA extraction( vortexing, boiling, centrifugation and collection of supernatant, storage at -20 degree Celsius) or would this be pointless at this time? My goal is to run PCR and then a gel.
EDIT:
Here is the composition of the lysis buffer:
In 20 ml of Lysis buffer:
final concentrations are $0.1 M$ TAE, $0.5M$ $\ce{NaCl}$, 0.2% SDS.
To $800 ul$ of Lysis buffer I added $5 ul$ of proteinase K at a concentration of $250 ug/ml$.
(Proteinase K was made via:  $ 0.0025 g$ up to $10 ml$ of TAE buffer( $1 M $))
This was in a $1.5 ml$ centrifuge tube that has been now sitting for 12 days.

Can you put in the composition of the lysis buffer here?

@Chris                    I put the composition of the buffer, thanks for reminding me.

What do you mean by 0.1M TAE? TAE normally stands for Tris-Acetate-EDTA, but you already have EDTA as a component.

@MarchHo              Yea your right, I was not thinking sorry let me fix that.

@Tegudet                 I have not done it yet, since im a slacker... I also dont plan on doing it any time soon. I am a novice at biology methods, so I wouldnt have any suggestions. Sorry and good luck.

It should be fine. Unless they have been contaminated with DNase, none of the components will damage or denature DNA. I've left purified plasmid DNA on the bench for weeks with no apparent degradation, so you should be okay (not that I recommend doing that on a regular basis). I would continue with the purification, according to your professor's recommendation, because you've already come this far. If worst comes to worst, you won't get anything, and you'll have to re-purify. However, the chances of your getting something are pretty high, so you may as well go with it.

Ironically I tried to continue my extraction and failed spectacularly, so I might have to redo the sample collection. This will help for the future though.

Your concentration of EDTA seems to be rather high. When performing lysis for DNA extraction, I usually use 1mM EDTA in the lysis buffer. Concentrations that are too high may result in inhibition of the PCR reaction later on, unless the DNA is first purified.
This could be a reason why your reaction failed.

I had less EDTA than that, the EDTA I mentioned previously was the final concentration of EDTA in my TAE, I removed it because I was not thinking clearly sorry. The final concentration of my EDTA in my TAE is 0.025 M i believe.  Also I have not ran my reaction yet, but many thanks for the advice.

@rosiv how then did you know your reaction failed? Boiling the mixture should result in precipitation of proteins, which should be removed by the spin. You will be left with the DNA solution which you can either use directly or use after desalting.


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what are examples of experimental designs on exposing materal for degradation
if one wanted to compare how sources of DNA would degradate in various conditions(environmental) how would they do this in an experimental fashion but also be best comparable to real world examples of Enviromental conditions? Sorry if this question is worded poorly, any suggestions would be appricated.
For example, if I were to expose my own blood to various conditions such as a wet enviroment versus a dry ennviroment, how would I best replicate these enviroments in real life(ie: bloodly water in a cup versus dried blood on a floor) without introducing confounding varables?
I would need some type of "standard" yes? And if so, then would using sterile controled conditions be appropriate, or should I literally be using these real world situations for "better" results?
I tired finding papers, but I guess my research methods are too poor to get anything useful.
EDIT:
My facilities I have access to are a small academic institution, I know basic autoclave use and have access to gel rigs and pcr machines. My samples do not have to be blood, it could be any human tissue or sample, like hair or spit. I suppose I would use the same sample, but kept in a sterile condition for a controo, maybe a petri dish?
I guess my mental protocol would be to try different degradation conditions and extractions, but starting with a boiling DNA extraction to see how effective a certain condition was compared to a control.
I could set up a time table of like 2 weeks to perform the experiment, and every 3 days or so, extract DNA from the control and the sample to then pcr with some human primers(I think we are using the fbi's CODIS primers that they use in foriensics, but only a subset due to cost) and then run an agarose gel to determine degradation( poorer resolution meaning more degradation I suppose?).
Another wuestion that popped to mind, for my time table and my DNA extractions, would I have to perform the pcr and subsequent gel elecrrophorsis as soon as I am done with my extraction, or could I store the extraction samples until I am ready to run a large batch of pcr tubes and a large gel? Would they degrade in a -80°C freezer?

You are going to need to add more details to your question. What kind of facilities to you have access to? If you are doing this in an academic or commercial lab, there are likely protocols for handling human tissue that needs to be followed. Human blood is a biohazard and there are likely strict rules in place as to what you can and cannot do. Also, what is your plan for processing and examining the DNA after your experimental time. PCR amplification, sequencing? What are your controls? Until you give these details, then it is hard to say.

@AMR.            I added more details, thanks for the suggestions. This is an academic lab, I have access to autoclave, pcr, gel rigs etc..(we are not rich, state school). I was using blood as an example, there are other tissues I can use, although I can get authorization for blood if needed. Controls would be a sample of tissue or product that is kept in sterile conditions, like a perri dish maybe? Or would that be a bad idea. A lot more detail is in my post above.

Since you mention examples, a colleague did a project on DNA degradation using cotton swabs with saliva (definitely not as hazardous as blood!). What I don't know for sure is if she used normal PCR, but I do know she didn't have access to qPCR (and she was really good at agarose gels!). My bands were never perfectly regular, though, and I was just testing for presence or absence.

Have you heard of qPCR? This method quantifies the amount of DNA in the sample. Another quantitative PCR method you might look into is taqman PCR. Traditional PCR + agarose gel electrophoresis is not going to give you a quantitative measurement of the DNA in your sample.
Here are the wikis on taqman and qPCR.
taqman https://en.wikipedia.org/wiki/TaqMan
qPCR https://en.wikipedia.org/wiki/Real-time_polymerase_chain_reaction
Also, if you have the choice between intercalating agents and fluorescent probes, go with fluorescence. Intercalating agents are hazardous.
Hope that helps.
Edit Adapted from comments -
We don't have access to a real time pcr intrusment sadly. All we have is a traditional pcr machine. Can I get your opinion on this quote I found on the quantitative messures of traditional pcr: '"No, though comparing the intensity of the amplified band on a gel to standards of a known concentration can give you 'semi-quantitative' results." From thermofisher.com/us/en/home/life-science/pcr/real-time-pcr/…. Are there ways to work with the intensity of the bands I get to be " more reliable"? – Ro Siv
Yes, quantification from traditional PCR can be done, though the accuracy is questionable. One method I have heard of uses a computer to analyze the intensity of the bands. You could probably pull this off with some Python code (check out the scikit-image python library). The other option is to do what you said, compare to known concentrations.
If you are familiar with HA titers in virology, you might be able to contrive a similar method, in which you carry out 10-fold dilutions of the sample until there is no more detectable DNA left. The point at which there is no DNA left is called the experimental end-point, and the titer of the original sample is simply the inverse of the dilution factor at the end-point. Check out hemagglutination(HA) in the context of virology. I think a method similar to this would be better than simply eyeballing the intensity of bands, because you will have some quantitative evidence.
If you want to eye-ball, you should use control bands at several different concentrations, so that you can say, 'the intensity of the band falls between control bands A and B, and so the concentratin of the sample is between concentrations A and B'
I bet you could pull off the serial dilutions. It will be good practice, too. To make a 10 fold dilution, just add 1ml of sample to 9ml of saline. Then, from that new solution you just made, do it all again. Take 1ml and add to 9ml saline. Repeat. Each time you decrease the concentration by 10^-1. You can scale it down too - 1ul sample to 9ul of saline. Repeat. Here is a SOP on HA. Honestly, I would go with the serial dilution thing. I bet ur professor would help you out with this. It is cheap, easy, and widely used. cfsph.iastate.edu/HPAI/resources/SOPs/HA_HI.pdf
Question: If I were to do both methods, then would ImageJ be a possible substitute for scikit-image? rsb.info.nih.gov/ij I think its GUI interface is alot more workable for me.
Response: From just skimming that link it looks like it might. You would probably be interested in the density analysis part of the software, but I dont think a computer is necessary, and ya you will have to produce that gradient of concentrations any way. If it were me, I'd first try to do the experiment without computer analysis. Produce the gradient of control DNA concentrations, compare your sample to the control gradient and see where your sample falls.
Then repeat the experiment while varying the independent variable, lets say its time. So take a sample at 5 min 10 min 15 min etc. and produce a plot of surviving DNA concentration vs time. It will probably end up looking something like a sigmoid curve. If you decide you need more precision in your measurement of the DNA concentration, then consider using the image software, but I doubt you will need it, though I admit it would be twice as badass.

We don't have access to a real time pcr intrusment sadly.  All we have is a traditional pcr machine. Can I get your opinion on this quote I found on the quantitative messures of traditional pcr: '"No, though comparing the intensity of the amplified band on a gel to standards of a known concentration can give you 'semi-quantitative' results." From https://www.thermofisher.com/us/en/home/life-science/pcr/real-time-pcr/qpcr-education/qpcr-vs-digital-pcr-vs-traditional-pcr.html.  Are there ways to work with the intensity of the bands I get to be " more reliable"?

Yes, quantification from traditional PCR can be done, though the accuracy is questionable. One method I have heard of uses a computer to analyze the intensity of the bands. You could probably pull this off with some Python code (check out the scikit-image python library). The other option is to do what you said, compare to known concentrations.

If you are familiar with HA titers in virology, you might be able to contrive a similar method, in which you carry out 10-fold dilutions of the sample until there is no more detectable DNA left. The point at which there is no DNA left is called the experimental end-point, and the titer of the original sample is simply the inverse of the dilution factor at the end-point. Check out hemagglutination(HA) in the context of virology. I think a method similar to this would be better than simply eyeballing the intensity of bands, because you will have some quantitative evidence.

If you want to eye-ball, you should use control bands at several different concentrations, so that you can say, 'the intensity of the band falls between control bands A and B, and so the concentratin of the sample is between concentrations A and B'.

My lab skills are lacking and I feel like I would mess up easily, do you have any "dummy" sources for doing the serial dilutions or using the imaging software?

I bet you could pull off the serial dilutions. It will be good practice, too. To make a 10 fold dilution, just add 1ml of sample to 9ml of saline. Then, from that new solution you just made, do it all again. Take 1ml and add to 9ml saline. Repeat. Each time you decrease the concentration by 10^-1. You can scale it down too - 1ul sample to 9ul of saline. Repeat.  Here is a SOP on HA. Honestly, I would go with the serial dilution thing. I bet ur professor would help you out with this. It is cheap, easy, and widely used. http://www.cfsph.iastate.edu/HPAI/resources/SOPs/HA_HI.pdf

This is the scikit-image website, though if you havn't used python before this might cause you some headache http://scikit-image.org

Either way, I think your best bet is to do some type of serial dilutions (either to your control or to your samples like in HA) and calculate a titer. Check out the link to the .pdf I sent you, but dont look at the HI section of it, just learn the HA part. If you like biology, you will have to learn serial dilutions at some point. There are used everywhere. Good luck! You can do it!

If I were to do both methods, then would ImageJ be a possible substitute for scikit-image? http://rsb.info.nih.gov/ij/      I think its GUI interface is alot more workable for me.

From just skimming that link it looks like it might. You would probably be interested in the density analysis part of the software, but I dont think a computer is necessary, and ya you will have to produce that gradient of concentrations any way. If it were me, I'd first try to do the experiment without computer analysis. Produce the gradient of control DNA concentrations, compare your sample to the control gradient and see where your sample falls.

Then repeat the experiment while varying the independent variable, lets say its time. So take a sample at 5 min 10 min 15 min etc. and produce a plot of surviving DNA concentration vs time. It will probably end up looking something like a sigmoid curve. If you decide you need more precision in your measurement of the DNA concentration, then consider using the image software, but I doubt you will need it, though I admit it would be twice as badass.

The extended conversation that pertains to the answer should be inserted into the answer as an edit. Comments are temporary and can be lost in time. To insure the information stays with the answer it should be added to the body of the answer. Please consider editing to add the information into the answer. Thanks,


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determining horizontal gene transfer between two genomes?
I want to determine if there is horizontal gene transfer between two genomes, in particular I was to use the parametric methods described in wikipedia since I would most likely struggle to understand the phylogenetic methods fully.
The two genomes in mind would be Lactococcus lactis and  Lactobacillus helveticus since they are used in the process of cheese making and therefore would be in close enough proximity/environment to argue for tentative events of HGT. (Correct me if I am way off base here in my line of thought...)
Could I just access representative genomes for each from NCBI and calculate/determine the various genomic signatures that are indicative of HGT via the previously mentioned parametric methods(Nucleotide composition, oligonucleotide spectrum, structural features, etc...)?
Or would the genomes need to be rendered and sequenced from a confirmed source where they are both located/habituated to properly argue for HGT?(In which case I believe NCBI does not have this data readily available?)

Since the parametric model is applied to only a single genome to see if there is evidence of recent HGT via a change in the average content in coding regions, it will not tell you from where the HGT came from, just that a HGT likely occurred in an area of the genome. Since you are trying to specifically see if there was a HGT between L. lactis and L. helveticus you would have to run a parametric analysis on both, find a HGT candidate on one of the genomes and then find that sequence as a non-HGT candidate on the other genome and via BLAST.
These papers give a good argument to why to use genome signatures instead of GC content as a parametric method of detecting HGT.
Review from where most of the Wiki figures came from
Genome signature paper
Newer Genome signature paper


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Can these "Promega Wizard genomic DNA Purification kit" be used for samples not stated directly?
I am not sure if this is a duplicate of my previous question, it is somewhat related, so sorry if I misunderstood.
The question is, can i use the above kit for samples like hair, fingernails, etc?
Here are the guides:
https://www.promega.com/~/media/files/resources/protcards/wizard%20genomic%20dna%20purification%20kit%20quick%20protocol.pdf
and the extended guide:
https://www.promega.com/~/media/files/resources/protocols/technical%20manuals/0/wizard%20genomic%20dna%20purification%20kit%20protocol.pdf
It says that for the animal tissue:
Animal Tissue (Mouse Liver and Brain), so I figure it wont apply given that these cells might have higher percentage of DNA that hair(roots/shaft) could have, or fingernails.

You may want to look for forensic kits. These are specially adapted for the needs you habe. But make sure that you have a seat when you read the price quotes, these kits are really expensive. It may be worth to contact a sales representative and tell them that you do a research project and are not a professional analysis lab. Sometimes you can get a good discount then.

If you have a question about a kit, I strongly suggest contacting the manufacturer instead of just asking random people on the internet.

In addition, the kit clearly says "DNA". "Genomic RNA" makes little to no sense in a biological context.

@MarchHo       sorry it was a typo, i fixed it

It is difficult to isolate good quality genomic DNA from fingernails. PCR for specific genes is much easier. What do you want to do ultimately?

The column size should be appropriate. And you have to solubilize enough for DNA to come out. But why don't you use kits showing gDNA extraction from nail. http://www.epibio.com/docs/default-source/forum-archive/forum-14-1---pcr-analysis-of-fingernail-dna-using-quickextract-dna-extraction-solution.pdf?sfvrsn=4 And this information may be useful. http://link.springer.com/article/10.1007/s12033-010-9273-6/fulltext.html

@WYSIWYG         I was going to PCR for specific genes, the CODIS standard 13 loci for the human genome, using extracted DNA from hair or fingernails, thanks for the reply.

@RoSiv You don't need to extract DNA to do PCR. You can simply use a small part of the sample. Like you do in colony PCR.

@WYSIWYG          so are you telling me I could just break down the hair/fingernail and then perform PCR on that solution? if so would you have some type of protocol for that?

@RoSiv See this article. And for hair you should use the hair root (that is where you will find viable cells)