text:
Hardy Weinberg Equilibrium problem

In a small tribal population, the frequencies of two alleles A and a
  at a particular locus were 0.3 and 0.7, respectively. However, not all
  the individuals with genotype aa could live up to the reproductive age
  and the relative fitness of this genotype was found to be 0.5. The
  remaining genotypes had a relative fitness of 1. What is the expected
  percentage of heterozygotes among newborns in the next generation?

My answer is : 37 % but the answer given 43.52 %
I did the following : First I assumed the population to be of 100 individuals and then I counted the no of individuals with respective genotypes. Then I assumed that each person leaves 1 offspring except the aa ones which leave 0.5 offsprings and then I calculated the new genotype frequency from this.

Are you saying that f(A)=0.3 and f(a)=0.7?

@fileunderwater yes.

Your reasoning is incorrect, because once you have the number of individuals surviving after the 50% mortality you can't just give them all one identical offspring, you have to mate them with one another.
However, I can't get the answer given, instead I get 47.9%
Here is my reasoning:

f(A)=0.3
f(a)=0.7

calculate genotype frequencies:

AA = 0.32 = 0.09
aa = 0.72 = 0.49
Aa = 2 * 0.3 * 0.7 = 0.42

(these add to 1 as expected)
use 1000 individuals for nice round numbers

number AA = 90
number aa = 490
number Aa = 420

Now apply 50% mortality in aa individuals:

number AA => 90
number aa => 245
number Aa => 420

now calculate new allele frequencies in mating population:

f(A) = (90 + 90 + 420)/1510 = 600/1510
f(a) = (245 + 245 + 420)/1510 = 910/1510

calculate proportion of heterozygote offspring

= 2 * f(A) * f(a)
= (1200 * 910)/(1510 * 1510)
= 0.479

I hope someone can see where I'm going wrong.

I got 47.89% when only working with frequencies, so your answer seems right. My feeling was also that both answers were incorrect, therefore my comment to the question.

thanks @fileunderwater, I've been tearing my hair out over this! You should post your calculation - I expect it is more elegant than mine.

This is pretty much what I was getting as well, and I couldn't figure out how to get the 43.52%.

This is basically the same solution as @AlanBoyd's answer, but since he asked me to, I will post my solution as well (also a reason to try out $\mathcal{MathJax}$ a bit more).
Assuming:
$f(A)=p=0.3, \\f(a)=q=0.7$
and the standard formulas:
$f(AA)=p^2\\
f(Aa)=2pq\\
f(aa)=q^2$
gives these genotypes in the parental generation (G1), before and after selection (using the fitness vector $w$):
$$
\begin{array}{c|cccc}
\text{genotype} & \text{freq G1} & w & \text{freq breed.pop} & \text{freq breed. rescaled}\\
\hline
AA & 0.09 & 1 & f(AA)\cdot w_{AA}=0.09 & 0.119\\
Aa & 0.42 & 1 & f(Aa)\cdot w_{Aa}=0.42 & 0.556 \\
aa & 0.49 & 0.5 & f(aa)\cdot w_{aa}=0.245 & 0.325\\
\text{sum} & 1 & & 0.755 & 1
\end{array}
$$
The genotype frequencies in the breeding population (rescaled so that they sum to one) are then used to calculate allele frequencies as:
$$f(A)=f(AA)+\frac{f(Aa)}{2} = 0.397\\
f(a)=f(aa)+\frac{f(Aa)}{2} = 0.603$$
These are then used to calculate the genotype frequencies in the next generation (G2), using the same HW-equations as in the beginning:
$$\begin{align}
f(AA)&=0.397^2=0.158 \\
f(Aa)&=2\cdot0.397\cdot0.603=0.479 \\
f(aa)&=0.603^2=0.363 \\
\end{align}
$$
I do not understand where the given answer $f(Aa)=0.435$ is coming from.


text:
What stops telomerase?
The telomerase is an enzyme that adds telomeres.
What stops the telomerase from adding too many telomere sequences ? What's the regulating mechanism ?

Telomerases are tightly controlled on all level: Expression, post-translational modifications and by external factors. I think for this the external factors, a protein class called telomeric proteins. They bind to the end of the telomere and regulate the telomerase.

The figure is from this paper, which looks into the topic quite extensively:

Regulation of telomerase by telomeric proteins.

source: Stack Exchange

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sort: votes


text:
2 types of telomerases?
As telomerase works by adding new nucleotides complementary to the RNA it contains, it cannot work for the complementary strand.
Say telomerase X has RNA complementary to the 5' to 3' strand it cannot elongate he telomere for the 3'to 5' strand.
So does a cell have 2 types of telomerases ? One for 5' to 3' and another for 3' to 5' ?

A second telomerase is not necessary, as the lagging strand is filled in by the DNA-Polymerase, see this figure:

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text:
How does GTP help in the step of codon recognition?
The anticodon of an incoming tRNA base pairs with the complementary mRNA codon in the A site.Hydrolysis of GTP increases the efficiency and accuracy of this step.
How does GTP do so ?

GTP based structural changes (even motor actions) are very common in biological systems. For e.g. G-proteins, Rab-GTPase (vesicular transport), Ran-GTPase (Nuclear export/import).
So all these GTP-bound proteins make use of an intrinsic or assisted GTPase activity to convert GTP to GDP. This conversion causes change in the structure of the associated protein. Going back to the GTP bound form requires proteins called GEF (Guanine nucleotide Exchange Factors).
So in the case of translation elongation, the elongation factor is a GTPase which changes confirmation upon GTP hydrolysis. This confirmational change twists the tRNA so that the bound amino acid moves closer to the peptidyl-transferase center (if P-site is in the left then the amino acid is bound to the rightward CCA tail of tRNA. The twist causes the amino acid to move leftwards- towards the P-site).
You can refer books like Genes by Lewin for details.


text:
How do ion channels transport only specific ions?
Ion channels, such as $Na^+$ channels and $K^+$ channels, are higly specific for ion permeability. But how do these channels achieve and maintain this specificity? Like how does a $K^+$ channel transport only $K^+$ ions (same for other channels like $Na^+$, $Ca^{2+}$, $Cl^-$, etc. channel)?

I am restricting the answer to only $Na^+$ and $K^+$ channels, assuming similar mechanism for other channels. In these 2 channels, such high level of specificity is achieved because of two main differences between $Na^+$ and $K^+$:

difference in size of $Na^+$ and $K^+$ ions.
difference in chemical properties of $Na^+$ and $K^+$ ions.

Lets discuss these points one-by-one:

Difference in ionic size: the ionic size of $Na^+$ ion is 0.96$\overset{\circ}{A}$ while that of $K^+$ ion is 1.33$\overset{\circ}{A}$. How this size difference of 0.38$\overset {\circ}{A} $ is exploited by channels will be discussed in later section.

source

Difference in chemical properties: the property we are concerned here with is hydration enthalpy. $Na^+$ ion has hydration enthalpy than $K^+$ ion, meaning $Na^+$ has higher tendency to remain bounded by water molecules than $K^+$. How this enthalpy difference is exploited by channels will be discussed in next section.
source

I will discuss different methods used by these channels one at a time.

$Na^+$ channels: $Na^+$ channels are less studied than $K^+$ channels, but some of the mechanisms used are known and explained below:

$Na^+$ ions pass through channels in partially hydrated form1, and these channels have 2 rings of selection filters2 in mammals.
The first (outer) ring contains amino acids EEDD (or EEMD)3 while second (inner) ring contains amino acids DEKA4. How these amino acids bind to specifically $Na^+$ ions is not completely known yet, but it is hypothesized that the inner ring, being more conserved, is more important as a filter than the outer ring. Also, it has been shown that by changing the amino acid K in DEKA makes the channel more permeable to $K^+$ and $Ca^{2+}$ ions, and by changing sequence from DEKA to EEEE makes the channel more selective towards $Ca^{2+}$ ions5.
$K^+$ ion, in hydrated form, cannot pass through inner filter due to larger size and presence of negatively charged D and E of DEKA, whereas $Na^+$ easily passes through due to smaller size and higher hydration enthalpy6.

Negative charge in channel is such that it mimics the hydration shell (regular octahedron) of $Na^+$ from side
source (1) source (2)

$K^+$ channels: $K^+$ channels have been studied more intensively, so their mechanism is much more understood. The main points to ponder are:

The filter of $K^+$ channel contains amino acids TVGYG 7 and is present in the narrowest region of the channel.
To pass this channel, $K^+$ ion needs to be completely dehydrated i.e. without any water molecule bound to it. The amino acids in the filter replace water molecules with polar oxygen atoms. On the other hand, $Na^+$ cannot get rid of water molecules so easily and hence, its passage through the channel is thermodynamically unfavorable8, partly also because dehydrated $Na^+$ is so small that it cannot even bind with all of the polar oxygen atoms of amino acids.
Here nature shows some clever techniques. The amino acids, TVGYG, having their electronegative carbonyl oxygen atoms aligned toward the center of the filter pore, form a square anti-prism similar to a water-solvating shell around each potassium binding site. The distance between the carbonyl oxygens and potassium ions in the binding sites of the selectivity filter is the same as between water oxygens in the first hydration shell and a potassium ion in water solution, providing an energetically-favorable route for de-solvation of the ions9.

This is how the passage of a $K^+$ ion through $K^+$ channel looks like:
source
The carbonyl oxygens mimic this configuration as this is how a $K^+$ looks in hydrated form (square antiprism):source
P.S. as more deep studies are made, more mechanisms may be revealed. Also, above mentioned points are just theories and not conclusive proofs.
References:

Hille, B. The permeability of the sodium channel to organic cations in myelinated nerve. J. Gen. Physiol. 58, 599–619 (1971).
Guy HR, Seetharamulu P. Molecular-Model of the Action-Potential Sodium-Channel. Proc Natl Acad Sci USA. 1986;83:508–512.
McNulty, M. M., Edgerton, G. B., Shah, R. D., Hanck, D. A., Fozzard, H. A. and Lipkind, G. M. (2007), Charge at the lidocaine binding site residue Phe-1759 affects permeation in human cardiac voltage-gated sodium channels. The Journal of Physiology, 581: 741–755. doi:10.1113/jphysiol.2007.130161
Favre I., Moczydlowski E. & Schild L. On the structural basis for ionic selectivity among Na+, K+, and Ca2+ in the voltage-gated sodium channel. Biophys J 71, 3110–3125 (1996).
Calcium channel characteristics conferred on the sodium channel by single mutations.
Heinemann SH, Terlau H, Stühmer W, Imoto K, Numa S 1992 Apr 2;356(6368):441-3.
Mechanism of Ion Permeation and Selectivity in a Voltage Gated Sodium Channel. Ben Corry and Michael Thomas
Chemistry of ion coordination and hydration revealed by a $K^+$ channel–Fab complex at 2.0 Å resolution, Yufeng Zhou, João H. Morais-Cabral, Amelia Kaufman & Roderick MacKinnon
Mechanism of potassium channel selectivity revealed by $Na^+$ and $Li^+$ binding sites within the KcsA pore.
Ameer N. Thompson, Ilsoo Kim, Timothy D. Panosian, Tina M. Iverson, Toby W. Allen, and Crina M. Nimigean
A comparison between two prokaryotic potassium channels (KirBac1.1 and KcsA) in a molecular dynamics (MD) simulation study; Mikko Hellgrena, Lars Sandberg, Olle Edholm, 1 March 2006


text:
What type of insect is this? Is it ant or something else?
I was sitting under morning sunshine when I saw this:

At first, I thought that it is a common Indian black ant. But it was moving much faster. Also, it seemed to have 2 (or probably more) eyes (sorry, couldn't take images as 'twas too fast). The most surprising part was when it leapt over the chair WITH A WEB! (just like a spider). Also, its mandibles(?) are much bigger than an ant's. Is it some kind of hybrid of ant and spider. I recently read that in some caves new varieties of spiders, which look like beetles (or maybe opposite) have been discovered. Is this related to them?
Details: I found it in Northern Plains, India. Its length is almost 1 cm (maybe bigger) and breadth is about 0.5 cm (actually slightly smaller than that).

This one is an ant,Common Indian black ant.Ant being an insect has 3 pairs of legs but this one his has 2 pairs,must have got it's body cut. The small projections at front are the antennae.

@another'Homosapien' I see you found the other half :p. Cool find.

Such a queer species. I thought it was an ant. But it is actually a spider.
These spiders belong to Salticidae family,commonly called ant-mimicking spiders / jumping spiders.

They are  Batesian mimics of ants, such as Sphecotypus in the Clubionidae.

They do not feed on their model organisms and keep them at an acceptable distance.
This one is from Myrmarachne sp. There are more than 20 species found in India.

Source:

Wikipedia
Myrmarachne

@another'Homosapien' If you are not an expert on the group, or can find extremely conclusive evidence that points to one specific species, you shouldn't push to add a specific species name. Species information on the internet is scattered at best, and you cannot expect to be able to identify every single species based on google searches and a couple of websites. There is no problem of leaving it at the family name or Genus sp., if that is what is relatively certain.


text:
Domains in cell membrane
How is movement of proteins and lipids between different domains of cell membrane prevented?
Why is the noncytosolic layer not able to do lateral movements between domains but cytosolic layer is able to do so?

First of all, often it is not. Many receptors for example move around the membrane. You might want to have a look at wikipedia's entry on lipid rafts though.

There are various mechanisms through which membrane proteins can remain localized in the membrane. See the below figure from MBOTC (book):

(A) They can aggregate together so that their relative positions are constant.
(B) They can be anchored to the Extracellular Matrix
(C) They can be anchored to the cytoskeleton
(D) They can be anchored via cell-cell interactions (adherens junctions, hemidesmosomes etc)
(E) Not mentioned in the figure; mentioned in the comments. Lipid rafts are membrane regions which are composed of rigid lipids like cholesterol and sphingolipids. Lipid rafts are thicker than regular membrane and do not diffuse into the latter. Some proteins are specifically anchored to/incorporated into the lipid rafts (T-Cell receptor, IgE receptor) and their relative position with adjacent proteins (co-receptors) remains constant.

Why is the noncytosolic layer not able to do lateral movements between
  domains but cytosolic layer is able to do so?

Where did you read this. Both layers can do lateral movements; if proteins are specifically "anchored" to one side of the membrane then the concept of domain applies to that side only.


text:
How are 6 "fixed" CO2 molecules joined toegther as glucose?
When we study calvin cycle, we study it with 6 molecules so as to form 1 glucose in a single cycle as:
6 RuBP + 6 CO2 => 12 3-PGAL => 1 Glucose + 6 RuMP
But if we look deep, then we know that the molecules are synthesized one-by-one & 6 cycles give 1 glucose, but:
1 RuBP + 1 CO2 => ... => 1/6 Glucose + 1 RuMP
My question: What is actually this 1/6 glucose (organic carbon fixed from inorganic carbon and how are such 6 molecules joined together?

Okay, now I understand that I need to change my question a bit because its actually drastically misleading.

It's not really possible to break it down this way. The CO2 fixated by the RUBISCO enzyme generates two phosphoglycerate (2 x 3C) molecules from one ribulose bisphophate molecule (5C), while the rest of the Calvin cycle serves to regenerate 3 ribulose bisphophate from 5 phosphoglycerate. Hence, one 3-carbon sugar (glyceraldehyde phosphate or dihydroxyacetone phosphate) can exit the cycle for every 3 CO3 captured. The regeneration of ribulose bisphosphate involves several enzymes, and the stoichiometry is rather complicated; it would take an entire essay to describe it all. I suggest you look the calvin cycle in the metacyc database, it's a nice interactive resource where you can explore all the details of the reactions. Wikipedia also provides some details on these reactions.
The glyceraldehyde phosphate produced by the Calvin cycle is then converted to glucose and other sugars by the enzymes of gluconeogenesis. The key enzyme is fructose diphosphate aldolase (or simply "aldolase") which condenses glyceraldehyde phosphate and dihydroxyacetone phosphate to one fructose-1,6-diphosphate. A chart of the pathway leading to other sugars is found here.

Glucose (and other hexoses) are not products of the Calvin cycle. Glyceraldehyde-phosphate (a triose) is the immediate product the cycle; 2 of these can be condensed to fructose-2,6-biphophate by aldolase, and from there on to other hexoses, like glucose.

You were asking about the "1/6 of glucose" and how it derives from CO2; this is via glyceraldehyde-phosphate. No, I did not imply that 2 CO2 makes 1 glucose, that's obviously not correct; but 2 glyceraldehyde-phosphate makes 1 glucose. And for net production of 1 triose, 3 CO2 must be captured. I don't think it makes much sense to talk about "turns" of the cycle, I hear this often about metabolic cycles, but I think it's better to just look at the stoichiometry of the reactions. (It's not actually a wheel :)  I will extend the answer with the aldolase part.


text:
Disadvantage of using Drosophila for breeding experiment
What should be the disadvantage of using Drosophila for experiments?
a)small size of larva.
b)short life cycle.
c)mating soon after emergence of flies.
d)large number of offsprings.
Options (b) and (d) should be advantages.
I think that the answer should be (a) as small larvae would be difficult to maintain.
Given answer is(c).
Why is that?

All options given have advantages but become disadvantageous depending on experiment you are trying to do. Here question is asked for "breeding experiment". In these experiments it is very important to keep track of genetics. If females mates with males of some undesired genotype, it will ruin your experiment objective.
As option (c) is 'mating soon after emergence of flies' , females and males from same vial (which is generally maintained as single genotype) will start mating soon. Generally this time period is 4 hours. Drosophila melanogaster starts mating after 4 hours at room temperature. This is the precise reason in Drosophila, virgin collection is done within 4 hours of eclosion.
Imagine you want to set up cross between wild type and some mutant. You will grow them initially in separate vials. Now for crossing , assume you need females from wild type and males from mutant. In this step it is important that females should be virgin else it will be difficult to track your genotype later on. Now if Drosophila starts mating soon after emergence of flies, it is disadvantage for your breeding experiments.
Note: There is sperm competition but that is special case


text:
Corneal transplant and HLA matching
Is HLA matching/ blood grouping required for corneal transplants ? I think,it shouldn't be, because cornea is avascular.
I tried searching on the net but most of the references are old and controversial. So please provide a reliable and latest reference for your answer.

Just because it's avascular doesn't mean immune cells can't/don't infiltrate. There are plenty of inflammatory eye processes where the cornea and lens can be targeted.

Cornea is considered as an "immune-privileged" site and tissue, neither HLA nor blood grouping is required for allogeneic corneal transplant.
In terms of reference:
This could be one: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2802514/


text:
Eye color genetics
I am trying to find a model to link the phenotype eye color to its genotypes.
I know that there exists a simple model from Davenport, which explains {brown,blue} eyes. Further, there is an extended model for {brown,green,blue,gray} eyes, based on the two genes bey2 and gey. There are plenty of articles suggesting further genes which may or may not have certain impacts.
Is there a model which is more precise than the above mentioned, but which is well applicable (i.e. does not introduce excessive complexity and has greater accuracy)? I am trying to come up with some probabilistic calculations, and could well handle one or two further genes. It would also be interesting to know about the accuracy of the model.
Many thanks!

Does this question: http://biology.stackexchange.com/questions/728/how-is-eye-color-in-humans-inherited answer your question?

Not really.. I had seen the question and also read the mentioned papers. However, what I am looking for is a still simple model, which goes into some more depth than the two gene model (also mentioned in linked questions comments: http://www.athro.com/evo/gen/genefr2.html)


text:
What is the smallest known viviparus
I want to know what is the smallest viviparus known at this time.
I was Googling, but I can discover this animal.
Thanks.

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text:
What is a triglyceride?
I'm confused on what a triglyceride is, from what my text book it says its a type of gylercide, then from a website it said

Glycerides can be subdivided into two categories. The first group, the neutral glycerides are nonionic and nonpolar. The second group, the phosphoglycerides contain a polar region, the phosphoryl group.

Which makes triglyceride not a directly under a glyceride but under one of these groups. Then it says

Esterification may occur at one, two or all three positions producing monoglycerides (monoacylglycerols), diglycerides (diacylglycerols), or triglycerides (triacylglycerols). The most prevalent and most important are the triglycerides.

So does that mean that triglyceride can be produced by either of the two groups phosphoglycerides and neutral glycerides. And if that's correct then how are monoglycerides and diglycerides produced.
Source

Welcome to Biology.SE. Perhaps Chemistry.SE may be a good alternative SE to post this question.

@chris or the answer should be brought over here as a CW with a link to the answer on Chem as the original source identifying the author from Chem. Closing the question will just allow people to ask it again since we can't cross exchanges to mark as a duplicate.

Good point. I retract my close vote.

The following answer was giving by Michael D. Dryden from https://chemistry.stackexchange.com/questions/24797/what-is-a-triglyceride/24799#24799
There is some minor argument as far as nomenclature goes for these lipids. Most sources I can find, including IUPAC have glycerides as only including esters of glycerol with fatty acids. Monoglycerides have a single fatty acid ester with two free OH groups, diglycerides have two fatty acid esters, and triglycerides have three. Phosphoglycerides are defined separately as esterified derivatives of phosphatidic acids, so you can think of them like glycerides where for one of the substituents, instead of a fatty acid, some derivative of phosphoric acid is present. However, the way the two terms are defined, they don't encompass any common molecules, i.e. there are no molecules that are both glycerides and phosphoglicerides and neither group is a subset of the other.
So: mono-, di-, and triglycerides are subsets of glycerides while phosphoglycerides are a different group altogether, though structurally similar.

Triglyceride. It has 3 fatty acids, which are non polar (water-fearing). so they are hydrophobic. These 3 fatty acids are connected to a glycerol molecule. This molecule is polar and is hydrophilic (water-loving). The glycerol is attached to the 3 fatty acids via  a dehydration reaction. When they are connected, they loose a water molecule, and form an ester.


text:
Should the infraspecific epithet agree in gender with the genus name?
Let's take the following plant name

Gymnocalycium mihanovichii

So we were to designate the yellow form of the plant, would it be

Gymnocalycium mihanovichii f. aurea

because forma is feminine or

Gymnocalycium mihanovichii f. aureum

because Gymnocalycium is neuter?
Hope the question is on-topic

This is governed by the International Code of Nomenclature for algae, fungi, and plants or by the International Code of Zoological Nomenclature.
For plants, infraspecific names are covered in Article 24. Article 24.2 states:

Infraspecific epithets are formed like specific epithets and, when adjectival in form and not used as nouns, they agree grammatically with the generic name (see Art. 23.5 and 32.2).

Article 23.5 reads:

The specific epithet, when adjectival in form and not used as a noun, agrees with the gender of the generic name; when the epithet is a noun in apposition or a genitive noun, it retains its own gender and termination irrespective of the gender of the generic name. Epithets not conforming to this rule are to be corrected (see Art. 32.2) to the proper form of the termination (Latin or transcribed Greek) of the original author(s). In particular, the usage of the word element ‑cola as an adjective is a correctable error.

Article 32.2 states that names are still validly published, even if their terminations are incorrect.
In this case, since "aureum" is an adjective, it should agree with the genus name.

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text:
The damage of cancer cells
I read about the molecular biology of cancer, and I have a mess on my head and a lot of questions.. .
My primary question is-
The damage of the cancer cells is in the dna sequence or in the gene expression(microRNAs)? or even something else?
Thanks:)

Cancer is commonly defined as uninhibited cellular replication caused by mutations to the genome.
Genes where cancer-causing mutations have been identified are known as oncogenes; the COSMIC (Catalogue Of Somatic Mutations In Cancer) database lists all of the known oncogenes (547 to date - 23rd Jan 2015 - 1% of all human genes!) [1].
The effect of a particular mutation would be to alter in some way the expression of a gene or genes. This may be directly, for instance rendering a tumour-suppressing gene unable to fulfil its role [2], or indirectly, for instance by affecting epigenetic mechanisms that in turn affect expression of genes involved in cell cycle regulation [3].
To my knowledge cancer is not 'caused' by just a change in expression of a gene, although it may be mediated by it. The change in expression or effectiveness of a gene (such as tumour suppressor p53) resulting in uncontrolled cell division is caused by mutations at the genomic level.
What causes the mutations?
Lots of factors can cause mutations, from chemicals (e.g. from cigarette smoke, not just restricted to the lungs either [4]) to mistakes in the DNA replication machinery as somatic cells undergo normal cell division [5].
The last reference there provides very compelling evidence for the reason that some tissues are more predisposed to cancer than others; tissues with higher cell turnover (and thus require more cell division) have higher incidences of cancer - see the below figure from [5]! This figure separates "lung cancer" into two groups to show that even non-smokers have risk of developing lung cancer, but not as high a risk as those who smoke.

http://cancer.sanger.ac.uk/cancergenome/projects/census/
Muller, P.A.J.; Vousden, K.H. (2013) p53 mutations in cancer. Nat Cell Biol. 15:2-8
Hamamoto, R.; Saloura, V.; Nakamura, Y. (2015) Critical roles of non-histone protein lysine methylation in human tumorigenesis. Nat Rev Cancer. 15:110-124
Cancer research UK report on smoking and cancer
Tomasetti, C. & Vogelstein, B. (2015) Variation in cancer risk among tissues can be explained by the number of stem cell divisions. Science 347, 78-81

Thanks! and what caused the mutations at the genome of a cell?

Hi @MalicOfSdom, see my edit!

No problem @MalicOfSdom. If I have answered your question please accept it. If you would rather wait to see whether others answer as well feel free, but vote up/down as appropriate, and accept an answer to help future users of this Q&A !

I would vote to your great comment but I have just 6 reputation in this site XD...and one more thing, why some tissue are less commonly to get mutation even if they divided quickly?  like muscles..

As you can see from the graph, it is not exact, but just a correlation between cell divisions and cancer - many other environmental factors affect cancer risk too, and some tissues may be more exposed than others? What makes you say muscle specifically?

Because I didn't hear about heart cancer for example...

Interesting point. No idea why cancers of the heart are so rare!

The following review rather nicely summarizes everything that encompasses cancer: Hallmarks of Cancer: The Next Generation, highly recommend reading it.


text:
Can genetic engineering be performed without a laboratory setting?
I'm becoming more interested in genetic engineering as I learn more about it, and it's becoming more and more apparent that there's very few resources on genetic engineering at home. A similar question was asked here, but the best answer linked to a failed indiegogo campaign. Is it feasible to genetically modify an organism without a laboratory setting? If so, what materials could be used to do this?

You could probably do very simple genetic engineering in a home lab. Getting the competent bacteria and plasmids to put them in might be hard, as suppliers will be reluctant to sell to you. You'll need some equipment like an incubator to grow the bacteria, and maybe a centrifuge to purify the DNA. Chemicals might be hard to get too. Isopropyl alcohol and ethanol are often used to isolate DNA, and can be obtained pretty easily. SDS, NaOH, and bacterial media might be hard to get. Also, don't expect to sequence DNA at home.

Your best bet at genes you could use at home would be green or red fluorescent proteins, you can get UV LEDs at radio shack, with a little soldering you can make a small UV lamp to observe the fluorescent colonies.

You'll have to be careful about the local laws, in some countries you need a laboratory with permission for handling GMOs, doing such work outside it would be illegal.

At the molecular level, you wont observe the requisite aseptic technique, pH monitoring, water purity or chemicals at home. The best bet at experimenting with genetics at home would be to cross plants to observe change ala Mendel. At least, in my opinion.

Just out of curiosity, why has this been downvoted? It's a valid question, I believe it follows community rules, regardless of how misinformed it was.

I downvoted as I strongly discourage promoting freewheeling with genetically modified organisms, especially by folks who don't even know how to do it. Why would he want to do it? What are the safety measures? Does he know about ethics?  Emergency plans? Infection dangers? Good Laboratory Practice? This question should be closed

The only reason I answered this was to try and demonstrate how hard it would be to do the simplest type of genetic modification, hoping it would discourage people. I've seen this type of question before, thought someone should at least explain how hard it would be.

Discouraging people from home experimentation and discouraging people from asking about home experimentation are two different things.

I wasn't aware that downvoting based upon opinion was encouraged.

@DylanKatz - it is not 'encouraged' as far as I know. It is my personal reason for downvoting, which I provided kindly on your request. We can continue this discussion on meta.

Thought I'd attempt to expand this into an answer, THOUGH THIS IS IN NO WAY MEANT TO SUGGEST YOU SHOULD ACTUALLY TRY THIS. THERE MAY BE LEGAL ISSUES INVOLVED IN CREATING A GENETICALLY MODIFIED ORGANISM, EVEN A HARMLESS ONE, DEPENDING ON YOUR LOCATION. SOME OF THE CHEMICALS REQUIRED TO HANDLE DNA ARE DANGEROUS, AND SHOULD ONLY BE HANDLED IN A FUME HOOD AND WITH PROPER PROTECTIVE EQUIPMENT. I HIGHLY RECOMMEND THAT YOU DO NOT ATTEMPT THIS.
First, you cannot do genetic engineering outside of a lab. You might be able to set up a lab at home, but don't expect to do this using standard household chemicals. Lets assume you're only interested in adding DNA to bacteria, because that's relatively simple.
The first step you need to add DNA to bacteria is to get the DNA. Your major plasmid suppliers probably won't like selling to a non-lab, but if you're lucky you might get some from Invitrogen, Aldevron, or another supplier. If you know someone who works in a molecular biology lab, you might be able to get some from them, but that might violate rules with their university or employer. If possible, I'd get a green or red fluorescent protein gene, as those proteins are easy to detect using a UV lamp you might be able to build with UV LEDs, you might also be able to use a black light. Note that I do not know what promoter would be best to use on your gene. The lac operon is often used to express proteins in BL21 E. coli using the molecule IPTG as an inducer, but that requires you to have IPTG and BL21 bacteria.
Speaking of bacteria, you need competent bacteria. E. coli is the most often used species, but several strains are available. DH5a E. coli is most often used to grow up DNA plasmids, which is something you'll want to do because you probably won't be able to get much plasmid, so you have to make more or you'll run out. But DH5a usually isn't used to produce protein. BL21 E. coli is most often used to produce protein, but you'll probably need IPTG to induce the bacteria to make the protein. You might be able to get IPTG from Sigma Aldrich, but good luck getting them to sell anything to you.
Once you have the bacteria, you'll need to grow them. You need bacterial media, which might be obtainable because it's relatively safe. LB media is a mixture of yeast extract, tryptone, and salt. If you want solid plates you'll need agar too. You can probably get the media sterile enough by boiling it. You'll need some ampicillin or kanamycin to make sure only bacteria with your desired gene is allowed to grow, again Sigma Aldrich might sell it to you.
Of course you can't just put DNA into bacteria, the bacteria must be competent. You can make chemically competent cells by carefully treating them with calcium chloride and magnesium chloride. You'll also need dry ice, these need to be kept very cold. So now you can add your plasmid your competent cells, heat shock them in water at precisely 37°C for precisely 60 seconds, and plate them on your agar media. Then you need to incubate them at 37°C overnight.
If you need to purify the DNA plasmid back from the bacteria, you need to pick a colony off that plate and put it in liquid LB media, also at 37°C overnight with antibiotic. Here you'll need a centrifuge to spin down the cells and remove the left over media. Then you'll need to lyse the cells to release the DNA. You might be able to do this with soap, but you'll probably need NaOH and SDS. Once the cells are lysed you need neutralize them with an acetic acid solution, vinegar might be good enough. Then you have to centrifuge the cell debris to pull the insoluble crap out and leave the plasmid DNA and RNA in the supernatent. At this point you can extract the DNA and RNA with a phenol:chloroform:isoamyl alcohol mix. Good luck getting that, as the vapors from that solution are harmful to inhale, and really bad if you spill it on you, and should not be used outside a hood. But if you manage to get the extraction to work, take the top layer and add an equal amount of isopropyl alcohol and put it in your freezer for a couple hours. Then spin it down, carefully remove the supernatent and you should have a pellet of DNA in the bottom. You might have to clean the pellet with a 70% ethanol solution (140 proof) and another centrifugation. Quantifying your DNA at home will be almost impossible.
Also, this all assumes you just want to put a ready-made plasmid into bacteria. Trying to change the plasmid will require restriction enzymes, PCR, etc.
So yes, you can do genetic engineering at home if your home has an incubator (preferably with shaking), a centrifuge, a water bath, a -80°C freezer, a fume hood, a variety of chemicals, and a decent set of pipettes. But if you have $10,000 you don't really need you might be ok.

I'd make the warning about phenol/chloroform more explicit, doing that extraction outside of a fume hood is a pretty bad idea. Phenol is pretty toxic and not something I'd use in home experiments.

I think you're overestimating the difficulty of buying cells and chemicals, I'd guess that registering a business might be enough to fool suppliers. But the other arguments are valid, you're likely to run into significant walls trying to do anything useful at home. Even with second hand equipment, a basic lab would still be a considerable expense.

@MadScientist Tried to emphasize the phenol chloroform risk a little better. Another thing to worry about is that setting up any lab in your home is a good way to get the cops to start bothering you, since 90+% of home labs are probably meth labs.

@user137 Amateur drug labs are often found by the local fire department for a reason.

@Chris Molecular biology usually avoids the worst chemicals, but isopropyl and ethyl alcohols and phenol chloroform are all flammable, so the fire department might still find your molecular biology lab when your house burns down. These experiments have some danger, and they should not be done without proper equipment, but it's probably a little safer (legally and health-wise) than meth cooking.

Ah okay, I wasn't aware that this was such a dangerous/illegal process. Thank you for your answer.

This answer strikes me as too pessimistic. For instance, we rarely use phenol/CHCl3 extraction to purify plasmids -- we use Qiagen kits or spin columns. You don't need dry ice to make competent cells, if you use them immediately, and anyway, the Krogers where I shop for groceries sells dry ice. And I think most of the companies involved will sell non-hazardous reagents to anyone with a credit card. The biggest problem is that it would be expensive. You'd definitely need a centrifuge of some sort. And of course the big barrier is that you need to have some idea what you're doing.

@LeonAvery The expense is why I mentioned phenol and chloroform, if you have the money for qiagen kits you probably don't need to worry about at home molecular biology. And I suspect the hard part about at home competent cell production is maintaining a culture of E. coli all the time, having a -80 freezer is nice for long term storage.

To put the hazards in perspective: my father has a home woodworking shop. There are half a dozen big power tools that could take off a finger in a fraction of a second of carelessness, and some mildly hazardous glues, finishes, solvents, and lubricants. Indisputably, Dad's shop is a more hazardous environment than my lab, yet I've never heard anyone suggest this is too dangerous a hobby. DIY mol biol would be expensive. We usually expect a full-time worker to spend about $1000/month on supplies, and the minimal equipment, even from eBay, would set you back thousands.


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Is it possible to label a DNA molecule using a radioactive sulphur?
The radioactive labelling of the DNA molecule is possible using radioactive phosphorus and tritium atom. But is it any how possible to label the DNA  molecule using a radioactive sulphur atom?

@AliceD I honestly don't understand the argument that his question isn't about biology. I can't really think of any reason to label DNA this way that wouldn't be part of a biological experiment. (of course adding the motivation would improve the question, but it is not necessary to make it on-topic in this case).

@MadScientist point taken. I'll remove the comment. However, adding background helps to add the 'prior research component' too. It would just greatly enhance question quality.

Yes, it is possible, and indeed this was the standard labelling procedure used in early Sanger sequencing.
You synthesise DNA using a deoxynucleotide with a sulphur replacing an oxygen on the α phosphate as shown below. This phosphate forms the phosphodiester link in nucleic acids so the sulphur is incorporated.
The image is of dATPαS

response to David's comments
Please note that:

DNA does not normally contain sulphur.
This technique is for in vitro labelling of DNA; as far as I am aware it isn't possible to label with sulphur in vivo.

I have down-voted your answer as the radio-active molecule produced by the method you suggest is not chemically DNA but an analogue thereof.

Please go to chat for extended discussions. Because of raised flags and the general negative tone,  I've removed most of the comments here. Please keep it civil.

http://www.nature.com/nchembio/journal/v3/n11/full/nchembio.2007.39.html


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How do the chemical components of these spices prevent fungal growth?
I am doing an EE on how spices affect fungal growth for the following spices -
oregano,
garlic,
cinnamon,
cumin and turmeric. Its been hard to find any sites that say why or how they affect fungal growth, as far as I can tell I am pretty sure they affect the Krebs (TCA) cycle and inhibit the production of ATP. It would be great if someone could help me explain why :)

What is the reason for your assumption that the inhibit ATP production?

What is EE? 2. Do you have any data/reference to say that these spices even have an effect on fungi? If you don't prove that first then the "how" makes no sense.

I have seen papers which talk about inhibiting ATP production, and that components of spice ( like curcuminoids and thymols etc ) can do that


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How do lipid-soluble substances diffuse through the cell membrane?
It’s said that water-soluble substances can diffuse through cell membrane with less ease than lipid-soluble substances because the former encounters impedance in the hydrophobic region of the phospholipid bilayer. However, does the same logic not apply for hydrophobic substances, in that they cannot traverse the hydrophilic outer/inner surfaces of the plasma membrane? How would they be able to enter or leave the cell with greater ease?

See this paragraph and image from The Cell: A Molecular Approach. 2nd edition.:

During passive diffusion, a molecule simply dissolves in the phospholipid bilayer, diffuses across it, and then dissolves in the aqueous solution at the other side of the membrane...Passive diffusion is thus a nonselective process by which any molecule able to dissolve in the phospholipid bilayer is able to cross the plasma membrane and equilibrate between the inside and outside of the cell. Importantly, only small, relatively hydrophobic molecules are able to diffuse across a phospholipid bilayer at significant rates (Figure 12.15). Thus, gases (such as O2 and CO2), hydrophobic molecules (such as benzene), and small polar but uncharged molecules (such as H2O and ethanol) are able to diffuse across the plasma membrane. Other biological molecules, however, are unable to dissolve in the hydrophobic interior of the phospholipid bilayer. Consequently, larger uncharged polar molecules such as glucose are unable to cross the plasma membrane by passive diffusion, as are charged molecules of any size (including small ions such as H+, Na+, K+, and Cl-). The passage of these molecules across the membrane instead requires the activity of specific transport and channel proteins, which therefore control the traffic of most biological molecules into and out of the cell.

As shown in above paragraph, molecules have to dissolve in phospholipid bilayer to diffuse through it. But since the hydrophilic part is already interacting with water, so dissolving is mainly for the hydrophobic part. Now, since hydrophobic part is non-polar, so it can dissolve only non-polar substances (like dissolves like). Thus, small gases like O2, CO2 and non-polar molecules like benzene easily dissolve in hydrophobic part and diffuse through it. Also, molecules like water and ethanol can also dissolve in it in small amounts due to their small size and very less polarity. That's why only some molecules of water can diffuse passively, large amount of water would require aquaporins. Now, since bigger molecules like glucose have large size and high polarity, they cannot dissolve in the membrane and thus require transmembrane channels even for diffusion. Similar case is with ionic substances too: they require ion channels for their diffusion.
Hope this helps. Comment below if you have any further doubts.


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Is nucleosomal DNA ever degraded?
A hallmark of apoptotic DNA fragmentation is the digestion of DNA into individual nucleosomes. In addition, in the following experiment that tried to isolate the components of the nucleosome, the micrococcal nuclease only cleaved the linker DNA and not the nucleosomal DNA.

I've tried searching the internet but I couldn't find a clear answer to my question. Is nucleosomal DNA ever degraded? Are there nucleases that degrade it, and if there are, are they common? If nucleosomal DNA is not degraded, what protects it? The histone proteins?

Are you specifically looking for a nuclease that cleaves DNA wrapped around the histone octamer or is your question why does such DNA not normally get degraded? Or both? Generally the histones proved a stearic barrier to nuclease digestion and so protected DNA is not degraded, but I seem to recall that both DNase I and MNase are capable to nicking such DNA at a low rate.

Heat the sample which will denature the histones then add excess nuclease and it will be degraded. Even if you add a large excess of micrococcal nuclease it will degrade nucleosome-associated DNA. For DNase assays, the amount of DNase has to be carefully titered to get just linker DNA degraded

@canadianer More of the latter, but both if possible.

Nice question! Nucleosome is quite a stable structure because of electrostatic attractions between the phosphate group of DNA and Lysine or Arginine of histone octamer1. In fact, both histone and DNA are known to protect each other from degradation: histone protects DNA from some kinds of damage2 and DNA protects histone protein from proteolysis3. Also, the histone protein gets modified whenever there is damage to nucleosomal DNA, so that DNA repair machinery can be activated4. Thus, nucleosome is not only structurally stable, but also tries to maintain its stability by its constituents protecting each other.
source
This stability has also been taken to a whole new level. In a research paper, scientists predicted that the reason for discovery of thousands of years old DNA, in intact form, is due to the stability of nucleosome5. They have even predicted that nucleosomal DNA can remain readable for even millions of years, because the time when histones start degrading is also the time when proteases and nucleases degrade, leaving very few chances for DNA to degrade.
But, nucleosomal degradation is not impossible. In a research, scientists concluded that the enzymes Caspase Activated DNase (CAD) or DNA Fragmentation Factor 40 (DFF40), together called CAD/DFF40, are indirectly required for degradation of nucleosome6. See this paragraph (I only pasted the main points):

We report here that in response to apoptotic signals from a death receptor (CD95 and tumor necrosis factor-$\alpha$) or mitochondrial (staurosporine) apoptotic stimulus, the core nucleosomal histones H2A, H2B, H3, and H4 become separated from DNA during apoptosis in Jurkat and HeLa cells and are consequently detectable in the cell lysate prepared using a non-ionic detergent. The timing of this histone release from DNA correlates well with the progression of apoptosis...Taken together, these data demonstrate that CAD/DFF40 functions indirectly in mediating nucleosomal destruction during apoptosis...In this study, we have found that core nucleosomal histones separate from chromatin in apoptotic cells, but that this is not simply a by-product of DNA fragmentation. This event is indirectly related to CAD/DFF40 in the sense that CAD/DFF40 is required but is insufficient for the apoptotic histone release.

Thus, though it was the only paper I could find, nucleosomal DNA can also degrade in the same way as linker DNA if larger amount of CAD/DFF40 is present to degrade it.
References:

Histone structure and nucleosome stability; Leonardo Mariño-Ramírez, Maricel G Kann, Benjamin A Shoemaker, and David Landsman
Nucleosomal histone protein protects DNA from iron mediated
damage; Helen U.Enright, Wesley J.Miller and Robert P.Hebbel
Actin and DNA Protect Histones from Degradation by Bacterial Proteases but Inhibit Their Antimicrobial Activity; Asaf Sol, Yaniv Skvirsky, Edna Blotnick, Gilad Bachrach, and Andras Muhlrad
Histone - Wikipedia
Degradation of ancient DNA; Zvi Kelman, Lori Moran
Apoptotic Release of Histones from Nucleosomes; Dongcheng Wu, Alistair Ingram, Jill H. Lahti, Brie Mazza, Jose Grenet, Anil Kapoor, Lieqi Liu, Vincent J. Kidd and Damu Tang


text:
Evolution of the common honey bee's stinger
Has the common Honey Bee evolved a stinger designed for penetrating human skin so it will cause as much damage possible even if it means death? A honey bee can sting other insects and mammals more than just once, but that is not the case when inserted in the skin of a human it will be the bee's first and last sting. http://www.todayifoundout.com/index.php/2014/04/differences-bees-wasps-hornets/
The current form of the honey bee's stinger has evolved barbs. These barbs will cause the bee to lose its stinger in human skin giving the stinger more time to eject the apitoxin and apis virus into the nervous system causing extreme pain and for some anaphylaxis a severe allergic reaction.
Question- With the information and references I have provided, is there evidence that the Honey Bee's stinger has evolved specifically to be more effective against humans?

[citation needed] what is your evidence that a honeybee's stinger is most efficient in penetrating human skin? Also remember that evolution works both ways; human skin may not have great evolutionary pressure to ward off bee stings, whereas something like bear's fur may be under a stronger pressure

Bees sting all sorts of animals to defend their hive/territory - birds, dogs, rodents, bears, moose, etc.

@MattDMo-can you name a animal allergic to bee stings?

I thought they were really awful at stinging us, no? Their stinger get's lodged in our gooey skin and they rip their guts out trying to escape! I imagine they're more aimed at damaging insects and just so happens that a swarm can even deter larger animals if needs bee. tehe!

@user5434678 - a five second google search shows that dogs can be allergic to bee stings.  Your premise seems flawed.

@User- can is a another word for possibility.Your google link is eralevent to my question.

Anaphylaxis isn't really that relevant for dissuading a predator; they could do a lot of damage before it kicked in. It's the pain of the sting that drives them off. Presumably we can agree that bee stings are painful for animals other than humans?

The answer to the question "has evolution designed the common Honey Bee's stinger solely for stinging man-kind?" is no.
A honey bee's barbed stinger remains in the skin of any mammal afterwards due to its elasticity (skin closes back around the base after penetration) but can be retracted after stinging another insect. It isn't a human-specific thing. Presumably this is because it takes more toxin to dissuade a mammalian predator than an insect given their size. A little dose of toxin is released straight away but in order to deliver a dose large enough to irritate a large predator the venom sac needs to remain attached. The resultant damage kills a sterile worker bee but removes an attacking predator that could do much more damage; it is a strategy that confers a selective advantage.
The reference you cited  doesn't appear to say anything about other mammals, just other animals, so this doesn't actually contradict your other source. Insects are animals too!

"Stingers in bees evolved from ovipositors", here is a good reference of how bee stinger have evolved.
http://www.askabiologist.org.uk/answers/viewtopic.php?id=4021

The defense of the honey bee, having a barbed stinger which continues to pump venom even after the bee is swatted away by the intruder, (be it a human or a bear or other animal), is called "sting autonomy." When defending against a large mammal, the more stings the more likely to have an impact.
The reason the honey bee colony can afford to lose many guard bees in this manner is that they are a highly social species, called eusocial, or truly social (the highest level of social structure). The colony typically has 10s of thousands of members, and the queen is constantly laying eggs to replace lost workers, which usually only live 4-6 weeks, in normal summer activity.
Only the social bees are likely to sting you. Most bees are not social. The honey bee is the exception, so most bees will not sting you (if you can even find them). There are 3600 other species in the US besides honey bees, (which represent one, single species). And furthermore, honey bees will not sting you unless you approach or open their nest, (or grab one in your hand, or crush one) which is unlikely to happen accidentally. They will not attack you unless they are defending their nest- never at a flower! I doubt you have ever been stung by a honey bee, as most people confuse them with yellow jackets, which are not bees, but social wasps. The yellow jacket also has a barbed stinger but much smaller barb (and a much more defensive temperament), so it may or may not get stuck in your skin.
You can read all about stinging insects in the wonderful book, The Sting of the Wild, by Justin O. Schmidt.
Bee Well! - Carl the Beekeeper (Cornell University Master Beekeeper)

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text:
Does becoming martyr have an evolutionary advantage?
This is related to
How does "be altruist to those who are similar to you" evolve?
Altruism that is

Not reciprocal
Not familiar

has little explanation. One possible explanation is that the trait itself may correlate well with genetics. One great answer there is that often the cost of altruism is small anyway. It can explain why people vote. Here the expense is small anyway.
Still there seems to be some factors that are even bigger.
Let's take a look at people that die for their ideology. Christian martyrs, Muslim suicide bombers, or Communist guerilla fighters. They seem to get so little and well, die.
And that's pretty common. It seems pretty easy for a leader or pedagogue to rouse men to be soldiers. Of course, becoming a soldier is a pretty shitty job, yet most men don't mind.
These people make a huge sacrifice for the sake of their country, ideology, or people that are not even genetically related to them.
Why?

Comments have been moved to chat; please do not continue the discussion here. Before posting a comment below this one, please review the purposes of comments. Comments that do not request clarification or suggest improvements usually belong as an answer, on [meta], or in [chat]. Comments continuing discussion may be removed.

Your question is quite broad and asks for explanations for various behaviours which can lead to self-sacrifice.
Religious reasons: The genetic influence here may be a predisposition to let others influence you. This is what gives rise to culture in the first place, in other words: the predisposition to at some point maybe sacrifice yourself because you are taught to do so can only die out if the basic behaviour which gives rise to culture dies out. Cultures which lead their members to die may decimate their own numbers, but they will not wipe out culture itself because in the bigger scale, those with culture do better than those without. (Plus, those who sacrifice themselves may have children as well, so any genetic influence on their behaviour can be carried on.) This also goes far into the field of memetic evolution, which is disputed but may be interesting to read about.
Political reasons: As in, dying for one's nation or country rather than because of teachings. This probably has a defensive behaviour towards one's own group as the genetic influence. Also, reputation plays a big role: see shigeta's excellent answer.
You also mention willingness to subordinate oneself which is a very common pattern not only in humans. Richard Dawkins touches on this in The Selfish Gene, but there are probably papers more focussed on this particular topic out there as well.
I think it is far-fetched to assume a genetic inheritance of in general "willingness to die for something" (which would be required for genetic evolution to work on it). Each thing that some people may be willing to die for can have completely different reasons. I think in these terms the willingness to die is usually an exaggeration of a behaviour which evolved for different reasons.

I like the predisposition to let others influence you theory. That make sense. Like telomere for example. Death it self doesn't help, but telomere does. The same way dying for ideologies doesn't help, but predisposition to let others influence you might. Thanks Armatus.

There isn an effect called "Indirect reciprocity" where individuals just give to everyone they meet without direct requirement of reciprocity.
This sort of benefit to others is common - hospitality to strangers, general politeness, good customer service all fall along these lines.  You hope they will come back and benefit you again, but maybe they will tell someone else who will know you are a good community member.
It is only sustainable in a system where the cost/benefit ratio is less than the reputation benefit of the act.  It sounds as if this is only good for public acts but if the benefit is transferred to a social entity that outlasts the individual (like your children, a relative's children, a religion or a corporation say), the result could still hold.
If you think about typical morality/ethics really it still makes sense to think that what we call altruism must still have a net positive benefit.  If there is no benefit long term or to anyone, it really isn't useful or even good, its random.  What we usually call altruism is usually some sort of reciprocal cooperation.
A soldier who dies in combat or someone who dies for their beliefs but everyone knows about it as a public statement benefits from their act indirectly.  I don't think its altruism in the pure sense of the word. Defending the nation, ones' beliefs or whatever is, in its sense its own reward.  Veterans come back from a war are hopefully respected for their work.  Having a purple heart can be a good thing to show people.  I'm not saying these people are adequately compensated for what they have been through, but just trying to draw a distinction between pure biological altruism and 'indirect reciprocity'.
Examples of Indirect reciprocity might be the use of tax money to build highways and build power and water infrastructure.  Its important - its the glue that holds a nation or a group together.  If you got punished for doing these things we wouldn't be hanging as a nation very long!
A martyr with no family at all who would benefit would still count as an altruism I think, but most acts of public piety and sacrifice do benefit the individual by reputation. Something to think about.

I don’t see the connection. The individuals certainly have no benefit from dying. There is no reciprocity in such an action towards the individual (there may still be towards alleles, if those are shared between the martyr and those (s)he died for) – the cost/benefit ratio is infinite. None of the benefits you list apply to martyrs, only to people who stop one step short of martyrdom.

Actually it does. Say a member of Thio family dies for his country. Perhaps Thio families get respected more. But that's far fetch. That's still reciprocal.

@Jim On the allele level, yes. But this answer makes it sound as if the individual had an advantage, and that’s patently not the case.

@JimThio Its an extension of reciprocal altruism - i think you have to stretch biological theories to cover some human behavior, but as long as the offspring or relatives benefit it still makes sense. I do think i mentioned this.

I would say a better question would be, "Why would anyone die for a cause?". People benefiting from a cause may not be genetically related. The cost is significant. The cause tend to benefit those who are similar, but because similarity doesn't mean genetically related, how come genes that say, "die for a cause" evolve?

I think you incorrectly describe 'indirect reciprocity'. Indirect reciprocity just means that there is some sort of reputation-like effect that allows you to receive reciprocity not directly from the person you cooperated with but from others who see your good reputation (which you maintain by cooperating). The classic paper on this is Nowak & Sigmund (1998). For a general intro, I mention this and other mechanisms for cooperation in a TEDx talk & blog post

You are seeing the exploitation of a normally benefical trait.
Publically putting yourself at risk for your community has a big advantage.
Communities often reward such people heavily, materially, socially,and even with greater access to mates. Often they reward the mates and chidren of such people long after they are dead. Look at firefighters police or other high risk community protection behavior. In hunter gatherers this may be guard or warrior. Humans a incredibly social so a lot of our institual behavior is about promoting social connections or social benefits. Doing things for the good of community esspecially publically carries massive social captial.
You are just seeing religion or something else highjacking this behavior. The fact religions often convince peole of some kind of rward after death just makes the eploitation easier. Hijacking a normally benifical behavior is not that uncommon, evolution has a hard time keeping up with human inventivness.
https://www.ncbi.nlm.nih.gov/books/NBK424875/#:~:text=Altruism%20can%20only%20evolve%20if,both%20rely%20on%20this%20principle.
https://www.sciencedirect.com/science/article/abs/pii/S1090513802001575


text:
Is lumen space of a thylakoid completely separate from the intermembrane chloroplast space?
The question I have is whether thylakoids form actually completely independent "vacuoles" (i.e. independent membrane enclosed spaces) or whether the lumen space is connected to the intermembrane space of the chloroplast. I have this question because electron photographs that show slices can be sometimes misleading and connected structures may appear to look independent on photographs of slices.


text:
Why bananas accumulate a radioactive isotope of potassium (K40)?
A quick google search reveals many pages that intend to calm consumers down and assure them that quantities of radioactive potassium in bananas (K40 isotope) is not sufficient to be concerned about, e.g. http://www.raw-food-health.net/Natural-Radiation.html. I am not worried that bananas may be harmful, but I wonder if bananas are actually enriched in K40 relative potassium in soil? Maybe bananas are not enriched, and so every potassium-rich food is equally radioactive... but if specifically bananas are particularly enriched in K40, then what is the mechanism of this process?

The reason, at least suggested for other food, is a high potassium content in general. In the last paragraph (on wiki), you might find that plants w/ high potassium content are also likely to have a high content in radium...perhaps K+ transporters / uptake mechanisms have a slightly higher affinity for Ra2+ as well ?


text:
Do organic veggies contain more pesticides than regular food?
Since organic farms can only use "natural" organic approved pesticides rather than frequently more effective "synthetic" pesticides in use by other farms, does it mean that, on average per kg of veggies harvested, a higher amount of pesticide is applied at organic farms in comparison to regular farms? And does it imply that organic veggies sold in stores have more pesticide inside them than regular veggies?


text:
Are there U-rich transcriptional pause sites?
I've heard a statement in a talk that U-rich sequences cause transcriptional pausing. The intuitive explanation for this was that the UTP concentration is lower in the cell than the ATP concentration. Reducing the concentration of an educt obviously reduces the reaction rate, leading to pausing of the RNA polymerase.
After reading up on transcriptional pausing, I haven't found any literature that shares this view. The recent papers I found don't show U-rich sequences and have completely different explanations on how pausing works. Those explanations mainly concern interactions at the edges of the transcription bubble.
Now, I guess that there might be multiple mechanisms of transcriptional pausing. But I couldn't find any references in the literature to U-rich pause sites and how they could work. Is there any literature on this? Either on the fact that U-rich sequences tend to be pause sites, or that the concentration difference in NTPs leads to pausing at certain sites.

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I am not sure about polyU's effect on transcription rate but I don't think UTP is ever in limiting concentrations. Poly-pyrimidine tracts (PPT) are present near splice sites and this paper suggests that PPT-binding protein (PTB) can affect the rate of polyadenylation. I am not sure if that is what you are interested in

Yes, there are: this is a feature of bacterial intrinsic termination. The mechanism of pausing is not as you describe, though.
In bacterial transcription, two forms of termination are recognised (to my knowledge):

Intrinsic termination, consisting of a hairpin and a stretch of Uridines.
Rho-dependent termination, consisting of a 'loading' site for termination protein Rho, and a pausing site, but not the stretch of Uridines you refer to.

If you were reading up on transcription in eukaryotes, or were reading about rho-dependent termination, that would explain why you found no mention of polyU tracts. When evolution provides many solutions to a problem, it can get tricky to keep on top of it all!
This lists a few types of termination, including attenuation which is fascinating, and does involve regulation dependent on the concentration of a substrate.
Intrinsic Termination
A palindromic sequence situated just before the termination site causes a hairpin to form in the nascent RNA inside the exit channel of RNA polymerase, if given time (and if anti-termination factors do not bind the RNA to suppress hairpin formation). It appears that formation of this hairpin "destabilises the elongation complex [RNA polymerase + elongation factors]", and is an irreversible step towards collapse of the transcription bubble and dissociation of the transcription machinery.
The polyU tract (~8nt long) proceeding the hairpin seems to have dual function: the A:U basepairing in the DNA:RNA hybrid is weak; the hybrid becomes less favourable. Since the hairpin (which is an RNA:RNA duplex) is adjacent to the RNA:DNA hybrid duplex in the bubble, they experience competition for formation. Weakening the hybrid duplex favours hairpin formation, which acts like a switch that separates most of the RNA:DNA duplex in the bubble - synthesis cannot proceed, and the unstable complex dissociates.
Also, the ployU seems to be responsible for pausing which allows time for the hairpin to form, but not for the reason you suggest:
The concentration of UTP in the cell is not unusually low. ATP concentrations are higher than other ribonucleotides since it is the cell's major 'energy currency', quite apart from nucleic acid synthesis. Hence I don't believe pausing can be explained as the polymerase waiting for UTP. The polyU tract probably acts as a 'back-tracking signal' to the polymerase, since the hybrid duplex in the catalytic site is weakened, and the repeated nature may be "slippery"(?). This back-tracking pauses the polymerase.

To summarise: The elongation complex passes the palindrome and reaches the polyU tract, where the hybrid duplex in the bubble is weak and tends to cause back-tracking/pausing. This allows time for the hairpin to form in the exit channel, which both unwinds the hybrid duplex further, and destabilises the elongation complex. The transcriptional machinery is now destined to dissociate and the bubble collapse: RNA is released from the DNA duplex.
It is interesting to note that intrinsic termination can be suppressed by proteins that bind the hairpin. In bacterial operons, where sets of (almost) concatenated genes are separated by intrinsic termination signals, the amount of read-through at each termination site determines the relative expression levels of each gene.
Rho-dependent Termination
Rho is a hexameric protein complex that is loaded on to the nascent RNA at a loading sequence. It hydrolyses ATP to move along the emerging RNA - apparently it "races" with the polymerase, and when it catches up to the polymerase, it causes termination. There are pause sites in the RNA which allow rho to catch up - these sites tend to be rich in A and U, so perhaps polymerase is slowed by destabilisation of the hybrid duplex - but it is nothing like the intrinsic terminator, since it depends completely on rho for termination.


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Core Biological concepts explained to a Computer Scientist?
I am a computer scientist delving into Bioinformatics and I need to gain insight in biological phenomena. How would you explain three core concepts as:
Evolution, Selection and Variation, to a Computer Scientist? I am looking for something in the middle. I read Futuyma's book and was very useful, but I would like an explanation I can relate with my background, something to start building "bridges"...
Bibliography suggestions are welcome.

You might be interested in mathematical formulations of evolutionary processes. Here are some book recommendations. As you are a computer scientist, I suppose that you are aware of what a genetic algorithm (artificial intelligence) is. Genetic algorithm also provide good analogies.

@Remi.b +1 for the genetic algorithms

how about just open a molecular bio textbook?

Read on fishers fundamental theorem, the price equation, the breeders equation, and evolvability

Evolution

Evolution is the accumulation of genetic mutations that results in phenotypic variation (physical characteristics) where surviving variations are more suited to the environment the organism lives in, thus allowing it to survive better and -- critically -- reproduce as-good-as or better-than its competing organisms.
In terms of computer science this would be like a starting with basic CPU design with all the absolute necessities. Now, let's pretend every generation of CPU after your first is going to be randomly designed by something called "Pressure OS". Pressure OS doesn't care if the CPUs it designs match the needs of the consumer. PrOS is unfeeling. An OS of pure logic. ALL it will do is make a bunch of random ones, note which ones sell the best, and make the best-selling ones to be the template for its next round of random designs.

Selection and Variation

Selection is the process by which environmental pressures (low moisture, high heat, high altitude, available food, extreme pressures at the bottom of oceanic trenches, etc.) dictate how well each successive generation of organisms survive.
In our analogy, the Pressure OS is the cause of Selection. Some CPU designs aren't going to meet the needs of consumers (first-gen Atoms which could barely operate a toaster). Those ones won't be produced again. Others will be very successful (like the Pentium-4 Series which lasted for years) and will quickly outnumber the inferior ones.
Some designs, as odd as they are, will find success in areas outside enthusiast desktops or workstations. Like ARM designs which were never part of the desktop market, but found lots of success in phones and business devices.
Market requirements/environments, as met by the random variations produced by Pressure OS, created Variation in the types of CPUs available.
ARM Snapdragons could never, ever compete in the desktop enthusiast market. That's the realm of Sandy Bridges, Haswells, Semprons, and Phenoms. Then again, they're dramatically different designs -- which stem from common designs decades ago that have been heavily modified over the years -- that don't need to compete. Snapdragons and Semprons can co-exist because they fill different niches.
Now, when consumer needs change again -- if everybody gets tired of mobile phones, tablets, and desktops in favor of cone-shaped personal assistants which go in your ear -- then designs will change again under that new pressure. Eventually CPU one design will become the standard for that particular piece of hardware, and you could say that CPU variation had evolved to get there via selective pressure from consumers.
Biology operates in the exact same way, except the selection process is instigated by environmental pressures to produce organism variations that can successfully reproduce. It's also been going on for >3 Billion Years.

I'm happy to see that someone came from the hardware point of view :) I really like your examples.

Please note that these are just analogies not exact definitions.
Okay so let's imagine DNA as string of 4 letters that is the program code of an organism. Also the running environment is a good analogue to the biological environment (RAM, CPU time, disk space - as resources like food, water etc.) Genes of organism could be imagined as methods of an object like in object oriented programing. Let's define some functions:
Reproduction: copies the string and creates a new instance of the organism (like a new instance of the program) - cell or an offspring - this stands for asexual reproduction. Sexual reproduction takes two instances of the program and randomly exchange their functions and create a new instance with this shuffled code (recombination).
Mutation: induces random changes to the string at random times. This ensures that different "versions" are present of the code. You need mutation for evolution to work.
Also you need Selection - or rather selective pressure -  that is like changing the environment - more efficient codes will survive, the rest die of (aka crash, run out of memory (food)) etc.) Selection drives evolution forward. Also programs can interact with each other and function as a selective pressure - think of anti-virus programs and trojans or viruses - you need better and better AV programs because new viruses come out, and bad guys need new viruses because AV virus programs keep getting better and better - they both put selective pressure on the other and drive each other's evolution.
(Genetic) Variation: think of a group of softwares with similar function: like text editing. These are like different individuals of a species because they can do the same thing but they are all a bit different. These "species" evolve by gaining new functions by mutations (the programmer adds new code sections - mutation), and after they gain enough new function they turn into a new software - new species. Evolution takes a lot of time to produce new species - as does coding a new software :).
I hope this helps.

It might be good to remind your readers that analogies are just analogies. One must not make the mistake of bringing such analogy to far away and complain about incompatibilities. Selection that is like changing the environment. A changing environment would rather be a change in selection pressure. For example the concept of variation is limited to genetic variation in the analogy you presented.

@Remi.b - Thanks for pointing things out, I'll edit and refine my answer.

Why the downvote?

I want to make a declaration of innocence for this downvote :) Unexplained downvotes are always bothering me too.

@Remi.b - I've not accoused anyone, I'd not assume that you or anyone would down vote a competing answer (if it has no obvious incorrectness etc.) - that's just low... But i see down votes as tool to indicate more serious problems with a post.

@Remi.b - Oh and by competing I mean friendly sharing of different opinions / viewpoints not some "who's the big boss around" type race.


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Darwin's first sketch of a phylogenetic tree
Coming from Darwin's notebook this first sketch of a phylogenetic tree became one of the most emblematic image from Darwin's work.

I have a hard time to read what is written on it.
What is written on this page?

Where did you obtain the image from - is it a reproduction? The source of the reproduction may hold clues perhaps. +1

Related: A "new view of the tree of life" was just published in nature microbiology.

This is from Darwin's Notebook B: Transmutation of species from 1837–1838. From what I understand, the tree is a hypothetical depiction of descent used to discuss differences and relatedness between forms/species. This is the text that accompanies and follows the sketch (notebook pages 36-44):

I think
 (sketch)
Case must be that one generation then should be as many living as now. To do this & to have many species in same genus (as is) requires extinction.
  Thus between A & B immense gap of relation. C & B the finest gradation, B & D rather greater distinction. Thus genera would be formed. — bearing relation
(page 37)
to ancient types. — with several extinct forms
  for if each species an ancient (1) is capable of making 13 recent forms, twelve of the contemporarys must have left no offspring at all, so as to keep number of species constant. —
  With respect to extinction we can easy see that variety of ostrich, Petise may not be well adapted, and thus perish out, or on other hand like Orpheus being favourable
(page 38)
many might be produced. — This requires principle that the permanent varieties produced by inter confined breeding & changing circumstances are continued & produced according to the adaptation of such circumstances, & therefore that death of species is a consequence (contrary to what would appear from America)
(page 39)
of non-adaptation of circumstances. —
  Vide two, pages back.
  Diagram
  The largeness of present genera renders it probable that the many contemporary, would have left scarcely any types of their existence in the present world. — or we may suppose only each species in each generation only breeds; like individuals in a country not rapidly increasing. —
(page 40)
If we thus go very far back to look to the source of the Mammalian type of organization; it is extremely improbable that any of his relatives shall likewise the successors of his relations shall now exist — In same manner, if we take a man from any large family of 12 brothers & sisters in a state which does not increase
(page 41)
it will be chances against any one of them having progeny living ten thousand years hence; because at present day many are relatives, so that by tracing back the descen fathers would be reduced to small percentage. — & in therefore the chances are excessively great against any two of the 12. having progeny after that distant period. —
(page 42)
Hence if this is true, that the greater the groups the greater the gaps (or solutions of continuous structure) between them. — for instance, there would be great gap between birds and mammalia, Still greater between
(page 43)
Vertebrate and Articulata, still greater between animals & Plants.
  But yet, besides affinities from three elements, from the infinite variations, & all coming from one stock & obeying one law, they may approach, — some birds may approach animals, & some of the vertebrates invertebrates —
  Such a few on each side will yet present some anomaly & the g bearing
(page 44)
stamp of some great main type, & the gradation will be sudden.
  Heaven know whether this agrees with Nature: Cuidado.

The text together with actual pictures of the notebook pages can be seen at http://darwin-online.org.uk. Pages ~38-41 are often seen as key ideas for Darwin's formulation of natural selection. Also note that the presence/absence of a horizontal line at the tips are apparently used to denote extant vs extinct groups (see notes in link above).


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Assumptions of Hardy-Weinberg rule
The post Solving Hardy Weinberg problems offers an easy explanation of Hardy-Weinberg rule. The current top answer explicitly does not talk about the assumptions of Hardy-Weinberg. A model makes sense only if one is able to tell its domain of definition and therefore it is critical to understand the assumptions underlying Hardy-Weinberg assumptions.
What are the assumptions of Hardy-Weinberg rule?

Here are the assumptions to the standard Hardy-Weinberg rule (HWr) formulation
$$p^2 + 2p(1-p) + (1-p)^2 = 1$$
See Solving Hardy Weinberg problems for more info about this formulation.
Assumptions
The locus of interest is bi-allelic
This is an obvious assumptions, however it is very easy to extrapole HWr to any number of loci.
Organisms are diploid
This is another obvious assumption that is very easy overcome. This also means that HWr does not hold for loci present on sexual chromosomes as those chromosomes do not display a simple diploid behaviour.
Only sexual reproduction occurs
If some individuals are able to undergo non-sexual reproduction, then the rule does not hold anymore. See also Panmixia as these two assumptions are related.
Panmixia
Panmixia is often called "random mating". Panmixia is the state where each individual is equally to mate with any other individual in the population (including itself). There is therefore no population structure and no mate choice.
Let $N$ be the number of individuals in the population, in absence of selection (see If selection, it must be on fecundity alone), the probability to mate with any given individual (including itself) is $\frac{1}{N}$. You will note that it requires that individuals are able to self (but not clone as reproduction must still be sexual).
If selection, it must be on fecundity alone
If selection occurs, then it must on fecundity (right before reproduction). If selection occurs on survival during the lifetime, then the selected genotypes will be in excess in comparison to Hardy-Weinberg expectations.
If migration, it must be right before reproduction only
For the same reason as above, if there is migration, then it must be right before fecundity. If migration occur during the lifetime, then it will have a very similar effect than selection. Selection would increase the frequency of selected genotypes above HR expectations. Migration would increase the frequency of incoming genotypes above HR expectations.
Non-overlapping generations
This means that everyone reproduce in the exact same time and die right afterward. Very few species would qualify for such assumptions.
Population of infinite size
If previous assumptions already seemed hard to meet in the real world, the assumption of infinite population is absolutely impossible to meet.
Deviation from this assumption will cause deviations from expectations. Such deviations are often tested via a Chi squared goodness-of-fit test.
Note by the way that if the population is of infini size, there is no mutation, no migration and no selection, then there is no evolution.
Other assumptions
Biology is a science of complex systems. There are always other assumption one might want to consider. For example I did not talk about sex-specific selection or sex-specific mutation rate. But I am hoping that with the above I went over the most important assumptions.
So what's the point of HWr?
All models are wrong but some are useful. There exist no real life example of a population that perfectly fit into HWr assumptions but it does not mean the model isn't useful. Actually most population approximate HW expectations quite well. You will note also that it is by understanding how a scenario lead to a specific observation that we can interpret how derivation from the expectations can be achieved.
So yes, HWr is one of the most basic and most important rule in population genetics. It is so basic, that I would hardly name it in any fancy way as it is just the simple application of basic probability theory. See Solving Hardy Weinberg problems for more info.

You missed that (i) generations are assumed to be discrete and without overlap and that (ii) allele frequencies are unbiased between sexes.

@AlexDeLarge Thanks. I added "Non-overlapping generations". When you say "allele frequencies are unbiased between sexes", is it any different from what I meant in his also means that HWr does not hold for loci present on sexual chromosomes as those chromosomes do not display a simple diploid behaviour.?

It just means that males and females do not differ in allele frequencies. If they did - and given the assumptions mentioned in your answer there is no obvious reason (you can construct it implicitly from the panmixia assumption, I guess, but this is too vague) why they would not -, the population would not be in HWE.

Yes... "males and females do not differ in allele frequencies" sounds more like a consequence of the violation of specific assumptions that we should make sure to include. I see the mention of this assumption in the wikipedia article. I would not know how to justify the addition of this assumption so I'll leave it out for the moment until someone can teach me more on it.

I don't like this Hardy-Weinberg formulation because it reduces to 1=1. Nevertheless, nice answer.

@canadianer: That's why I don't like Euler's identity. 0=0 ... come on.


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Is it possible to have different genes in different parts of our body?
I want to understand genetic mutation specially in the context of multicellular organisms like humans.
I studied biology only till high school and I can’t fully understand wikipedia pages on this subject.
I know that genetic material is in chromosomes inside the nucleus of a cell. When that cell multiplies, the chromosomes too generates a copy of themselves and both child cells get one set of the chromosomes.
I would like to know:

Does genetic mutation mean an error in chromosome generation at fission stage or will it occur later in the life of the cell?
Multicellular organisms begin their life from a single cell (zygote). Under normal circumstances, every cell that grows from this single cell should have the same genetic material. Can genetic mutation eventually result in us having different genetic material in cells of different parts of our body? For example, when only a part of our body gets exposed to radiation.
If answer to question 2 is yes, which genetic material will control the behaviour of the cells? Let’s say, for example, that the genetic material of cells in our stomach favour high growth rate of hair but the cells in the scalp themselves do not have that particular gene. What will be the result?

Welcome to Biology.SE! 1-Genetic mutation means error in base sequence, not chromosome generation. 2- No. No effect would be so powerful that it would alter your genetic material. That'd mean that you are half human and half elephant (or something worse). 3- the result would be no hair at all (stomach would burn the hair on its lining, and scalp wouldn't generate hair at all). If you're satisfied with this, then I can post it as an answer with some more details.

@another'Homosapien'  I don't agree, there are many ways DNA can be altered, and smaller genetic changes in single cells happen due to errors in all the time.  Of course this does not turn you into half-elephant, but it is certainly possible that the different cells in the body have differences in their genetic material.

@Roland I know, I just gave an introduction to these topics and said that I would give more details on this. However, iayork has already posted an answer which, I think, answers many parts of the question. :)

More information on protein variation among despite little to no genetic variation: More variation in proteins than genes. Why?

@Kanj, I think your question (3) is causing some confusion. What do you mean by "which genetic material will control the behaviour" ?  Each cell has its own copy of the genetic material (genome), and if the genome of one cell is changed by a mutation, various things can go awry in that particular cell, but it does not affect other cells in the body.  Perhaps you can clarify your stomach--scalp example?

@Roland- When asking question 3, I assumed that each cell has the entire genetic material not just the part that's relevant to it. I hope that's correct. What I want to know is that if cells in separate parts of the body develop conflicting genetic material due to mutation, genes of which part of the body would control the organism. The answer, I gather from this discussion, is that cell's growth and behaviour would depend on the genetic material it has; not on the genes present in other parts of the body. So high hair growth rate cells of the stomach can not affect hair on the scalp.

The general answer is that no, it's not possible to have different genes in different parts of the body.  There are two interesting classes of exceptions, but they are exceptions.
The first is that mutations can and do occur in cells during their growth.  Most of these are probably neutral - they occur in the vast wasteland of genetic junk in the chromosome, and nothing happens.  But some of them are harmful, and this is what puts cells on the pathway toward cancer.  Outright cancers, that we can detect, are the result of at least a half-dozen mutations occurring in the same cell lineage, that cumulatively allow the cells in that lineage to grow in uncontrolled manner, to avoid immune clearance, to encourage their own blood vessel growth, and so on.  (In fact, cancer cells generally have far more than a half-dozen mutations, because a route toward getting the mutations they need is to turn down DNA repair, allowing mutations to accumulate with minimal control.  For example, Genomic landscape of DNA repair genes in cancer, Genomic profiling of pediatric acute myeloid leukemia reveals a changing mutational landscape from disease diagnosis to relapse.)
The second set of exceptions is in the immune system.  Both B cells and T cells specifically modify their chromosomes during their development, making huge numbers (trillions) or new genes.  The catch is that these are all in the same region, the antibody or T cell receptor genes.  It's part of the mechanism by which the adaptive immune system "remembers" which pathogens it's interacted with in the past.  The wikipedia article on V(D)J recombination is a starting point.

Good, but your examples show (in contrast to the first sentence) that the general answer is yes, it is possible to have different genetic material in different cell types of the body.  "Different genes" sounds strange, but definitely different alleles of genes.

Genetic mutation usually refers to any errors made while copying DNA. This can certainly occur in the lead-up to cell division, when chromosomes are copied, although they can also occur when repairing DNA that has been damaged.
I'm reading your use of the term genetic material as referring to DNA. Genetic mutation can change the sequence of DAN, but it doesn't really change what genetic material we have in any given cell. I think that it's important to understand that all of the cell in our bodies contain the same genome, or set of genes. What differs from one cell type to another is which genes are active (or "expressed" as biologists say). Mutations can alter gene activity. Say, for instance, that the deletion of a single nucleotide causes a frameshift; this can lead to the loss of that gene product in the affected cell and its daughters.
Understanding that all genes are present, but only some genes are active/expressed should help clear up your third question.

For (2), how do you figure that a genetic mutation does not change the genetic material?

@Roland - DNA remains DNA despite any mutations. At least, that was the way that I interpreted the OP's question. It sounded like he was confused about really basic things like what genetic material is. I felt that a more complicated answer risked straying too far off-target and becoming a broader biology lesson. I'll edit the answer to make that a little clearer, though. :-)

I agree that (2) is unclear. Personally, I also I find the expression "genetic mutation" a bit ridiculous and I would only expect non-biologist to use this term instead of just "mutation".

By definition, the DNA sequence changes with mutations, which means that the "genetic material" has changed. I think the OP's question 2 is pretty clear: the question is whether somatic mutations occur. (And yes, they do.)


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A diagram of a crossover
How can one draw a crossover between ABK and aBk where genes A and B follow the Mendel's law of independent assortment and gene K does not i.e. K is linked to B?

Welcome to BiologySE! Where have you looked for help with this so far? Is this a homework question?

It's just an exercice that I'm interested in

Your question is unclear. What kind of a drawing do you want. Moreover, this questions seems to be primarily opinion-based.

I'm looking for a representation of the genome in a cell

I am voting to close as unclear mainly because we don't know to what locus is gene K not independent.

I'm not sure if this is what you're asking for, but in the following image, allele K (or k) is linked to B while A (or a) and B are independent.

Again, this is just a guess because your question seems a bit unclear to me.

Yes, that was the thing I was looking for

Oh, upvote and select it as correct then...! ;)


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What do bloodsucking animals actually feed on?
A number of animals, including mosquitos, leeches, ticks and so on, feed on blood. And yet, at least in mammals, most stored nutrients can be found in body fat as fat, muscles and liver as glycogen and digestive system as undigested nutrients, leaving very little in the blood itself. Normal blood sugar before a meal is 70-99 mg/dL, which at the high end means blood contains roughly 3.8 kilocalories per liter. This means that to gather a single kilocalorie from blood glucose, it would take 26 mL of blood, more than any leech could reasonably hold. Estimating the mass of a leech at 20g and scaling down human caloric needs linearly, 2500 kilocalories per 70 kg, yields a leech caloric requirement of 0.714 kilocalories per day. By this estimation, a leech would need to feed at least once per day to meet its energy needs, and yet data from the American Museum of Natural History states that a leech need only feed once every few months. The same math holds for other bloodsucking animals.
So what in blood do bloodsucking animals actually feed on?

Lets find out how much calories are there in the blood. I am using this site for main reference, but will also add more references where needed. But before that, we should know that one donation of blood is about 1 pint (or 450 ml) blood1. But here, I calculate with volume 500 ml.

First calculate calories for plasma. Blood is denser than water by six percent2, so multiply that 500 ml donation times 1.06 to get to grams (because calorie content will be calculated from grams). Multiply that by 55/100 for men or 60/100 for women to get to grams of plasma. Now, multiply that by .07, because plasma is only 7% protein3, to get to grams of protein. Finally, multiply that result by four to get protein calories. Here, considering 55/100, I get 81.62 calories.
Now for sugar in plasma. Normal fasting blood sugar is around 0.09 grams per 100 ml of plasma (more familiarly expressed as 90 mg/dl4). Multiply the amount in grams time 2.75 for men or 3.00 for women, i.e., equal to how many hundreds of mls of plasma there are in 500 ml of blood, and then times four to get to calories. Result should be 1 calorie.
For plasma calories from fat, use 0.5 grams per 100 ml5 of plasma, times hundreds of mls of plasma, times nine - for calories from grams of fat - to get to calories.  Result is roughly 12 calories.
Next comes calories from red blood cells. RBCs are mostly water and protein, the protein almost entirely hemoglobin. Hemoglobin does not conform to the rule of four calories per gram because the heme portion of the molecule is not metabolized for energy. Use average hemoglobin values of 160 g/L for men or 140 g/L for women6, multiplied by 0.5 to get to the blood donation volume of 500 ml, multiplied by 0.96 to correct for using only the non-caloric heme portion of the hemoglobin molecules, then multiplied by four to get to calories. Hemoglobin is only 90% of the dry weight of RBCs7. Multiply one-tenth the amount of the hemoglobin weight in 500 ml times six (see below for why six) and add that to red blood cell calories. I get 353.28 here.
Finally, estimate calories for the other types of cells. Of the 500 ml blood donation, roughly one percent will be white blood cells and platelets8. Figure five grams, times one-third to get to dry weight, times six, to get to an estimated 10 calories. The "times six" is because some of the dry weight is protein or carbohydrates, which both have four calories per gram, and some is fat, which is 9 calories per gram.

Add everything up. The total should be approximately 425 calories for women and 460 for men in 500 ml blood i.e. even 10 ml of a man's blood contains about 9.2 kcal (there's no definite answer about how much blood a leech drinks at a time). Now, as you say in your question that a leech requires about 0.714 kcal, it means that a leech can survive for almost 13 days by sucking just 10 ml of a man's blood (if they have to metabolize everything present in blood (except, of course, water)), which justifies your statement.

I see my error was assuming the only value in blood is in the glucose, and ignoring everything else

@theenvironmentalist yeah, but since the parasite has got only that much amount as its sole source of energy, it would definitely do everything to extract as much energy as possible ;)