text:
A question related to qPCR analysis
Here is the thing. I am using a method, called TU-Tagging, to isolate cell type specific RNA. You can find more about the method here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2783170/
To explain it very briefly, there is an enzyme called UPRT (Uracil Phosphoribosyltransferase) which is expressed in Toxoplasma gondii. Under normal circumstances UPRT creates UMP from host cells' uracil and this UMP incorporated in RNA. However, they found that this enzyme cannot distinguish uracil and uracil analog 4-Thiouracil (Basically has thio on 4th position of the uracil). So, when 4-TU provided externally, UPRT incorporates 4-TU into RNA and you get thio-RNA. Then with basic biotinylation and streptaividin isolation you can get thio-RNA from your total RNA isolate. (Of course UPRT should be put to specific cell types of your interest)
Anyway, after the explanation (maybe it was unnecessary though) here is my question.
After I isolate my so called specific RNA, I check the purity by qPCR by using cell type specific markers. I do not have a reference gene. The only thing I am interested in is the presence or absence of markers (and also the fold change of course). Now, I have some data but I do not know how to present them (There is nobody in my lab experienced with qPCR and my experience is just so limited).
Do you have an idea how I can overcome this issue? I looked into some calculations but most of them are needed for reference genes or some other stuff. The only thing that I have is cycle numbers and my primers' efficiency. Do you think I can do something with these inputs? (I know that cycle numbers mean nothing in a plot, so I do not want to put cycle numbers basically.)
Thank you for reading it. Any help/idea would be very appreciated. I am so desperate. Thank you.

Great/clear/easy to follow explanation of the TU-tagging technique. However, I am confused as to what you are really asking for. You isolated a cell specific RNA and you want to check the "purity" of your isolate? What do you mean by this?

Thanks. So imagine like, I have a fly line which has the UPRT in their neurons. When I do the TU-Tagging experiment, in theory I just isolate RNA from neurons. So, I should not see any glia specific markers lets say. So, with qPCR I am checking cell type specific markers in order to see my RNA is clean or contaminated by other cells.
However, I do not know how to plot these qPCR results. I just have cycle numbers and do not know how to present them.

Does your qPCR software not provide you with the progressive graphs where you can see each sample crossing the threshold? That might be a nice picture to show.

OK, let us start from the beginning. We know what makes one cell type different from another cell type is its expression - i.e. what genes are actually being transcribed into RNA. Therefore, there should be certain RNA in one cell type that should not exit in another cell type. If you isolate RNA from a certain cell type, say a neuron and you want to show that your sample RNA contains only neuronal RNA, than you have to prove 2 things:

That your sample contains certain RNA sequences that are known to be in neurons
That your sample does NOT contain certain RNA sequences that are known NOT to be in neurons

There are several lab procedures for identifying the presence/absence of certain RNA sequences in a sample, your chosen technique is qPCR. Here is a brief explanation of how qPCR works.
You put your RNA sample along with a sequence specific primer in the qPCR machine. The primer will bind to a specific sequence and then that strand will be replicated. This will keep on repeating, cycle after cycle. So if you start with 1 sequence of say sequenceA, after cycle 1, you will end up with 2, then 4, then 8 and so on.
Anyways, if your goal is to use qPCR to prove your RNA sample comes from a neuron then you must find some sequences that are known to be specific to neurons. Then find primers for these sequences. Then use these primers to amplify some RNA from your sample. If you get amplification, then you must have had that sequence in your RNA sample. To further support yourself, you may also want to look up a few sequences that are known NOT to be expressed in neurons and using the same principle prove that these sequences are NOT in your sample.
The above will give you qualitative data, it will simply tell you if a certain sequence exits or does not exist in your RNA sample. Since you are only interested in the presence or absence of markers, this should be sufficient. Howver, if you would like to quantify your data, i.e. find out how much a certain sequence is expressed then read on.
You can also get quantitative data from qPCR (after all qPCR stands for quantitative PCR). The number of copies of an RNA sequence after a certain number of cycles is proportional to the initial number of copies of that sequence in your sample. In other words, if your initial RNA sample has a lot of sequenceA and a little sequenceB, then at any cycle, you should see more sequenceA.
We can take advantage of this relationship. There are two general methods you can use to quantify your results. One is called Absolute quantification and the other Relative quantification.
The idea behind absolute quantification is that you run two qPCRs. In one, you do your RNA sample. In the second, you run a standard sample, for which a standard curve is available. You can then compare your RNA sample results with the standard's results to get an idea of the number of copies in your sample.
The idea behind relative quantification is that you compare the qPCR results for your sequence of interest with the qPCR results of a refrence gene. This will only give you an idea of how many times more or less your sequence of interest if expressed than the reference gene. Since you do not have a refrence gene you cannot use this method, but you can use the absolute quantification method explained in the paragraph above!
Here are very useful links on quantifying using qPCR:
http://en.wikipedia.org/wiki/Real-time_polymerase_chain_reaction#Quantification_of_gene_expression
http://relative.gene-quantification.info/
Let me know if you need further clarifications.

Hey thanks! As you told also I am just interested in to show presence and absence. I already did lots of qPCR experiments with neuronal and glial primers and have the data as cycle number. So I just want to show them but I can not show the cycle number, I need to express it as some numbers which will show fold change for example. I need to plot the data. So can I just assume that every cycle will double my cDNA and could use an equation like this: 2^-Ct ? Or it is not the way?

if "C" is your initial concentration, and "t" is the number of cycles, then yes your equation will tell you the fold change. Sorry for the late response, haven't been on here for a while.


text:
What cells don't have a primary cilium?
It is often stated that most cells in the human body have a primary cilium.
Which ones don't? For which cells is it unknown?

Hi, if you found my answer acceptable, it would be a nice gesture to show this by marking it as accepted.

Thank you for the answer, @leonardo, but I was asking about unciliated cells in particular. I'll wait to see if anyone can provide a more authoritative answer saying there are none, or an example of cells with no cilia.

It seems that, by and large, most animal and plant cells have primary cilia. To quote from this open access paper:

".[..] organisms that form cilia have a basal body or centriole-like structure as their microtubule-organizing center, whereas those that do not [e.g., yeast, higher plants] use morphologically distinct structures for organization of their microtubule cytoskeleton."

Other cases where cells lack primary cilia are when they possess motile cilia (e.g., sperm are mono-ciliated, respiratory epithelia are multi-cilliated).

Fry AM, Leaper MJ, Bayliss R. The primary cilium: Guardian of organ development and homeostasis. Organogenesis. 2014 Jan 1;10(1):62-68. Epub 2014 Apr 17.

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text:
How do you merge SNP data with a reference genome?
My Data
I have a 23andMe file listing SNPs in the form:
rsid       chromosome      position        genotype
rsXXXXX         1           PPPPPP          CT
rsXXXXX         1           PPPPPP          GG

Fields are TAB-separated and each line corresponds to a single SNP. For each SNP, four fields of data are supplied.

An identifier (an rsid or an internal id)
Its location on the reference genome.

The chromosome it is located on.
The position within the chromosome is is located on.

The genotype call oriented with respect to the plus strand on the human reference sequence.

The reference genome is the human assembly build 37 (also known as Annotation Release 104).
My Question
How do I merge the SNPs into the reference genome?
For example, take the first line in my SNP file:
rsXXXXX        1           PPPPPP          CT
Part 1
I can see that I need to replace the nucleotide at position PPPPPP on chomosome 1 of the reference genome with a nucleotide from the genotype field, but which nucleotide am I supposed to use? C or T? And why?
Part 2
Where am I supposed to start counting from on the reference genome? Looking at chromosome 1 of the human assembly build 37, the first ~10,000 characters (excluding the first line description) are N. Is the first N number 1? eg. If PPPPPP was 100,000 would I replace the 100,000th character in the reference genome with the correct nucleotide from Part 1 of this question? Or should I start counting from the first non-N character in the fasta file?

First, you need to know which genome sequence does the SNP file refer to. They must have mentioned the reference sequence that they used.
As others mentioned the case of CT is heterozygosity. If you just want to mark the changes then discard the residue that is already present in the reference genome and use the other allele. However, you want to keep a track of the haplotype then you have make sure that a set of SNPs come from the same chromatid. This is difficult- you might still be able to know it for SNPs that are close enough to be mapped by a single read but it is almost impossible for SNPs that are separated well enough.
As Endre said, you have to start from the first nucleotide. However, it seems dubious that you are getting $\ (NNNN)_n$ in the beginning of chromosome 1. Complete assembled chromosomes do not have such stretches. Below are the first 10 lines of the chromosome 1 fasta file. See for yourself.
>gi|568815364|ref|NT_077402.3| Homo sapiens chromosome 1 genomic scaffold, GRCh38 Primary Assembly HSCHR1_CTG1
TAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAAC
CCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCAACCCTAACCCTAACCCTAACCCTAACCCTAA
CCCTAACCCCTAACCCTAACCCTAACCCTAACCCTAACCTAACCCTAACCCTAACCCTAACCCTAACCCT
AACCCTAACCCTAACCCTAACCCCTAACCCTAACCCTAAACCCTAAACCCTAACCCTAACCCTAACCCTA
ACCCTAACCCCAACCCCAACCCCAACCCCAACCCCAACCCCAACCCTAACCCCTAACCCTAACCCTAACC
CTACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCCTAACCCCTAACCCTAACCCTAACCCTA
ACCCTAACCCTAACCCTAACCCCTAACCCTAACCCTAACCCTAACCCTCGCGGTACCCTCAGCCGGCCCG
CCCGCCCGGGTCTGACCTGAGGAGAACTGTGCTCCGCCTTCAGAGTACCACCGAAATCTGTGCAGAGGAC
AACGCAGCTCCGCCCTCGCGGTGCTCTCCGGGTCTGTGCTGAGGAGAACGCAACTCCGCCGTTGCAAAGG

How to replace $N^{th}$ residue is quite a straightforward task. But that is a programming question and not the scope of this forum. Assuming that you have solved the part 1 problem and have a tab separated sorted file like this:
chromosome  position    residue
 1           79989           G
 1           100232          T
 3           341342          A

This script may not be the best but would work in a linux/*nix/Cygwin terminal, to replace the residues (ensure that you have gawk version >=4.0):
gawk -F "\t" '(FNR==1){x++} (x==1){a[$1][$2]=$3;next} (x==2){if($0~/>/){h=$0;sub(/^.*chromosome /,"",h);sub(/ .*/,"",h)} else{seq[h]=seq[h]$0}} END{for(i in a){s=0; for(j in a[i]){m=m substr(seq[i],s,j-1) a[i][j];s=j+1} m=m substr(seq[i],s); print ">Chr"i"\n"m}}' SNP_file Genome.fa | fold -w 60

Unfortunately I cannot explain how the script works, in this forum

"TAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAAC" blats to position 10,000 according to UCSC.  And look at it, as I said, it's repetitive and awful.  The OP just has a masked sequence.

Hmm.. yes.. I didn't notice that.. nonetheless the start is from the residue#1..

Genetics 101, you have 2 copies of all your DNA at every position, one copy from your mother, one from your father.  So for the "CT" one, you have one copy with a C, and one with a T.
And yea, it's normal for the first several thousand, or million letters to be N's.  The genome is repetitive and yucky there, but it's counted for numbering purposes anyway.
Honestly, I wouldn't do this with a giant text file of the genome.  Just search for your SNP in ensembl.org using the rs number, and you'll get the SNP, and some flanking sequence, and some context.  Search it in PubMed if you want to see if it's ever turned up in any publication

Part 1:
According to Lior Pachter, 23andme data are not phased. Which means that for each entry in the genotype field, you do not know which chromosome copy it came from. This happens since modern microarray platforms are not able to tell which of the two copies of a chromosome a snp came from.
You can solve this problem for most snps by comparing your alleles to the reference genome, but this would take some programming chops. You could use https://github.com/endrebak/qc_gwas as an example, which does the same thing, but for plink files.
Part 2:
I'm assuming that you would like to do this programatically, and not by copying and pasting the snps into the reference genome.
The short answer is that the first N is the first nucleotide. But, you should rather use a package such as Biopython to do the counting for you, it might be knottier than you think (you need to adjust for line endings in the fasta file, for example).

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text:
What is the suitable terminology to describe this study approach?
I need to know the correct term(s) which are usually used in the parlance of both biology and bioinformatics for this study approach:
About 11 transcripts were investigated using qPCR for a number of samples (about 200) and then  the gene expression data were subjected to data mining tools: principal component analysis (PCA), cluster analysis (CA) and the results were interpreted using other supportive data that were not included in PCA in order to reveal the nature of acquired clusters.
Clusters obtained were then predicted from the gene expression data using machine learning classifiers. In short, it is a blend of molecular biology, data mining tools, and machine learning classification (predictive modeling).
Please if you have ever done this kind of data analysis, what should be the appropriate term to describe this approach?
Likely candidates
Gene expression profiling study
Transcript profiling study
Transcript Wide Analysis Study or TWAS for short

I would bet the author is furthering a global screening approach (probably micro arrays). You don't really have enough info given , can you cite the paper? Right now There's a few different things going on here, like you deduced.

it isn't a microarray, it is a 96-well based gene expression analysis using real-time quantitative PCR (sample maximization approach, not gene-maximization). Unfortunately, I am not aware of any paper that did the same thing.

I didn't say IT was a microarray, I said the intial study could have been a microarray, and this experiment you describe is now "pin-pointing" genes from that microarray data, as is usually, but not always, the case. As of now I think all this experiment can be parlanced into would be gene expression and linking that to omics data.


text:
What are the known natural biochemical reasons for a dead human's body not fully decaying?
What are the known natural biochemical reasons for a dead human's body not fully decaying (decomposing)?
EDIT:
I am interested in a scientific explanation of those cases, in which human body would not fully decay, for example, some parts of skin and hair would still be there, and I am not talking about such cases like hand-made mummification (like, say, those Pharaoh's mummies in Egypt).

Please clarify your question a bit. Are you asking under what circumstances a body might not decay, and the biochemical reasons thereof? Or do you have a specific circumstance in mind?

@jarlemag - "Please clarify your question a bit" - Sure. I am interested in a scientific explanation of those cases, in which human body would not fully decay, for example, some parts of skin and hair would still be there, and I am not talking about such cases like hand-made mummification (like, say, those Pharaoh's mummies in Egypt).

@brillant You can edit your question to add your clarifications. Additionally you should add some research you already did. For example try checking about a relation of humidity and temperature to decay.

related posts- 1 and 2

@brilliant are you talking about bodies preserved in bogs and ice.

@potterbond007: "are you talking about bodies preserved in bogs and ice" - Not really. I'm talking about those cases when a body in a coffin for some reason is not fully decomposed while all the surrounding natural conditions apparently should bring it the state of full decomposition (except, perhaps, for the bones).

question requires case study reference and clarification!


text:
Is there a correlation between brain size and amount of sleep?
As far as we know, sleep seems to be the part of the daily cycle when executive functions are resting and memories are fortifying. Many, but not all, of the functions that become dysfunctional upon sleep deprivation seem to be situated in the frontal lobe or associated with the neocortex.
My question is whether there is a correlation between percentage of the day spent sleeping and brain size (either the whole brain, or a part of the brain such as the neocortex or frontal lobe). How do other species correlate compared to us? Either in absolute brain size, or in brain size relative to body size.

I'm closing this question as it is cross-posted on CogSci already at http://cogsci.stackexchange.com/questions/6440/is-there-a-correlation-between-brain-size-and-amount-of-sleep

@MadScientist not sure, they're complaining about the cross-posting over there too and neither one has an answer. I'm not sure which site is a better fit. Darko, could you please modify your question  to fit the different communities more specifically?

Changing the question would not alter the outcome and as such is stupid. But ok. Since the question is more specific towards the correlation between species, I will leave it as it is here. Cognitive scientists have nothing to add to that. I will edit the Q on CogSci to make it a better fit.


text:
Help with the Price equation
The Price equation describes mathematically the evolution of a population of units from one generation to the next.

$\bar{w}\Delta \bar{z}$ = $Cov (w_i,z_i) $+$ E(w_i\Delta z_i)$

I would like to know how to actually employ the equation to some data. Perhaps a simple online "walk-through" type guide of the Price equation would help. It should simply show the calculation of the Price equation using numbers from an example population. For example, I'd like to see how the Price equation is applied to the following scenario:

A population, $P$, of 5 individuals reproduces to produce population
  $P'$.
The trait value of the $i^{th}$ individual is $z_{i}$ where $z_1$,
  $z_2$ and $z_3$ all = 1 and where $z_4$ and $z_5$ both = 2 and $\bar{z}$ = 1.4.
Absolute fitness is $w_i$ for the $i^{th}$ individual where $w_1$,
  $w_2$ and $w_3$ all = 1, and $w_4$ and $w_5$ both = 5.
Relative fitnesses, $\omega_i$, are $\omega_{z=1}$ = 0.077, and $\omega_{z=2}$ = 0.385.
Thus the population $P'$ has $n$ = 13, with 3 individuals where $z$ = 1
  and 10 individuals where $z$ = 2 and $\bar{z}'$ = 1.769.
$\Delta z $ is the transmission bias and is equal to 0 in this case
  (perfect transmission of the trait score $z$)
The value $\Delta \bar{z}$ = $Cov (w,z)/ \bar{w}$ = ....

Here's an R script to create the above information:
# Define two trait values:
z1 = 1
z2 = 2

# Define two fitness values:
w1 = 1
w2 = 5

# Set number of units possesing each trait in P population:
n1 = 3
n2 = 2

# Create data
df = data.frame(c(rep(z1,n1),rep(z2,n2)),c(rep(w1,n1),rep(w2,n2)))
colnames(df) = c("z","w")

df$omega = df$w / sum(df$w)

n_P = length(df$z)
    n_O = sum(df$w)
z_P_bar = mean(df$z)
    z_O_bar = sum(df$w*df$z) / sum(df$w)
omega_z1 = mean(df$omega[df$z==z1])
omega_z2 = mean(df$omega[df$z==z2])

# Parental population size:
n_P
# Offspring population size:
n_O
# Parental mean trait:
z_P_bar
# Offspring mean trait:
z_O_bar
# Realtive fitnesses:
omega_z1
omega_z2

Here is a simple example using your data in which both terms of the Price equation are needed, since the value of the character for $z_2 $ changes in the second generation. I used your suggested change $z_2'=(9\cdot 2 + 1\cdot 3)/10 = 2.1$.
The Price equation or theorem is:
$$(1)\hspace{10mm}w\cdot \Delta z =  \text{cov}(z_i,w_i) + E(w_i\Delta z_i)  $$
While the idea here is just to give a credible calculation using both terms in the right side of the equation, and while the intuition behind the equation is essentially mathematical (or is it? $^1$), Steven Franks' paper, 'George Price's Contribution to Evolutionary Genetics', J. Theor. Biol. 175 (1995), 373-88, is a good introduction. His characterization of the right side may be the best one can do:

"The two terms may be thought of as changes due to selection and transmission, respectively. The covariance between fitness and character value gives the change in the character caused by differential reproductive success. The expectation term is a fitness weighted measure of the change in character values between ancestor and descendant. The full equation describes both selective changes within a generation and the response to selection..." p. 376.

We work with reference to the following data and will define variables below.
$$\begin{array}{c | c | c | }  n_i & 3 & 2  \\ \hline
z_i &1  & 2  \\ \hline
w_i &1& 5   \\ \hline
n_i' & 3 & 10  \\ \hline
z_i' & 1 & 2.1  \\ \hline \end{array}$$
All cites WK are to the Wiki page on the Price equation:

(1) We can write $\text{cov} (w_i, z_i)$ as $E(w_iz_i) - wz.\hspace{10mm}$ WK eq. (7).
Explicitly:
$$ \text{Cov}(w_i,z_i) = E(w_iz_i)- wz = \frac{ w_1z_1n_1 + w_2z_2n_2}{n_1+n_2} - wz $$
$$ = \frac{1\cdot1\cdot3 + 5\cdot2\cdot2}{3+2} - (2.6)(1.4) =\frac{23}{5} - (2.6)(1.4)= 0.96$$

(2) We can write $E(w_i\Delta z_i) = E(w_i z_i') - E(w_i z_i).\hspace{10mm}$ WK eq. (8).
Now $E(w_i z_i') = \frac{1}{n}\sum w_iz_i'n_i\hspace{40mm} $ WK eq. (9a).
$ = \frac{1}{2 + 3}(1\cdot 1\cdot 3 + 5\cdot(2.1)\cdot 2) = 24/5.$
$E(w_iz_i) = 23/5$ from (1) above.
So  $ E(w_i z_i') - E(w_i z_i) = \frac{24}{5} - \frac{23}{5} = 1/5$

(3) Finally we have $\Delta z =  z' - z = \frac{2.1(10) + 3(1)}{13}-\frac{3\cdot 1+2\cdot 2}{5} = \frac{29}{65} $
and $w = \frac{3\cdot 1+ 2\cdot 5}{3+2} = \frac{13}{5} = 2.6$
So $$w \Delta z = (2.6) \frac{29}{65} = 1.16 $$
$$= \text{cov}(z_i,w_i) + E(w_i \Delta z_i) = 0.96 + .2 = 1.16 $$

$n_i$ is the number of elements in group $i.$
$n_i'$ is the same for the filial generation.
$z_i$ is the value of a character for group $i.$
$z_i'$ is the same for offspring of $z_i.$
$w_i$ is a fitness weight, often the number of offspring an element $z_i$ will have.
$w$ is the average fitness for the parental generation.
$z$ is the average value of z for parental generation;
$z'$ is the average of z for the filial generation.
$z_2' - z_2$ (for example) is the average value of $z_2$ in the second filial
  generation minus the average of $z_2$ in the parent's generation.

$^1$ This site condenses some critical discussion of the Price equation. I have not worked through it yet but it addresses some lingering doubts I have about just what this equation means. Strongly recommended.

Thanks - I've worked that out using my R script & got the same answer! I know it was not in the original question but could you help explain the second term on the RHS ($E(wiΔzi)$) which shows the transmission bias. Perhaps if I said that one of the $z$=2 parents has 4 offspring where $z$=2 and one where $z$=3, the other $z$=2 parent has 5 offspring of $z$=2.

This example only furnishes the requested calculation but there is no functional relationship between the trait z and fitness w. A more instructive example would be Wiki's note on 'altruism' at the linked page.

This is a nice numerical walk-through and explanation, see this webpage.
As requested I've sketched out a solution to the specific case above.
A nicer way for caclulations is to rewrite the price equation as:
$$ \Delta z = Cov(w_i/\bar{w}, z_i) +E(w_i/\bar{w}, \Delta z_i) $$
So lets draw out some important terms.
In the current population average for $z$, the average trait value in the second generation $z'$  and, the average relative fitness of the parents $\bar{w}$ are:
$\bar{z} = 1.4$
$z' = 1.769$
$\bar{w} = 0.2002$
So we an brute force the $\Delta z$ by doing $1.769-1.4 = 0.369$. However we shall also show this using the price equation (note for sample data the correction is $n-1$ not $n$ as shown below).
$Cov(x,y) = ((x_1 - \bar{x})*(y_2 - \bar{y})+(x_2 - \bar{x})*(y_1 - \bar{y})+ ... (x_n - \bar{x})*(y_n - \bar{y}))/n$
Using the data provided we can say:
$Cov(w_i/\bar{w}, z_i)= ((3 * (0.077 - 0.2002)*(1-1.769)) + (2 * (0.385-0.2002)*(2-1.769)))/5 = 0.07392 $
This is a per capita change. $0.07392 * 5 = 0.3696$ (rounding error).
Expectation
So the OP identifies a situation where transmission effects are non zero. Lets just consider that the mutation that causes z=2 is a  super-synergistic and causes its offspring to be z=4. The expectation term in this case is:
$E(w_i/\bar{w}, \Delta z_i)= ((w_4/\bar{w})*(z'_4-z_4) + (w_5/\bar{w})*(z'_5-z_5)) /5$
I've ignored the first 3 individuals because the transmission effect will make their terms 0 (1-1=0).

Thanks for sharing @Sanalphatau. Rather than providing a link-only answer, we typically ask community members to provide a brief summary or excerpt of the salient point(s) from the linked material (see http://biology.stackexchange.com/help/referencing). If for any reason your link gets broken in the future, this answer would become useless without any additional info.

Thanks, I'll take a look shortly (@DanielStandage raised a good point so perhaps you would like to elaborate on the answer). I've also edited the question so that it makes a greater attempt to draw fuller answers.

Apologies, not very well versed with the guidelines. I'll read through and update my answer in the coming day or two (so its more stand alone).

Thanks @Sanalphatau - I look forward to it. If you can then it would be good if you could help me solve the above problem, I think this would help me get my head around it, my main confusion is just knowing which numbers to use where

The first part of your calculation agrees with part (1) of my answer above (divide cov by w = 2.6). Your calculation works but I think by definition $\bar{w}= (1/[n_1+n_2])(w_1 n_1 + w_2 n_2).$ If you finish the second part and show the two sides equal I would upvote. OP added the second part after he got the first part.


text:
Protoporphyrinogen (IX) formation in heme synthesis

This picture shows one of the steps of heme synthesis. In this step two propanoate groups of coproporphyrinogen III are decarboxylated to form protoporphyrinogen IX. The enzyme that catalyses this step is an oxidase. Oxidase enzymes catalyze the removal of hydrogen  in the presence of oxygen to form water or hydrogen peroxdide.
So, will a water molecule form in this step? 2H+ will come from the two carboxylate groups and oxygen will combine with it to form water. Will a water molecule form in this way?

Oxidase enzymes catalyze the removal of hydrogen (addition of oxygen).. Oxidases don't add oxygen; they use oxygen as a cofactor or electron acceptor. Oxygenases are the ones that add oxygen. And all oxidases give rise to either $H_2O$ or $H_2O_2$

Nonetheless, your title and the diagram is not really related to your actual question. Please clarify what exactly you want to ask.

@WYSIWYG, I have edited the question.

so, will a water molecule form here?

Seemingly the enzyme uses molecular oxygen in the reaction and one of the end products is water.
This reaction scheme is more detailed and presumably accurate.
http://www.hmdb.ca/reactions/3063
In addition there is also a set of papers detailing coproporphyrinogen oxidase which was also on the website, hopefully one goes into more detail on the reaction.
http://www.hmdb.ca/proteins/HMDBP00251


text:
problem with natural selection
I fail to see how natural selection can build any kind of new functionality.
New functionality in a design requires sacrificing a complex series of meanwhile useless steps before the new functionality works and becomes advantageous.
For example, if I want to upgrade a stationary chair to a wheelchair, there are many intermediate steps that must be done (which are not advantageous) before the added functionality becomes advantageous.
If a human being sits there and tries to intelligently assemble the wheelchair in such a way that it will be advantageous at each step, he will not be able to do it. it just doesn't work like this.
Can someone fill me in as to how this works and whether there have been experiments that demonstrate this, for example, having someone assemble a simple functional design with the limitation that every few step adds advantageous functionality.

This is a common misconception of natural selection: Not everything which appears needs to be new (there are szenarios in which other organs change) and not every step needs to be advantageous. It is enough if it causes no negative effects.

@Chris let's say for example sonar in bat navigation. how many changes are needed in coordination b4 the functionality becomes advantageous?

have you ever tried to build a chair like this? it just doesn't work.

Evolution by natural selection does not require that every intermediate step produces some kind of useful functionality - you are assuming some kind of cost to fitness imposed by intermediate steps which is great enough for selection to be effective. Evolution via natural selection leads to change because deleterious changes are selected against, and advantageous ones are selected for - however, selection is not the only force affecting evolution and not all changes to traits have fitness consequences (or strong ones at least).

There are homo sapiens who can guide themselves with echo location.  How can you argue that it's impossible to evolve when we humans already have it, without requiring specialized adaptations?

@Chris if the intermediate step is neutral (neither advantageous nor disadvantageous), then you no longer have the pseudo-intelligence of natural selection helping you and it becomes more or less random.

Mutations are random.

@Chris right. so you dont have the help of any pseudo-intelligence and cannot expect a complex intelligent design to emerge from this process.

Why do you expect that there is some help necessary? Evolution simply happens. And it takes time - a lot of time.

This is fundamentally a teleological argument.
The error is in assuming that the intermediate steps were a precursor to the present functionality. For example, interpreting an 'intermediate' bird wing as a fully functional wing, intended for flight. In fact, there is no prerequisite that present characteristics or functions have evolved from intermediates that were intended FOR that characteristic or function.

what you say is correct, but some things are totally useless without a combined and coordinated functionality and they are irreducibly complex. bat sonar for example requires sending out sound waves, a biological transducer, a signal processing etc. before there will be any useful functionality from this. what intermediate steps could possibly be useful here?

You CAN get useful functionality from systems before they are in their modern configurations.  The structure of the eye, the bombardier beetle; intermediates CAN have uses.  How can you hope to prove that every single element of every single complicated system didn't?

@swbarnes2 true, but don't you agree that for some systems there is a minimum complexity before they can be of any advantageous functionality. and that minimum is in fact enormously complex.

There are so many wrong-headed premises here, one hardly knows where to start.
First of all, natural selection is the process of changing the frequency of alleles in a population, mutation is what creates new ones.
Second, just because you can't think of every intermediate step doesn't mean it's impossible.
Third, you are assuming that natural selection is so uber powerful that every single stop must be beneficial, and there's no evidence that that's the case.  Evolution preserves lots of neutral and nearly neutral mutations.
Fourth, you are assuming that each step in some kind of path way can only possibly be used for the pathway it's in today.  That's not true either.
If you want somewhere to start in the literature, try some papers by Lenski:
http://www.ncbi.nlm.nih.gov/pubmed/22992527
http://www.ncbi.nlm.nih.gov/pubmed/23918358
If you really want to argue that it's impossible for, say, E.coli to evolve the ability to metabolize citrate, because it's too hard to get from here to there, you need to address the empirical fact that these bacteria did just that.

perhaps E.coli had this functionality built in to the dna. I have seen papers which claim the organism has the ability to modify the dna on its own.

If the functionality was pre-built, why don't all E.coli have it?  Did you read the paper, or even the abstracts?  Modify its DNA with intent?  I'm sorry, but there is no evidence of that.  I don't see what the point of asking questions is if you are going to make up facts to bolster your per-determined conclusions.

pre-determined conclusions? I follow the truth wherever it leads me. for E.coli the process of how it evolved this ability has not been proven that it was through random mutations, correct? We just know it has an ability the parent did not have. but it could well be that there is some kind of pre-built mechanism in the E.Coli for making various "intelligent" variations of daughter cells and these variations.

regaring the E-coli, I found this which plays it down "but it’s doubtful that Lenski’s E. coli have achieved any more than two mutations, so have not even reached Behe’s edge, let alone progressed on the path to elephants or crocodiles". from http://creation.com/bacteria-evolving-in-the-lab-lenski-citrate-digesting-e-coli  any thoughts? thanks for your patience

e-coli already had some ability to metabolize citrate


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Are there issues with filling PCR tubes to capacity?
I'm planning to scale up a PCR reaction, and I'm wondering if filling the PCR tubes to the maximum volume of 200 ul would be a problem. It would mean a lot less pipetting as I would only need 1/4 of the tubes.
The typical protocols I've seen always use 50 ul for a PCR reaction, I'm wondering if there are any issues with larger volumes, e.g. differences in heat transfer, that could cause issues if I scale up the volume in one tube.
Is scaling up the volume problematic? Any specific aspects I should consider?

Too long for a comment: I would say it depends on the PCR. I have personally used maximum volumes of 50ul, if I needed to prepare higher volumes, I made one mix which subsequently got distributed to more tubes with 50ul max.
The problem with big volumes is to get a fast and homogeneous heating and cooling. If the outside of the tube is faster, the reaction there starts already while this may not be the case in the middle. This can lead to uneven denaturation and amplification of your template. The later is especially problematic when you amplify short sequences. There the amplification time might already be over and the PCR program is moving on before the template is finished, which will result in less of your full-length product and the enrichment of shorter versions.
There is another problem that might occur in big reactions: Due to gradients in reactivity because of temperature gradients I think it is possible that reagents (dNTPs, Mg-ions) can form gradients which further inhibit a good yield.
Finally I tested one thing on one of our PCR machines: The PCR tube is set into the heating/cooling block. It is not completely set into the block but stick out partly, so if you fill it up to maximum capacity, the upper 75-100ul (approximately) would be outside the heating block and we have a thermal problem. The reaction mix there would only heat up due convection.

(Also too long for a comment.) This question reminded me about an anecdote told by Arthur Kornberg concerning the approach to scaling up that was adopted by Reiji Okazaki (discoverer of Okazaki fragments).
Here is a quotation taken from For the Love of Enzymes: The Odyssey of a Biochemist by Arthur Kornberg

Reiji’s research style is not readily gleaned from his publications,
  but it is vivid in my memory. One example I call the Okazaki maneuver. In purifying an enyme, he used a heating step: 10 milliliters of
  the enzyme solution was held in a test tube at 70°C for ﬁve minutes;
  then the coagulated impurities were removed by centrifugation.
  When he came to the point of scaling up the procedure to several
  liters, he simply repeated the original heating procedure several
  hundred times. I was embarrassed to have to report such an unsophisticated procedure in our publication. But then I realized that
  he was able to complete this step in a few hours and saw no point in
  wasting precious time and material in learning how to do the heating in a large beaker or flask. Later, when another of my students
  puriﬁed an enzyme with a heating step and had to scale up his
  procedure 2,000-fold from 3 milliliters to 6 liters, I advised the
  Okazaki maneuver: he added 3 milliliters to each of 200 test tubes to
  carry out the heating and centrifugation step, repeating the procedure nine times. Another student who tried heating a large volume
  of this enzyme in a single step lost it in a thick coagulum.


text:
Were there any flying dinosaurs?
I've seen some articles which came in contradiction with each other.
The first article was talking about flying dinosaurs, dinosaurs with feathers and so on.
A couple of other articles are talking about misconceptions about dinosaurs one of them being that there are no flying dinosaurs but just flying reptiles (from scholastic.com and livescience.com).
So, which one is right?
Also if possible please provide a source for argument.
I cannot find the first article again.

Beside the question of "Could the Pterodactyle fly?", there is the second "What is a dinosaur?". This question is related to the second one. But anyway, @kmm already provided a very good answer that you could accept.

The title of the question is a little bit scary u know. I was under the impression that there is currently no flying dinosaurs :D

Related: If dinosaurs could have feathers, would they still be reptiles?

Birds are both flying dinosaurs and flying reptiles. Yes, that's potentially confusing.
To understand the apparent contradiction, you have to understand how modern classification of organisms works (phylogenetic systematics). Under the old (Linnean) classification system, Reptilia (reptiles) was an order and Aves (birds) was a separate order. Phylogenetic systematics, which has completely replaced the Linnean system, views all organisms as interrelated in a nested set of monophyletic groups (clades). It's like a set of venn diagrams, where all organisms fall into a giant circle and then successively smaller circles classify more and more specific groups.
The clade Reptilia includes snakes, lizards, crocodiles, and lots of extinct groups, including dinosaurs. So all dinosaurs are reptiles. The clade Dinosauria includes all the extinct dinosaurs (Stegosaurus, Triceratops, sauropods, etc.), including theropod dinosaurs, which include well known dinosaurs like Tyrannosaurus and Allosaurus. Based on a mountain on anatomical evidence, including lots of transitional fossils, living birds are a sub-group of theropod dinosaurs.
So all birds (Aves) are theropod dinosaurs (Dinosauria: Theropoda). All dinosaurs are reptiles. Therefore, birds are dinosaurs and reptiles. They are just more closely related to dinosaurs than to other reptiles.
The tricky part is that most people have an intuitive idea of what "reptiles" and "dinosaurs" are. To a systematist, whose job it is to classify organisms, these terms don't mean the same thing as they do to most people. Systematists think about groups like Reptilia and Dinosauria and how those groups are related to one another. So they have no problem saying that birds are dinosaurs and reptiles, because birds are nested within both of those groups.
A few words about pterosaurs
Along with birds and bats, pterosaurs are the other clade of vertebrates capable of powered, flapping flight. Pterosaurs fall within Reptilia (and Diapsida and Archosauria) along with Dinosauria, which includes birds. There are a lot of other extinct lineages in the tree that are not shown, e.g., ornithodirans that are not dinosaurs and not pterosaurs. Pterosaurs and birds share anatomical features that all reptiles, diapsids, archosaurs, and ornithodirans have, which is how we know that they are more closely related to each other than to other groups, like crocodiles. But their flight structures evolved independently and are anatomically distinct fro one another. So pterosaurs are flying reptiles but not flying dinosaurs.
These images might help you understand the above explanation.

Nice answer, but having said that, there's no reason why dinosaurs can't be a paraphyletic group. (I don't know if they are, but it's potentially a taxonomic leap to equate monophyly with calling them the same name.)

"Flying reptile" is often used not to mean "a reptile which flies" but instead as a synonym for Pterosaur.

This is a good comprehensive answer - but I think the OP needs to also understand that pterosaurs are not dinosaurs, and that this is a separate question from whether birds are flying dinosuars. You might want to edit your answer to include this information, since it's also a matter of systematics.

The most important take-away being that ostriches (Struthio camelus) are the largest remaining dinosaurs :-) And sure @Sparhawk, dinosaurs can be a paraphyletic group in the sense that you can define a jargon term any way you like. But cladists will refuse to utter the word with such meaning.

@SteveJessop I'm an evolutionary biologist (amongst other things), primarily in protists, a polyphyletic group. There are certainly other poly/paraphyletic groups that are defined as such (e.g. fish), although I agree that most of them are not useful from a classification perspective. I am unfamiliar with dinosaur taxonomy, but I was just making the point that birds being nested in the dinosaur clade doesn't necessarily imply that they are dinosaurs. I think the answer has to explicitly mention the claim that dinosaurs are monophyletic.

@Sparhawk: sure, I think statements like "views all organisms as interrelated in a nested set of monophyletic groups (clades)", are intended to make the more general claim that clades are the only groups used in formal classification and hence dinosaurs necessarily must be a clade if it's a classification at all. This is what cladists want us to believe, that there's no taxon to describe what you study and you should come out and call it "radishes, emus and spanners" or whatever ;-)

@SteveJessop Oops. I totally missed that quote. Good point.

A 2017 study suggests that Theropoda are not under Saurischia. Not that this detracts from your answer at all, but it is interesting :)

@M.M A lot of people disagree with that study.

to further blow your mind, flight likely evolved at least twice in dinosauria, with sort of bat like wings in the Yi lineage and feathered wings in the bird lineage.

In addition to kmm's excellent answer, I'd like to present the xkcd point of view.

By any reasonable definition, T. Rex is more closely related to sparrows than to Stegosaurus.

Separation by time
Phylogenetic distance
Physical similarity

Birds aren't descended from dinosaurs, they are dinosaurs.
Which means the fastest animal alive today is a small carnivorous dinosaur, Falco Peregrinus.
It preys mainly on other dinosaurs, which it strikes and kills in midair with its claws.
This is a good world.

I'm not an expert, but I think that you have to be specific about the flying animals to which you are referring. Pterosaurs are not classed as dinosaurs, whereas modern birds are descended from theropod dinosaurs which is where feathers appeared.

I don’t rightly know what to make of it, but there seems to be some evidence for feather-like structures on non-theropod dinosaurs.

Asides from flight-capable modern birds and their early ancestors1, there are several other therapod dinosaurs which palaeontologists suspect were capable of flight, "but in a manner substantially different from that of modern birds":
Dromaeosaurids

Image
Dinosaur
Source

Microraptor
Scapular orientation in theropods and basal birds, and the origin of flapping flight, Acta Palaeontol

Changyuraptor
A new raptorial dinosaur with exceptionally long feathering provides insights into dromaeosaurid flight performance, Nature Communications

Sinornithosaurus
Feathered coelurosaurs from China: new light on the arboreal origin of avian flight, Feathered dragons

Deinonychus (juveniles)
Morphological Variations within the Ontogeny of Deinonychus antirrhopus (Theropoda, Dromaeosauridae), PLoS ONE

Rahonavis
Glorified Dinosaurs: The Origin and Early Evolution of Birds, Sydney  Gravity-defying Behaviors: Identifying Models for Protoaves, American Zoologist  Avian ancestors. A review of the phylogenetic relationships of the theropods Unenlagiidae, Microraptoria, Anchiornis and Scansoriopterygidae, SpringerBriefs in Earth System Sciences  The Theropod Ancestry of Birds: New Evidence from the Late Cretaceous of Madagascar, Science

Zhenyuanlong
A large, short-armed, winged dromaeosaurid (Dinosauria: Theropoda) from the Early Cretaceous of China and its implications for feather evolution, Scientific Reports

Troodontids

Image
Dinosaur
Source

Jianianhualong (not guaranteed)
"Barb geometry of asymmetrical feathers reveals a transitional morphology in the evolution of avian flight", Proceedings of the Royal Society of London B: Biological Sciences

Paraves (basal)

Image
Dinosaur
Source

Anchiornis (possibly juveniles)
*The wings before the bird: an evaluation of flapping-based locomotory hypotheses in bird antecedents, PeerJ

Scansoriopterygidae
And interestingly, not using feathered wings but membranous ones similar to bats or pterosaurs:

Image
Dinosaur
Source

Yi qi
A bizarre Jurassic maniraptoran theropod with preserved evidence of membranous wings, Nature

Ambopteryx longibrachium
A new Jurassic scansoriopterygid and the loss of membranous wings in therapod dinosaurs, Nature (2019)

Sources:
 • 1. A Jurassic avialan dinosaur from China resolves the early phylogenetic history of birds, Nature
 • Wing bone geometry reveals active flight in Archaeopteryx, Nature Communications
 • The wings before the bird: an evaluation of flapping-based locomotory hypotheses in bird antecedents., PeerJ
  Note: flight in Anchiornis only suspected of being possible in juveniles

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Is fluoride toxic, and how worried should I be about it?
A recent flurry of "fluoride is bad!" posts are appearing on my social network news feeds.  Usually I can simply ignore them after a brief look, but this one, stemming from a recent article in The Lancet, isn't easy enough for me to understand and apply or ignore.
The posts link to a March, 2014 article, Neurobehavioural effects of developmental toxicity, from The Lancet Neurology, Volume 13, Issue 3, which has the summary (emphasis added):

Neurodevelopmental disabilities, including autism, attention-deficit hyperactivity disorder, dyslexia, and other cognitive impairments, affect millions of children worldwide, and some diagnoses seem to be increasing in frequency. Industrial chemicals that injure the developing brain are among the known causes for this rise in prevalence. In 2006, we did a systematic review and identified five industrial chemicals as developmental neurotoxicants: lead, methylmercury, polychlorinated biphenyls, arsenic, and toluene. Since 2006, epidemiological studies have documented six additional developmental neurotoxicants—manganese, fluoride, chlorpyrifos, dichlorodiphenyltrichloroethane, tetrachloroethylene, and the polybrominated diphenyl ethers. We postulate that even more neurotoxicants remain undiscovered. To control the pandemic of developmental neurotoxicity, we propose a global prevention strategy. Untested chemicals should not be presumed to be safe to brain development, and chemicals in existing use and all new chemicals must therefore be tested for developmental neurotoxicity. To coordinate these efforts and to accelerate translation of science into prevention, we propose the urgent formation of a new international clearinghouse.

I don't have full access to the article, so I can't refer to the epidemiological study it says shows fluoride to be a developmental neurotoxicant.

What is a developmental neurotoxicant?
How strong is the research that claims fluoride is a developmental neurotoxicant?
What relationship, if any, does this report or research have with typical fluoride compounds used in US water treatment at the levels typically present in US water (sodium fluoride, fluorosilicic acid, or sodium fluorosilicate at 0.7 mg/L)?

The PDF of the paper can be found here. I'll have a look at it later and write an answer about it.

The paper references the following paper regarding the fluoride meta-analysis: Choi AL, Sun G, Zhang Y, Grandjean P. Developmental ﬂ uoride
neurotoxicity: a systematic review and meta-analysis.
Environ Health Perspect 2012; 120: 1362–68. This appears to be available here: http://ehp.niehs.nih.gov/1104912/ Thanks for reviewing this!

I don't really understand your third question.

@Chris I should probably rewrite that.  Just because fluoride may be considered toxic doesn't mean that any or all of the compounds used deliver effective levels of fluoride to the brain, so I'm asking if this information about fluoride toxicity applies to fluoride as it is currently used in our water systems.

Well, that is the question. The Choi paper does its meta-analysis on research which has been conducted on water fluorine levels. So this is not unimportant.

I don't care about additional reputation. If my answer doesn't fit your question, there is no need to accept it. You can also add some points which are not covered and I will probably try to answer them. I only remove obsolete comments.

First of all: Yes, fluoride is toxic, but the toxicity depends largely on the form (soluble vs. unsoluble, which fluoride salt etc.) occurs. It also depends on the environment since insoluble salts which are subjected to strong acids can release fluorine ions.
The certain toxic dose for adults is 32-64mg/kg body weight, a 75kg adult needs to take up between 2,4 and 4,8 grams of fluoride ions (for sodium fluoride this would be between 5,3 and 10,6 gr of the salt). For children this is about 5mg/kg body weight.
For the water the added dose of fluorine is much lower, somewhere between 0,7 and 1.2 mg/l. Other sources of fluroride are food (especially sea food) and also black tea.
The toxicity of fluoride is mediated by different ways: First it forms an insoluble salt with calcium in the cells, effectively causing hypocalcemia. Calcium is an important second messenger in different signal transduction pathways as well as highly important for the functioning of nerve cells (which also explains why it is neurotoxic in the development of nerve and brain cells). It also causes the inhibition of a number of different enzymes as enolase (disturbs the glycolysis) but also phosphatases and katalase. For all of this have a look into the Wikipedia if you want to know more details.
About the paper: It is a review of published research articles which sums up the situation in this field. The paper mentions fluoride only twice: Once on the abstract and once in a table about newly identified developmental neurotoxins (table 2 to be precise). It references only one meta-analysis on this topic.
The cited meta-analysis ("Developmental fluoride neurotoxicity: a systematic review and meta-analysis") which did a statistical meta-analysis of published papers and their data. They find a significant relation between the fluoride content of the drinking water and the IQ of the children.
However this is not undisputed (to say it mildly), since while a finding can be statistically significant, it doesn't necessarily mean that there is clinical importance. The other important point which @Doctor Whom mentioned is that a correlation doesn't imply a causation. So even if there seems to be a correlation between two things, they are not necessarily connected (see the famous example of storchs and birth rates).
This paper ("Developmental fluoride neurotoxicity: clinical importance versus statistical significance.") is published as a comment on the original paper and claims exactly this. They say the the mean difference in IQ is about 7 points, which is not of clinical importance. Another paper critizes the relatively low quality of the original papers used for the study ("Fluoride and children's IQ.").
They also mention a low consensus about what is a high concentration of fluoride in the drinking water and also show the very wide variation of the fluoride concentration in the original studies. The highest concentrations mentioned are around 10mg/l which is about 10x the concentration used for adding fluoride to the water. Even if we take in account that children are more sensitive to fluoride and also need lower fluoride concentrations to cuse some developmental damages (below the fatal concentration) this would still add up to quite absurd amounts of water they have to drink.
Regarding your questions:

A developmental neurotoxin is a substance which interferes with developing neurons or nerve cells. It either inhibits their growth completely or at least impairs the cells.
Given on the articles I found (and cited above) I would say that fluoride is a developmental neurotoxin. Nevertheless it seems to me that it is not very strong in this context as the current studies are contradictory. Thinking about the amounts of fluoride present in water (even if the concentration is much higher than recommended) makes me doubt if this is really the causative agent.

Well written, Chris.  I would recommend the addition of two points.  One, to the "significance" discussion, the point that correlation does not infer causality.  That study had a strong likelihood for bias, as there are MANY regional factors beyond yes/no fluoridated water that could influence this marginal difference in IQ results.  Secondly, to the final point (#2), I would comment on the issue of dose.

Good points, thank you for mentioning. I added them.

7 IQ points is rather significant - 10 points is supposed to be one standard deviation.  Do you mean that the IQ difference was not statistically significant?

The original authors say that 7 IQ points difference is statistical significant. We are less than 1 sigma away from the mean here.


text:
Trimming of tRNA precursors
From Molecular Biology of the Cell (4th edition) by Bruce Alberts et al. (Chp 6, Pg 338) :

Both bacterial and eucaryotic tRNAs are typically synthesized as
  larger precursor tRNAs, and these are then trimmed to produce the
  mature tRNA. In addition, some tRNA precursors (from both bacteria and
  eucaryotes) contain introns that must be spliced out.

What's the difference between the two statements (and between trimming and splicing) ?

Trimming = removing RNA sequences from one end.

Splicing = removing introns and joining exons back together.


text:
What's the biggest obligate anaerobic organism discovered till now?
Beside many anaerobic single cell organisms, there are some annelid worms that are obligate anaerobic at least in their early development stages. Probably, due to low concentration levels in nature, some of the other respiration methods (like uranium or iron reduction) can limit the maximum size an organism will grow. Given the lower energy level extracted compared to the oxygen respiration, what size limits enforces the sulfate, sulfur or methanogenesis respiration? What's the biggest discovered organism, extinct or alive, that is obligate anaerobic?

There are three worms which have been found in the sediment of the mediterranean seafloor, which not only live without oxygen but also do not tolerate the exposure to oxygen. They belong to the metazoans, for more details see either the report (reference 1) or the original article (reference 2). They reach a size og about 1mm.
References:

Scientists discover first multicellular life that doesn't need
oxygen
The first metazoa living in permanently anoxic conditions


text:
Why isn't phosphorus or nitrogen a limiting nutrient for animals?
Nitrogen and Phosphorus are usually the limiting nutrient for plants, especially for algae.  Phosphorus is used for DNA, ATP and phospholipids, and Nitrogen is used for pretty much every protein a cell might want to produce.  That is, their need for biological processes is not tied specifically to photosynthesis: anything that lives is going to need them, pretty much for anything it might want to do.  It would make sense for them to be a limiting nutrient for almost anything that's trying to grow, plant or animal.
Yet for animals the limiting "nutrient" seems to always be energy, ie: food.  Why aren't animals limited by lack of nutrients in the same way that plants are?  Obviously animals need these nutrients, too.  Or to reverse the question, why do plants need so much more phosphorus/nitrogen than animals do?
My best guess is that an animal's digestion of plant material is relatively inefficient energy-wise but relatively efficient nutrient-wise.  So for an animal to eat enough food to have sufficient energy to survive, it's probably eaten more than enough Nitrogen and Phosphorus for its needs.  But I'm just guessing and I can't find any data that would back up that guess.

More a thought: I think it is because plants a bound to one place. They have to take up what the soil in which they grow contains. Animals on the other side do not have this limitation and as they either feed on plants (which then have these subtances in them) or other animals they do not have this problem. For a number of animals salts can be a problem though.

Nice thought, but not all plants are static.  Consider algae, which float in the oceans and get carried by currents.  They're not exactly swimming against the currents, but neither are the zooplankton which feed on them.  Yet I don't think zooplankton is directly nutrient limited in the same way algae clearly is.

Thats right. The question is if algae have this as limitations.

From wikipedia: "Freshwater algal blooms are the result of an excess of nutrients, particularly some phosphates" (http://en.wikipedia.org/wiki/Algal_bloom#Freshwater_algal_blooms).  So yes, algae are nutrient limited in the same way that terrestrial plants are.

Phosphorus
Your suggestion that if we are meeting our calorific requirement we will be getting enough is true for phosphorus.
Most foods contain lots of phosphorus. The maximum dietary requirement occurs during adolescent growth, estimated at 1250 mg per day. Assuming a calorie intake of 2500 kcal we can calculate a 2500 kcal equivalent phosphorus content for various foods:
skimmed milk contains 7,400 mg phosphorus per 2500 kcal
roasted chicken breast contains 7,500 mg phosphorus per 2500 kcal
cooked white rice contains 3840 mg per 2500 kcal
(Calculations are based upon values obtained via this site.)
Nitrogen
Our requirement for nitrogen is met by our protein intake: inadequate protein intake manifests as kwashiorkor which is essentially due to a dietary deficiency of essential amino acids. In other words, the only way to achieve a nitrogen-deficient diet is to not eat protein, and this would not be alleviated by any inorganic source of nitrogen, even if we could consume enough of such a N source.

Thanks!  Numbers always help actually determine what's going on :)  I suppose fundamentally it's a consequence of thermodynamics: matter is conserved during protein synthesis and digestion, but energy is not.  You can't disassemble a protein and get back all (or even most) of the energy required to build it.  But you can get back most of the amino acids used to build it.

As you already mentioned N and P are major components of important biomolecules. In Sterner & Elser, ecological Stoichiometry, 2002, fig 2.2 demonstrates the percentage of N and P in biomolecules. As you can imagine these biomolecules are important and require forms of P and N to be consumed for an organism to function.
Animals are limited by nutrients such as Nitrogen (N) and Phosphorus (P). From an ecological perspective, many aspects of an organism’s life and subsequently their evolution are affected by nutrient limitation. For example, the brood mass of an aquatic snail can be limited by a low amount of dietary P (Tibbets et al., Phosphorus-mediated changes in life history traits of the invasive New Zealand mudsnail (Potamopyrgus antipodarum) 2010). Another example is a riparian crustacean growth limited by a low P treatment (Danger et al., Phosphorus content in detritus controls life-history traits of a detritivore, 2013).
There is even a ratio of the required elements for animals to survive/grow in an environment, threshold elemental ratio. The threshold elemental ratio is often a carbon to nutrient (i.e. N or P) ratio; different clades/species have differing ratios (see figure 2 in Frost et al., Threshold elemental ratios of carbon and phosphorus in aquatic consumers, 2006).
Thinking about animals getting their energy from food is too simple.
Consider this easy example; we, humans, require protein to properly function; a 150 lb adult – who requires about 55 grams of protein a day (these are estimates, I am not an nutritionist). That person can eat about one chicken breast and fulfill that daily requirement or they can eat 25 ounces of potato chips to achieve that. If they only have potato chips available then they have an N limiting diet. Of course, plants and animal have different requirements for energy, but animals are limited by nutrients just as plants are.
https://www.jstor.org/stable/40864578
https://besjournals.onlinelibrary.wiley.com/doi/10.1111/1365-2435.12079?__cf_chl_jschl_tk__=pmd_j7iq6cCQINSFmxVZ.Cvds9jOQmS2OHgpvYjw1t.gTU8-1635260689-0-gqNtZGzNAjujcnBszQvR
https://onlinelibrary.wiley.com/doi/full/10.1111/j.1461-0248.2006.00919.x?__cf_chl_jschl_tk__=pmd_g7eFplMHGUViCzJfN9vFQvHm4vmZabdJLJLo180WrCc-1635260692-0-gqNtZGzNAlCjcnBszQyl

Welcome to Biology.SE. We're looking for long answers that provide some explanation and context. Don't just give a one-line answer; explain why your answer is right. In addition, please include the complete reference information since links can break. One easy way to get that information is to search for the paper on Google Scholar and click on the ‟ symbol to get reference information. This is a good example of how to format references. Answers that don't include explanations may be removed.

Thank you that is much better!  ——— If possible, it would be helpful if you added links to online versions of the sources you mention — that will make it easier for other users to follow up.

Off the top of my head:

Plants are photosynthetic so have unlimited access to energy. If an animal had unlimited access to energy it would likely have Nitrogen or Phosphorous or something else as the limiting nutrient.
Animals eat plants and/or each other. Whatever animals eat will have to a greater or lesser degree sufficient protein/fat/nucleic acids etc to satisfy minimum nutritional requirements. As noted in Chris' comment there can be some species-specific limitations like availability of salt in a herbivore diet, or the human requirement of an external source of vitamin C.

Light access can very easily be a limiting agent, though.  Mature forest floors, for instance, have little undergrowth for exactly this reason.  In situations where there's an algae bloom, the top of the water is essentially opaque.  Yet in most ecosystems (certainly temperate/tropical oceans) the total biomass production of producers is not limited by light but by nutrients.  Likewise if animals were energy efficient but nutrient inefficient during digestion, it's conceivable that nutrients would be more limiting than energy.


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Why do bananas turn black after some time?
Why do bananas turn black after some time? Please don't just give hypotheses but concrete references to experiments

Banana skin consists of plant cells and cellular tissue. This tissue contains phenolic compounds. On getting old, the cell membranes of the banana get weak. When the membranes weaken, the phenolic compounds mix with polyphenol oxidase (an enzyme present in the cells cytoplasm). As a result of this interaction, the phelonic compounds oxidize and produce a brown compound called melanin which results in the colour of the peel turning black. Also, the green skin of banana contains a gaseous plant hormone, ethylene, which diffuses into the fruit and hastens the process of ripening. It is yellow when the fruit is ripe and turns black with the production of more and more ethylene.

Good one potterbond007

@speedoheck Thx. I added some more details btw.


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Does a walk after a meal help with digestion?
I am a bit confused with the notion that "walking after meals helps you in digestion ",
Some say that it helps, whereas others oppose it. Can someone come up with a valid explanation for this?

This seems like a job for Myth Busters :D

apparently walking helps in the movement of food into the stomach and improves digestion. Also helps in decreasing blood sugar after meals, which decreases cardiovascular risk and potential signal diabetes by helping muscles absorb glucose in the blood. Here is the link to a study done comparing the results of walking after food and after a drink. Also a study was conducted where when people with Type 2 diabetes took a 20 minute walk just 15 minutes after eating, their post-meal blood sugar levels were lower than if they had walked before dinner or not walked at all. Here is the link to another similar study.

Well it depends what you mean by helping digestion.
This answer in skeptics may shade some light:

a walk after my lunch [is] a healthy habit that helps with digestion.

Walking may be a healthy habit but it does not specifically assist digestion.

Digestion is a process which takes place in resting conditions. Exercise is characterised by a shift in blood flow away from the gastrointestinal (GI) tract towards the active muscle and the lungs.

From: Is the gut an athletic organ? Digestion, absorption, and exercise. [Sports Med. 1993] - PubMed - NCBI
So it's seems walking help sugar level (but this is independent to having eaten just before) but seems to not be beneficial to the digestion (in particular stomach contractions ― nutrient absorption will only start in general two hours after your meal, once the food leave the stomac)


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Exercise vs stimulants, which is more effective for promoting concentration?
Stimulants are the first choice for treating ADHD. But we also know that exercise helps to improve concentration.
We know that both stimulants and exercise increase bloodflow to muscles and to the brain by activating the sympathetic nervous system. Is this is the MAIN cause of the effect of improved concentration, rather than, say, specific activation of parts of the brain responsible for learning or planning or something similar?
What I'm asking is, do drugs and exercise have different effects on the brain, what are the differences, and what are the consequences of these differences on concentration and learning? Which is more effective for promoting concentration and why?

exercise stimulates brain regions that are involved in memory function to release a chemical called brain-derived neurotrophic factor (BDNF) which is a protein that helps in the survival of neurons and promotes the growth of new neurons. BDNF rewires memory circuits so they work better.
Memory enhancers or smart drugs or Nootropics as they are called help in improving the efficiency of neurotransmitters and its associated receptors in cognitive function. Three systems that are stimulated by these drugs which I could find are:
1) Cholineric System
2) Glutamatergic System
3) Dopaminergic & Serotonergic Systems
You can read about about them here along with links to published articles on their effects. Details of different nootropic drugs are mentioned in this article along with their effects.
Of course naturally improving concentration would be the way to go considering the hazards of long term use of drugs. Some links to the side effects are this and this

Thanks but can you give a quantitative comparison for example, by how much does exercise improve working memory capacity compared to modafinil? By cholineric do you mean cholinergic? I'd vote you up if I could.

Cholinergic is the abbreviated term for acetylcholine which is in fact the primary component of the cholineric system so you can say that both of them are basically the same thing.. Sadly, as of now, I cant find a published paper on comparing smart drugs with exercise. I would suggest you read papers on how much exercise improves cognitive function like this one (http://dev.europepmc.org/abstract/MED/17414812/reload=2;jsessionid=KueHPX5d2GFw4mgwWuGZ.0), read a paper on how modafinil affects cognitive function (http://link.springer.com/article/10.1007/s00213-002-1250-8) and form a comparision.


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Neuronal Architecture of the Brain
To what extent do brains (e.g. of humans) contain recurrent  connections?
I am studying artificial neuronal networks and frequently encountered the statement, that recurrent neural networks are closer to biological neuronal networks than for example feed forward networks. But I didn't find information on the question if feed forward or recurrent architectures dominate the brain architecture.

The recurrent patterns of connections in a network are known as network motifs.
You can check this paper out. They have identified common network motifs in different types of real networks including neural networks (of C.elegans though).
Apart from feed forward loops, bi-fan is also a common network motif in neural networks.
Perhaps the connectome project has data for human brain which you can analyze for identifying network motifs. You would have to request for the data, though.

Ok, let's talk about mammalian neocortex rather than about the entire central nervous system.
The vast majority of synapses within the cortex are formed between neurons within the same cortical area (Binzegger et al 2004). Although most of these synapses will not be self-connections (from a single neuron back to itself), they are recurrent in the sense that there is a high degree of interconnectivity within a cortical area. In visual cortex, connections within the superficial layers of cortex (layer 2/3 <-> layer 2/3) make up around 70% of all excitatory synapses in visual cortex!
In contrast, the "feed-forward" pathway into visual cortex makes up less than 1% of the excitatory synapses in visual cortex (Costa & Martin 2011).
If you change your scope to look only at inter-cortical-regional projections, then there is comparatively less recurrence (i.e. strong bi-directional connections between two cortical areas), although it still exists. Connections between cortical areas seem to be correlated with physical distance across the cortex (Vezoli et al. 2004). Connections between adjacent areas (V1 and V2, for example) are strong in both directions, and appear to project to similar cortical laminae in both directions. In contrast, projections over longer distances are comparatively weaker, and target different cortical laminae in either direction.


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How does a biologist decide when she has enough results to publish a paper?
Biology is so exciting! Answering a question leads to  thousand more questions! There is no limit to how much one kind find out about a phenomena…
So I have always wondered how someone can decide that it is time to publish some fixed amount of research they have done. How do biologists decide when to publish a paper? How do biologists know that results are sufficient enough for a publication?

haha... when reviewer is satisfied :P

@WYSIWYG And I believe there are  money constraints too!

not much.. just advertising constraints

@WYSIWYG By money, I mean funding ... What exactly is advertising ?

Reviewers/referees are indeed the gatekeepers and they hold the key and they can make it quite difficult to publish a good work! Money is most certainly a constraint for the scientists that have to pay for the paper especially to make it open-access although many funding bodies these days pay for the publication costs! The journals however take advantage and they charge astronomical amounts for advertising and only allow the highest bidder to advertise as they self impose a space limit, hence they become choosy over it, which becomes a constraint on their part.

I agree with all the responses so far; however I thought I should add that to publish a paper in a decent internationally peer-reviwed journal, more often than not, a paper has to tell a story, ideally a novel story and not just the same data that has been published before or at least address an old question in a new manner, that provides a fresh insight into the field or the question. A publication can't just be a bunch of random small and unrelated questions and experiments, at least not in any peer-reviewed journal. The key to a successful paper is that it should have ideally one message, which can be identified in the title, since believe it or not thats how most scientists vet whether a paper (abstract/summary) worth looking at or not. So as correctly mentioned, you identify a gap in the knowledge and attempt to address it having considered what is know about it so far, if any. Writing a paper follows a global formula, which has been elaborated in Chris response. Hence the key is that the paper has to tell ideally one story and the experiments used to address it has to make a logical progression to address the question. So you can't just jump from a small preliminary experiment which is questionable in its reliability into a large scale experiment. Some times you have to make the leap of "faith" in your experimentations and just do a certain experiment but the chances are your previous experiments have given you an indication as to whether its going to work or not. Be very mindful that most of the time the order in which you do your experiments is not the order in which you put them in the paper so what usually happens is that you have a central question, you do a bunch of experiments to address it and then you shuffle them around to tell the story in the most concise way and again the key word here is story.
Now not only a paper has to tell a concise story but it has to be of general interest to the scientific community, specially in high impact journals. You probably know a recent paper about STAP cell lines that got into Nature and attracted world-wide attention in which the authors described how exposing the cells to stimulus/stressors such as acid or pressure can turn it pluripotent, which the media linked to personalised treatments. Now I don't want to get into all the controversy that followed it but its just to make the point that a research like this is not only of interest to the scientific community but also the public hence it got published in a highly respectable journal. Now whether thats the right thing for scientists to do and send important research to the top journals, which is hard to access by many countries is a whole different argument but I hope you can begin to see publishing a paper in a journal is not only related to its scientific merits but also to what extent it is of interest to the general or scientific community and what story is it telling or implying (to put it a bit more crudely). Now not every paper makes it to Nature and most of the time publications are highly specialised work which not everyone on the planet might be interested in them but they still follow the points I talked about.
hope this helps!

When you do science you start with a question or a hypothesis. How is Gene A regulated? Or "does hormone B have an effect on the immune system". Or whatever.
Then you start by thinking how you can prove or disprove your question/hypothesis with experiments. You then do your experiments and see if they are enough to prove your question. It often happens that you have to do additional experiments to cover side-questions which appear during the work or to exclude some side-effects which may also be important. If you have done all this (with replicates) and looked from different angles on your problem, then you can start writing an article.
This includes some introduction from the literature and a classification of your results into the things already known. If you make strong claims, then you will need a lot of arguments (=results) to prove your point. It is quite hard to argue against "common knowledge".
The question of how much research is enough is quite philosophical, since you usually don't "finish" a topic. You look only at certain aspects from a certain angle. This can be quite different for other researchers.

"..since you usually don't "finish" a topic".. I just love this line !

It is really like this. Working on one question often throws up two or three new related questions. That's what makes science to exciting. Of course you need quite some tolerance to frustration, as not everything works as intended or as it should.

It's all about "Is this paper interesting enough to get published?"  And people just get a feel for that when they are reading papers all the time, and submitting papers frequently.  For instance, maybe publicizing a big cool dataset was useful enough a few years ago to be published as is, but now, you might need a good finding that you found from that dataset, and followed up on, before the paper will be considered by your journal of choice.

Thats right. Standards change and people get used to some findings if it is shown the 10th time.


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Do axon grows after cutting/damaging of some of its part?
Do axon grows after cutting of some of its part to near original place?
Do axon restores after local damaging of some of its part?
I take https://class.coursera.org/neurobio-001/ classes and learn that axons are very long. So it is interesting if they able to restore connection to far places parts of body...
UPDATE

https://en.wikipedia.org/wiki/Axon_guidance

yes they do.. I'll post a long answer when i get time.. meanwhile you can look for Axonal regeneration. (A lot of experiments have been performed on regeneration of sciatic nerve and DRG neurons)

Well look at this picture from Junqueira histology book:

In an injured or cut peripheral nerve, segments of axons distal to the injury lose their support from the cell bodies and degenerate completely. The proximal segments can
regenerate from their cut ends after a delay. The main changes that take place in an injured nerve fiber are shown in the picture above.
In the nerve segment distal to the injury the axon and myelin, but not the connective tissue, degenerate completely and are removed by macrophages. While these
regressive changes take place, Schwann cells proliferate within the connective tissue sleeve, giving rise to rows of cells that serve as guides for the sprouting axons
formed during the reparative phase.
The axon grows at the rate of 0.5–3 mm/day


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What is this snake
I took a picture of this snake in Switzerland (Geneva Area):

It looks to be an adder but cannot be sure about which species.
In Switzerland we have two kinds of adder:

Vipera berus
Vipera aspis

For me it looks like a Vipera berus, but all the images I saw from both species (and the variations) I cannot be sure.

amazing that you stood long enough to take a picture of an unknown snake.. I would be running my lungs out..

I was at reasonable distance and with a 70-200mm it helps. But yes I recognised an adder (lightly venomous) but I know they are quiet as long you don't go next to them.

An generally speaking, snakes in Europe tends to escape before attacking

I'm not an expert so don't feel qualified to answer, but a bit of reading suggests to me that it is Vipera aspis because the head looks rather broad and there is no clear dorsal zigzag.

I think it's an Vipera Aspis.
from wikipedia:

The dorsal markings vary strongly, but only rarely take the form of a
  clear zigzag, as in V. berus.

Your Snake in Maximum RGB Color (Broken ZigZag)

Vipera Aspis from Google Image

Thanks for your answer. After searching about the repartition of both snakes around Geneva, I found these maps that confirm vipera berus is not present in Geneva area as vipera aspis is


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Fatty Acid Synthesis

I have a problem in my reasoning on the fatty acid synthesis in the human body.
In the synthesis process you have this homodimer.
So the synthesis starts with the transfer of a acetyl group from acetyl-CoA to the sulfhydrylgroup of the condensing enzyme (CE) with help of the acetyltransferase enzyme (AT) and this on 1 of the 2 monomers.
At the same time a malonyl group from malonyl-CoA is transfered to the sulfhydryl terminus of phosphopantotheine from the ACP, and this on the other monomer and with help of the malonyltransferase (MT) enzyme.
AND HERE THE PROBLEM STARTS
The acetyl residue will be condensing with the malonylACP and at the same time there will be a decarboxylation (CO2 goes off) and CE goes off from acetyl. At the end acetoacetyl-ACP is formed. So if I got it right; the acetyl residue is being 'cut off' from the CE from the first monomere and binds to the malonylACP on the other monomere. Right?
And after that the acetoacetyl-ACP will be swept back to the other monomer (to the reduction part), is this also right?
Then the reduction-dehydration-reduction steps are happening and at the end of the road you will get butyryl-ACP which will cut off from the ACP and migrate on the same monomer to the cysteine residue at the condensing enzyme (CE) (= translocation).
And after that you can start a new condensation-reduction-translocation cycle and go on until you end up at palmitoyl-ACP.
So the actual question is; is my reasoning right about how the product is going from one monomer to the other several times?
In my book it's a pretty messy explanation and so I want to be sure I'm right.
I hope somebody can help me out =)
Greetings

It might be best if you draw a diagram of your proposed pathway and post it in your question as an edit so that it's easier to follow through your question.

I have a few pictures about it I can post eventually. I will try to fix that up in a few minutes. If that doesn't help I will draw it more in detail tomorrow and post =)

I'm afraid this picture is too small... I'll make another one tomorrow.

The textbook descriptions of fatty acid synthesis can be confusing because although the underlying chemistry of the process is universal, the way that it is organised is different in the systems that have been characterised, which include E. coli, yeast and vertebrates.
In vertebrates:
The fatty acid synthase is a dimer of identical multifunctional single polypeptides. The synthesis process involves two -SH groups: one is the terminal group of the pantothenate of the acyl carrier protein domain (Pan-SH) and the other is an -SH group of the condensing enzyme (CE-SH).
For the first condensation step the initiating acetyl group is attached to the CE-SH of one monomer and the incoming unit (malonyl CoA) is attached to the Pan-SH of the other monomer.
The condensation reaction between these two results in the new elongated unit being attached to the Pan-SH. This unit then goes through the reductase/dehydratase/reductase steps to form the new acyl CoA which is finally transferred to an CE-SH group, opening up the Pan-SH for the next incoming malonyl CoA.
This will happen repeatedly in each cycle of the process. Obviously since each monomer has both -SH groups a single fatty acid synthase dimer can be engaged in two elongations at the same time, but these will always include a transfer. It is thought that the initiating acetyl group comes in via the Pan-SH group.
You say:

And after that the acetoacetylACP will be swept back to the other monomere (to the reduction part), is this also right?
Then the reduction-dehydration-reduction steps are happening and at the end of the road you will get butyrylACP which will cut off from the ACP and migrate on the same monomere to the cysteïnresidu at the condensing enzyme (CE) (= translocation).

The diagram that you included clearly shows that the acetoacetyl group is formed via the reduction-dehydration-reduction steps on the same Pan-SH where its precursor was formed by condensation. Only then is it transferred to the CE-SH group. The diagram also indicates that the acetoacetyl group is transferred to the CE-SH of the same monomer. This implies that a growing chain never transfers from one monomer to the other. I have seen other sources which seem to suggest that this step does involve a transfer between monomers.
In fact it would appear from the discussion on the WP page for fatty acid synthase that this is an unresolved issue - see for example:
Joshi et al. (2003) Engineering of an Active Animal Fatty Acid Synthase Dimer with Only One Competent Subunit Chemistry & Biology 10:169 - 173

Abstract
Animal fatty acid synthases are large polypeptides containing seven functional domains that are active only in the dimeric form. Inactivity of the monomeric form has long been attributed to the obligatory participation of domains from both subunits in catalysis of substrate loading and condensation reactions. However, we have engineered a fatty acid synthase containing one wild-type subunit and one subunit compromised by mutations in all seven functional domains that is active in fatty acid synthesis. This finding indicates that a single subunit, in the context of a dimer, is able to catalyze the entire biosynthetic pathway and suggests that, in the natural complex, each of the two subunits forms a scaffold that optimizes the conformation of the companion subunit.

So if I got it right, everything takes place on 1 monomere? And the translocation step is also on the same monomere?

But why does my book tell me then that the synthesis starts with the transfer of a acetylgroup from acetylCoA to the sulfhydrylgroup of the condensing enzyme (CE) with help of the acetyltransferase enzyme (AT) and this on 1 of the 2 monomeres and that at the same time a malonylgroup from malonylCoA is transfered to the sulfhydrylterminus of fosfopantetheïn from the ACP, and this on the other monomere and with help of the malonyltransferase (MT) enzyme?        It clearly tells me that it occurs on the 2 monomeres... So what is the conclusion then? =S

As I tried to hint at, I don't think anyone really knows. The cited paper concludes that a single monomer can do everything as long as it is in a dimer. But of course that doesn't mean that's the way things normally happen. It's clear however that the prevailing textbook version does describe the cooperation of two monomers, as shown in your diagram 3.

Okay I understand what you say =) Thank you very much. It makes sense now. I will follow the teacher her book that describes the cooperation of two monomers. Because if I would say like 'nobody really knows' she will be like what are you trying to say? Haha =P And her diagrams show that there is cooperation of two monomers as you say so then I'll have to explain it that way on the exam too (if she asks). Thank you very much!


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Is there a superterm combining "animal line" and "cell line" in disease models?
Biologists researching diseases will frequently use animal models. The way I understand it, there are species of animals, such as "mouse", and lines of mice, such as Black six, NMRI or also genetically engineered lines like B6.Cg-Tg(CAG-cre/Esr1*)5Amc/J. But they also sometimes take cell lines such as HeLa and transplant them into animals, or treat them in vitro.
Is there a word which covers both "animal line" and "cell line" and is in widespread use? I thought that "model organism" would be a good way to express it, but a biologist working in disease models told me that when she hears that, she only thinks of animals, never of cell lines. She wasn't able to come up with a term which covers both. Her best try was "experimental system", but she conceded that, if used out of context, no biologist would recognize that it is about animal and cell lines.

'disease models' sounds pretty good actually.  maybe 'model system'

Is there any relevance in discerning or not discerning cell line and animal line apart from terminology? If you combine a transplant with a host - and there is no rejection - this might still not be an "animal line", as there are - in spite of non rejection of transplant  - are different, allogenic MHC cells, in that animal line. It is not a "cell line" either. You are not asking about combining allogenic cells  i.e. you are not asking for a term that denotes transplanting cell line into animal line?

There is no super-term that I can think of but you could say genetically modified (mouse) samples/specimens?

No, because not all mice or cells are genetically modified. The Black Six and NMRI I listed above are examples of wildtype mice, and they are still lab lines.


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Definition of Sexual Selection?
How do you define Sexual Selection (SS)?
(One might want to subdivide SS into intra- and inter- SS to answer)

Is SS clearly different from Natural Selection (NS)?
Is SS nested within NS or are NS and SS two different and (anti- or not) parallel processes?
Is the evolutionary processes due to sexual conflict are SS processes?

Sexual conflict arises when the reproductive interests of males and females are not aligned, generating sex-specific selection on shared traits such as mating rate (from this article)

(One may want to subdivise sexual conflict into intralocus and interloci conlict to answer)

Are the evolutionary processes of sexually antagonist genes SS processes?

Sexually antagonist genes are those genes where one allele is favored in females while another allele is favored in males (my own definition)

Can SS be accurately defined or is there a continuum of kinds or processes from complete SS processes to complete NS processes?

Stated differently, is SS defined as the color orange (it is a continum) or like a square and a rtiangle (no continuum)
(I talk here about kinds of processes, not about the relative importance of SS and NS in explaining the evolutionary dynamic of a trait or a locus)

If you define SS based on some other concepts that might be subject to various definition, please define this other concept. For example, if one says "SS occurs on a trait whenever this trait undergoes directional selection due to sexual competition", he will necessarily need to define "sexual competition" as well.

Below is a list of scenarios where you can answer by yes or no whether SS is involved in the evolution of some feature. In all of these scenarios, we'll consider cases where the males have to find a mate…

The males need good ears to find the females before other males. Is SS involved in the adaptation of ears abilities?
The males need good flying abilities (supposing we talk about flying animals) to have access to females before another male. Is SS  involved in the adaptation to good flying abilities?
The males need good flying abilities  to have access to females although there is not much between male competition because the vast majority of females won't never be fertilized. Is SS is involved in the adaptation to good flying abilities?
The males need good flying abilities to be able to fly a long time without spending to much energy otherwise they will die before finding a female. Is SS is involved in the adaptation to good flying abilities?
The males need good flying abilities to be able to fly a long time without spending to much energy otherwise they will die before finding a female. There are quite a few females but there the competition is so rough to find a female that is still unmated Is SS is involved in the adaptation to good flying abilities?
The males need good camouflage because when they fly to find a mate they may get eaten by a predator and die before reproducing. Is SS is involved in the adaptation to good flying abilities?
The males need good camouflage because when they fly to find a mate they may get eaten by a predator and die before reproducing. Here the difference is that the predators are attracted to the spot if they can sense many males. So the presence of the other males influence the probability of finding a mate of a given male. Is SS is involved in the adaptation to good flying abilities?

It looks like there are a ton of questions in my post but they are so related to each other that it would be stupid to ask them separately. All these questions basically sums up to the first question: How do you define SS? I welcome some references to papers that offers interesting definitions of SS.

hey.. check this article out.. came just yesterday..

Is SS clearly different from Natural Selection (NS)?
Is SS nested within NS or are NS and SS two different and (anti- or not) parallel processes?

Darwin, in The Descent of Man, and Selection in Relation to Sex defined sexual selection as a type of selection that "depends on the advantage which certain individuals have over other individuals of the same sex and species, in exclusive relation to reproduction." Throughout, he distinguishes between natural and sexual selection. This suggests to me that Darwin thought of them as different processes.  A spot check of various evolutionary texts show the authors all using some variation of Darwin's definition.
In my opinion, the two are are clearly different but not necessarily separate. Both NS and SS affect fitness, a major component of the evolutionary process.  I tend to think of SS as nested within NS. NS affects fitness indirectly. Beneficial traits increase survivorship.  The longer individuals survive, the more reproductive opportunities they will have and fitness will, on average, increase. But, survivorship does not guarantee reproduction. Thus, I think natural selection acts indirectly on reproductive success.
SS operates directly on reproductive success because males selected by females will reproduce, increasing their fitness. Sex is, after all, a natural process. In my view, female choice is the "environment" of the male (as far as reproduction) so variation of male traits in the female choice "environment" differentially affects the fitness of the males. That is natural selection.

Is the evolutionary processes due to sexual conflict are SS processes?

Absolutely. Sexual selection ultimately arises because of a difference between genders of energy investment in gametes. Males produce lots of gametes and relatively little energetic cost. Females produce relatively few gametes with lots of energetic cost (think of tiny sperm vs large, yolk-filled eggs). It benefits males to mate with as many females as possible because, even if a mating produces no offspring, he lost very little of his energy investment. Females will be choosier because they can't afford to waste gametes. Thus, there is an inherent conflict of interest between males and females.

Are the evolutionary processes of sexually antagonist genes SS processes?
Sexually antagonist genes are those genes where one allele is favored in females while another allele is favored in males (my own definition)

Are these genes related exclusively to reproduction?  If so, then that would be consistent with the original concept of SS. However, sexually antagonistic genes are not necessarily the result of or a cause of SS.  For example, Rice (1992) argued that sexually antagonistic genes may explain the evolutionary reduction of recombination between primitive sex chromosomes.
Rice, W.R. 1992. Sexually antagonistic genes: Experimental evidence. Science 256: 1436-1439.

Can SS be accurately defined or is there a continuum of kinds or processes from complete SS processes to complete NS processes?

I think SS is accurately defined, but whether is is a type of NS or not is (I think) open for debate. As I described above, I think of SS as a particular type of NS, one that operates directly on reproductive success rather than indirectly.

Below is a list of scenarios where you can answer by yes or no whether SS is involved in the evolution of some feature. In all of these scenarios, we'll consider cases where the males have to find a mate…
The males need good ears to find the females before other males. Is SS involved in the adaptation of ears abilities?

Depends. Do males and females also use their ears for other purposes, such as detecting prey or predators?  Is hearing ability much greater in males than in females? Darwin specifically addresses such a scenario. (Last sentence of page 256, first part of page 257.)
I think these ideas play out for most of your scenarios. It depends on if the traits differ between the sexes (not specified in your scenarios) and the traits lead directly to increased male reproductive success. But I will address one more.

The males need good camouflage because when they fly to find a mate they may get eaten by a predator and die before reproducing. Here the difference is that the predators are attracted to the spot if they can sense many males. So the presence of the other males influence the probability of finding a mate of a given male. Is SS is involved in the adaptation to good flying abilities?

In this case, I would say not SS. The camoflage is necessary for survival, not direct reproductive success. This is natural selection.  Increasing the probability of finding a mate is not the same as guaranteed reproduction.