text:
Anaphase Microtubule Disassembly
Centromeres move toward the poles as the microtubules that connect them shorten. This shortening is due to the removal of tubulin subunits from the kinetochore ends of the microtubules.
I'm confused as to how the centromeres can be pulled closer to their respective poles while tubulin subunits are being removed. To me, this is similar to pulling an object by a rope while simultaneously cutting pieces of the rope out. How do the centromeres remain connected to the spindles while tubulin subunits are being removed?

I don't think the microtubules shorten. The disassembly of tubulin (dynamic catastrophe) happens from its + end which in this case is protected by the kinetochore proteins. The separation of chromatids, I guess, happens via a dynein (and in some cases kinesin) mediated movement.
The wikipedia article on kinetochore is quite detailed and you can have a look at it.

Sorry, I was unclear. I meant that the length of the microtubule spindle fibers shorten due to the removal of tubulin subunits.

yes.. but it does not happen thay way as I can recall. the removal of tubulin subunits happens from the + end which is now protected.

How exactly do the kinetochore proteins protect the + end?

In different species it's different - in some it's packman like ie disassembly from the + end but in some the microtubules are reeled in (from the centriole end)

I know this question was asked a very long time ago, but for future viewers, below is a useful snapshot taken from my Campbell's Biology Textbook. As you can see, the motor proteins are not located at the very "tip" of the microtubule, so they are still able to carry the chromosome to the pole while the tubulin subunits disassemble on the kinetochore end. For more about motor proteins, go here, to YouTube, or wikipedia.


text:
Theoretically, is domestication of (virtually) any animal possible?
Looking at ones that manage well alongside us human animals, such as dogs and cats, we see that this is possible for evolved, distant animals to have heritable, preferable traits around people. However, when especially looking at lions and the like, it doesn't seem to work out as well.
Some people have tigers as pets, but in general it is believed that they are more "wild" and not as tame and domesticated as other animals (such as dogs and cats).
Is it possible to selectively breed and enable any animal to be more like dogs and cats? Even sharks? Tigers? Alligators?
If domestication worked so well with dogs and cats, such as them living (for the most part) peacefully and well with people, wouldn't the process be beneficial for other animals so we could all live better side-by-side?
In short, can you theoretically get any animal to have heritable traits?

I understand your overall question, but your last question doesn't really fit in: all animals have heritable traits.

Domestication of animals was not performed so that we live better side by side but because they were beneficial for human needs so we domesticated them. Best example is dogs that were used as protection for live stocks. I'm no zoologist to respond to your question but so long as they have a nervous system that can learn, I don't see what not. even snails and drosophila can learn tasks such as maze solving but that doesn't necessarily domesticate them so i guess it depends on how developed their NS is and what you define as domestication.

have you heard of the 40 year long Russian experiment to tame foxes? Quite interesting. Have a look at it.

Maybe the first question is. Are dogs and cats domesticated because they are predisposed to domestication?

It depends somewhat how we define domesticated - I keep flies in a lab, just as a farmer keeps cows in a field, but is this the same as training a pet?

@Bez: But a lot of work had to be done on the ancestral wolf before it could become a reliable livestock guardian - and indeed, many dog breeds don't work as guards.  So what was the initial impetus?  One idea is that dogs basically domesticated themselves, having discovered that there were advantages to living with humans.  Some would go so far as to suggest that dogs domesticated humans...

As the previous answers clarify, all organisms have heritable traits that may be manipulated through selective breeding. It is the pragmatics that can be prohibitively challenging. From an (zoo)archaeological point of view, few animals have actually been domesticated, and only recently in our species' history. The dog is an unusual case, perhaps domesticated 14,000 years ago; most domesticated animals only show skeletal changes within the last 10,000 years. Cats, compared to livestock's total dependence on humans, are 'barely' domesticated--they got used to humans while camping out in Egyptian storehouses where all the mice were, perhaps around 4,000 years ago, but even today a fluffy house cat will revert to a feral state if abandoned.
Many animals are behaviourally unsuitable for domestication. If an animal is dangerously aggressive, for example, they cannot be penned and isolated--so the many controlled generations it takes to reduce their baseline aggression cannot occur. Humans also tend to co-opt pre-existing social structures in a species, such as becoming the 'alpha' in a dog pack or the head 'ram' of a sheep herd. Species without a hierarchy or herd mentality are difficult to control and keep track of, and so do not lend themselves to human care.
You mentioned tigers in your question. Tigers have little to offer people (other than pelts), they're massive/aggressive, and they're jungle loners. You can't raise a herd of tigers; they'll kill each other and the survivor will kill you. That they're carnivores is also challenging, since a carnivore is much more expensive to feed than a bunch of grass-munching sheep. Altogether, there was never a situation in prehistory that would have turned tigers into giant house cats. House cats eat unwanted mice; tigers eat your cattle (and children). The occasional tiger 'pet' won't change that.
Domestication, outside of recent experiments (like the Russian foxes mentioned above), has always been a protracted, indirect process. People started interfering with animals that were already useful in some way(s). Dogs offer warmth, hunting aid, defence, transport, and (in a pinch) food. Alligators, tigers, and sharks are not useful enough to make the danger and cost of raising them worthwhile. Even if you did eventually produce a 'human-friendly' shark, there would still be a 'wild' population ready to eat you--and your complacent pet sharks, too!
For a very readable explanation, try the chapter on domestication in Jared Diamond's (1997) Guns, Germs, and Steel.

I understand the question as "can you get any animal to have heritable traits selected by humans?"
This definition of domestication implies that a population of animals can be bred for a sufficiently long period of time, so that humans can select hereditary traits that fit their needs. Humans could provide selective pressure that creates a new variety with different traits. So according to the laws of evolution, I would say it could theoretically be done for any living being.
But there may be species that could be reluctant to such a control, e.g. animals that we have difficulties to reproduce in captivity for whatever reasons (polar bears?), or isolate from their wild congeners (genetic isolation is a generally a pre-requisite to domestication). For them, domestication could take too much effort or a longer time than humans would be willing to spend.

So, are you supporting his theory that all animals could be domesticated? Just that some take more time than others.

It really depends on the definition of domestication. I'll edit my answer to clarify.

I understand the question as "can you get any animal to have heritable traits selected by humans?" : replace "heritable traits" with "the specific set of heritable traits that we call domestication" & you'll be there.

As everybody, I don't fully understand your question. Can you please add your definition of domestication?
Would you consider domestication as soon as human can select for heritable traits? If yes, then the question may be split in two:
Do all animal populations have heritable traits?
Yes! But Depending on what kind of traits you want to consider no variance (yielding to no heritability) may exist in the population. For example, you'll have a hard time to select crocodiles to have fluffy hair as there is no variance in "hair fluffiness" in the population. Crocodiles have no hair.
However, some practical issues exist. For example, it might be hard to select for a given behavior if the animal is so small that we can hardly observe them during a sufficient amount of time to know whether or not the individual display this behavior. Typically, it might be hard to select for specific traits in a population of a species that live inside another species (endosymbionte, endoparasite).
Are humans able to breed any animal species?
No, we're not! Many species do not breed in captivity or do not even survive in captivity. This is due to our lack of knowledge of the ecology and social behavior of the species in question.

Not all animals are equally predisposed for domestication. To be easily domesticated, animal should have:

Flexible diet - and not compete with humans for food
Reasonably fast growth rate
Ability to be bred in captivity
Pleasant disposition
Temperament which makes it unlikely to panic
Modifiable social hierarchy

Wikipedia link above has plenty of details.
So sharks, tigers and alligators are (according to above) are NOT good candidates, because of 4 and 6 at least. Alligators are bred in captivity in farms but are not really domesticated.
See also dates and places of domestication.

There are also two very different kinds of domestication.  Most domesticated species we keep around as a source of food, so their domestication equates to being able to conveniently keep & raise them.  A few we form working partnerships with: notably dogs & horses, but to some degree camels, draft cattle, llamas, and a few others.

No and yes.
What you perceive as domestication has a lot to do with intelligence or even social intelligence of animals.
Common fish is too stupid (from our point of view), to have any social bond with humans. Mammals are usually much closer and have similar structure of intelligence and patterns of behaviour.
That only if you consider domestication as something more and not just human utilization as with breeding fish for food, spiders and snakes for fun (or even snakes for rat-catching, as some African tribes did according to wiki).
So not all animals could be domesticated, they need certain qualities, mostly connected (or we are connecting them) with intelligence.
However, once you look at mammals, which usually have enough social intelligence, you could breed them into domestic animals. It would be hard, there would usually be no other purpose than "We can, so we do", but you could. There were various experiments. One is famous Russian experiment with foxes, another is infamous Hitler's experiment with cows (experiment with bringing back Aurochs, Heck cattle, cows were "undomesticated"). There, in controlled environment, true genetic plasticity of behaviour were showed.
Note that as other posters wrote, this is theoretical. In nature and by natural means, domestication was always hindered by immediate usefulness (not even potential future usefulness). Most of domesticated animals are highly social in their natural form and not very aggressive. Even big cats are quite close. Tigers not as much as cheetahs, which were traditionally bred (or kept as pet) from ancient times.

In short, can you theoretically get any animal to have heritable traits?

All animals have heritable traits. That's genetics.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
Are there any cases of observed extreme speciation
Is there an observed (direct not indirect) speciation on record showing a species shift within the span of history of recorded science?

I think this post may interest you. It is maybe even a duplicate.

a simple google search would have provided this page showing examples of speciation, even artificial ones (http://en.wikipedia.org/wiki/Speciation)

I'm looking for something more along the lines of a fruit fly evolving into a june bug or an ape evolving into a human. Obviously those examples are ridiculous, but they explain my point. I'm looking for something where one kind becomes another... and I hate using that word...

I should add that I don't expect to find anything like this, but I figured this would be the place to ask.

Darwin in origin of the species makes several examples from live stock and pets.  During his time creationists argued that all (or many) of the different dog breeds came from different origins, each of which was created separately by god. Darwin makes good arguments for conversion by man, your modern creationist is unlikely to argue the multiple dog origin in light of  modern science.  The lesson here is that, your creationist, has been fed, a hand picked question that can not be satisfied, and when it can they will pick a new question.

Rebuttal question "Show us documented proof where the amputee has their limb instantaneously restored"

This question seems to involve an attempt to respond to ID rhetoric. Instead of asking a precise but open-minded question OP is asking for an example of something that may not be directly observable. This site wastes too much time (IMO) responding to faux-naif questions from evolution deniers masquerading as open-minded middlemen.   There are plenty of these questions in the record and on the net. This is not the forum for them even if the OP is in fact well-intentioned.

As much as I can agree with what you are saying daniel, I am asking because I had hopes that someone WOULD have an answer. I have already answered my debater with this: https://docs.google.com/document/d/1S5tX2H4J4hR41mD7-oT5qw3o9cq46u6ipgV2SQFeJS4/edit?usp=sharing

So to sum it all up, the question still stands. My reason being that surely someone has either an example that I can use to both answer and respond to these types of questions as well as something that will educate me. I TOTALLY get that ID rhetoric is a huge problem for the scientific community. But just ignoring it won't make it go away... it makes them think they have valid questions. Then they go and get valid lawmakers to support them... ugh

How on earth is this 'off topic'????
I am asking for biology-based evidence of speciation. I didn't realize that my REASONS for asking a question would matter one whit. This is fairly ridiculous and casts quite a pall over all other questions that anyone can ask on these boards as far as I am concerned. I thought that the clarify, simplicity, and reasoning behind my question followed ALL of the 'scope' requirements of this board. There wasn't a drop of philosophical or any other non-biology related characteristics to my question. Simple biology 101. Someone needs to re-review this hold.

ID proponents' belief that their questions are valid is not a reason to entertain them here. You are not asking for evidence of speciation, you are asking for "fruit fly to june bug" speciation. You can raise the issue at the Meta site. I don't expect in my lifetime to see fruit flies turning into june bugs.

Fair enough. THAT makes more sense than the blanket hold with standard answer. Thanks @daniel

But I do think Remi.b's comment is responsive to this question. Also you should post a question on Meta so we don't drag this out here.

Hi @randomblink.  Please note that your question was put on hold by the community and up till now has had no moderator intervention.  Privileges are earned by the amount of reputation a user has on the site, which is a indicator of how trusted that user is.  In this this way, it is the community that determines the scope of the site.  I can see that you have made efforts to improve your question to get it out of the hold - can I ask why the first question linked to would not be a duplicate before I vote to reopen?  At a glance it seems to provide you with an answer.

@RoryM the reason that the question linked to would NOT be a duplicate because the questioner in that instance is referencing reproductive isolation as the definition of another species. This is something that fruit flies are famous for as well as several lizards and a few plants and bacteria. I am searching for a more pronounced evolutionary step whereby more than just reproductive isolation or minor coloration is the defining marker of speciation. I'm looking for a larger gap between the original species and the new one.

Could not fit in a comment…
What kind of observations will you accept to be an observation? If we can demonstrate showing genetic data that two current species where actually only one some time in the past would it represent an observation to you? Or does it has to be a lab experiment (experimental evolution)? Experimental evolution with big animals take much time, I am afraid we probably have no evidence (not counter-evidence) of a mammal species that evolve to be phenotypically speaking as different than a fruit fly and a june bug (example coming from your comment). Would you accept considering microorganisms (I have no example in head though right now)?
As you noted yourself I think, it is difficult to know how different (phenotypically or genetically?) should two sister populations (populations who derived from a common ancestral population) be so that you would consider that one of these populations at least evolved into another "kind" (compare to the ancestral population).

I 'knew' that there would not be an answer that would give me what I wanted after 'thorough' online searches. But I had hope that someone would have an obscure link that Google had missed. The level of evolutionary steps I was searching for are just not going to happen within the tiny historical steps as little as decades or even millenia. I was being WAY too optimistic.

but I had to try!

Good to try $\ddot \smile$ Hope you agree that you have to decide 1) what you will accept as being an observation (Not all methods of observation in science are easy to understand for non literate) and 2) what kind of differences you are interested in.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Hiding identical sequences in NCBI web interface
Sometimes there are identical sequences in Genbank/Genpept, most often coming from the same species but different strains. Ie if I look up "bacteria chitin synthase", the 624-aa protein from Dickeya dadantii shows up three times. There even is an "identical proteins" link.
Is there any filter that I can use to get only one sequence from every group of identical ones? I mean, other than parse downloaded file on my own computer.

Use the NR database and restrict to the species of interest

@WYSIWYG you mean the "partially" non-redundant database? :P

What's your end objective? It is trivial to download the sequences and only keep one but would that be OK for you or do you need this to happen on the web site itself? Using RefSeq will bring the duplicates down to 2 for your example but since multiple sequences exist for different strains, it will be hard to avoid them altogether from the NCBI databases. What is your end objective here? There may be better ways.

@terdon.. LOL.. yeah partially non redundant..

I've written a little script to remove identical sequences from fasta to get what I need. To print the list of removed sequences, uncomment line 22
#! /usr/bin/python3
# Removes identical sequences from fasta file

import sys
from Bio import SeqIO
sequences={}
#This is where sequences will be stored
#likely calling str(seq.seq) on every test will be slower
with open(sys.argv[1], 'r') as fasta:
    parser=SeqIO.parse(fasta,'fasta')
    for seq in parser:
        sequences[seq.id]=str(seq.seq)
l=list(sequences.keys())
for j in range(0,len(l)-1,1):
    try:
        s=sequences[l[j]]
        for k in range(j+1,len(l)-1,1):
            if sequences[l[k]]==sequences[l[j]]:
                del sequences[l[k]]
    except KeyError:
        pass
        #print(l[j],file=sys.stderr)
for j in sequences.keys():
    print('>',j,'\n',sequences[j])

This is for offline execution for which many other tools can also be used- EMBOSS or even awk. Wasn't your question about the online search.

I'm not sure if there's a way on GenBank, but UniProt offers UniRef where you can cluster redundant sequences or specify a lower cutoff (like 90% identity).

I don't need clusters, I need non-redundant set of sequences, preferably with a proper access (ie reading entire nr to find what I need is too much). But thanks for answer anyway.

well, just take one sequence from each cluster! if you download the UniRef databases, you actually get the non-redundant set.


text:
Do females living on mountains have more RBCs than a normal male
I got this doubt when I was studying about haematocrit value. According to my NCERT textbook males have greater number of RBCs than females. But who will have more RBCs when comparing a normal male and a female who lives at a higher altitude?
*edit
the magnitude of altitude would be less than 8,586 m (28,169 ft) as the woman I know is not exactly at the top summit of Kanchenjunga so what would be the answer then?

Why should it be different there?

@Chris i didn't get you

http://en.wikipedia.org/wiki/High-altitude_adaptation

@Raghavakrishna i have read that article but my doubt is who will have more no. of RBCs now a normal male living at normal sea level or a female living at higher altitude? because normally males have more no or RBCs when compared with females

@agharehanabbas You can not compare this directly since the conditions are completely different. And if men and women are both at high altitude, I would expect men again to have higher counts.

@agharehanabbas May be this could be useful http://www.ncbi.nlm.nih.gov/pubmed/11256567

your edits still do not provide enough clarification and suggest that it is medical advice you seek (it regards someones specific RBC count).

@GriffinEvo what more should i add in my question then

Specific altitudes that you had in mind. The male and female. <8586m is not specific, it is anywhere from 0-8586.

Currently impossible to give a definite answer... It depends what altitude you look at.
Going from @Alan_boyd's answer the normal range is 40-50% for males and 36-44% for females. If the altitude at which a person is acclimatized to correlates well with red blood cell count (RBCC), and this effect is not gender specific (i.e. both sexes are affected similarly), then an average woman from high altitude should have a higher RBCC than an average from low altitude. But whether or not the high altitude female RBCC exceeds that of the male depends on the altitude of the two measured.
This rough graph, assuming RBCC and altitude correlate and that male RBCC is higher than female RBCC, shows the problem. Female (red dashed line) A is from a higher altitude than the selected male (blue dashed line) and has lower RBCC. Female (red dashed line) B is from a higher altitude than the selected male (blue dashed line) and has higher RBCC.

Define altitudes and the question may be answerable.

i have edited my question now what must be the answer

According to the MedlinePlus site these are the normal ranges for haematocrit:
Male: 40.7 - 50.3%
Female: 36.1 - 44.3%
Unfortunately it isn't clear if these ranges are for people living at low altitude, but since most people in the USA do, I think this is a safe inference. So clearly there is already some overlap.
The paper accessible here reports various changes in haematocrit due to moving between different altitudes. Broadly speaking these changes are in the range of 10 - 15 percentage points (e.g. a change from 39% to 49%).
So yes, a female who has moved to a high altitude is likely to experience an erythrocytosis (or polycythaemia) which would mean that her haematocrit would exceed that of many males.


text:
FRET only works for interactions between 1nm to 20nm.
FRET only works for interactions between 1nm to 20nm.
How can you be sure that the interaction that you want to study isn't less than 1 nm/greater than 20nm apart?

To get an elaborate answer on this one, I guess you should ask at physics. Very basically, FRET works by that an excited chromophore transfers energy to a nearby chromophore, through dipole-dipole coupling, which in turn emits energy (light) which can be detected. This is a quantum mechanic effect, i.e. these are very small energies. The emission energy between from the donor to the acceptor chromophore is inversely proportional to the distance between to the power of six according to the equation:

Where r is the distance and R0 the Förster distance between the donor/acceptor-pair (distance which the energy transfer efficiency is 50 %).This means that the energy to be detected very rapidly decreases. The Förster distance is in the range 2-10 nm for different chromophore pairs, which leads to the upper limit of FRET use.
The lower limit I don't know if it's due to steric effects or some quantum mechanical effect I do not know about. But since proteins are in the size range of the lower limit they must be in really close vicinity in order for their interaction to be detected using FRET.

The answer is to perform a FRET experiment.
FRET is most commonly used to find out whether something is nearby something else in this range.  Its chosen as a technique when two points of attachment for FRET probes might be within 20 nm, but are not known to be, or might be only in certain conditions.
There are some rules of thumb though. 1 nm, or 10 Angstroms, is about the length of 6 chemical bonds.  To be that close the two FRET probes (which are fluorescent molecules) would typically be attached to the same molecule.   3-4 amino acids apart in a peptide, at the opposite ends of a steroid.  These are schemes for a FRET experiment you would typically avoid out of hand.
FRET is often used for proteins, which are often wider than 20 nm.  For instance FRET probes might be attached to specific positions in two proteins which are known to bind to one another.  A FRET signal would indicate whether the two attachment points of the FRET probes are physically in proximity, allowing one to narrow down the orientation of the two proteins which are binding.
So its more or less an educated guess as to whether to do a FRET experiment, but using simple spatial reasoning you make a safe bet.

While this is true, FRET is not a fool-proof experimental approach, and can give either false positives or false negatives. I think Bioguy wants a way to confirm FRET results.

good point.  FRET is pretty hard to do.. its not my favorite sort of evidence.  its used in so many contexts - we're not necessarily talking about proteins here for instance - that its hard to go too deep...

That's also true, I assumed the discussion of proteins.

I'll add on to shigeta's and RickardSjogren's answer. Firstly, I agree that the upper limit for Forster interaction distance is ~ 10-11 nm due to the rapid fall off of the effect. If I infer from your question correctly, you seem to be asking how to confirm a lack of FRET interaction is a result of no interction, or steric hindrance.
Classical methods of confirmation can be learned from biochemsitry. For instance, co-immunoprecipitation and intermolecular linkage with pull-down.
If the FRET interaction doesn't show a positive result, perhaps it's because the interaction is so tight and the probes are so close that they are prohibited from the FRET effect. That would suggest a strong interaction, and a co-immunoprecipitation should readily show you that you can pull down one protein, run the results on a western blot, and probe for the other protein. The second permutation is to pull down protein B, and probe for protein A. This is a confirmation that both proteins exist in complex. Failure to co-immunoprecipitate both proteins (especially when trying both permutations) would likely indicate that proteins A and B do not interact, or that their interaction is highly transient or very weak. Co-IP can be demonstrated in vitro using purified recombinant proteins, or in vivo, in their native state from cell lysates.
Enter the second technique. Various small molecule compounds of different molecular length can be used to make inter-molecular, amine-to-amine linkages. See BS3 for example. This works best in vivo, where incubation with a compound such as this would create cross-links between neighbouring proteins only with the reach of the englth of the compounds. If two proteins interact, then by definition they must be spatially close to each other, and therefore some percentage of your proteins should be in complex together. From there, you can run a western blot and show that you can probe for both proteins, that run at the same apparent molecular weight defined by the sum of both proteins molecular weights (and therefore both proteins will run higher than expected because their mass is modified by the addition of the interacting protein + linker). Modern versions of this approach involve using mass spec identification of cross-linked fragments, which is much more sensitive and quantitative that western blotting.
A third method could be quantitative colocalization by immunofluorescence microscopy. Prepare cells for immunofluorescence, probing for both proteins of interest, and quantitatively assess whether the proteins co-localize with each other. By eye (and not so rigorously), you would expect that both proteins should exhibit very similar spatial distributions within the cell if they are in fact interacting.
Failure of the above two methods strongly supports the idea that the proteins do not interact, or that they do interact in very weak or very transient conditions. The only way to truly exclude the idea that they do interact in a very weak/transient manner is if you know that the protein complex does something in a cell. If they do something while in complex, then you can knock one protein out, or express a recombinant mutated form of the protein, and assay for the lack of the normal action.


text:
Which point mutations in proteins are OK, and which cause significant change?
I heard that some point mutations in proteins are OK, like from alanine to glycine (I'm not sure, it's just an example), some will change the protein significantly. I want to understand deeper but don't know the right keyword. I have tried some but none of them works. Can you give me a good keyword to start searching? Thank you.

Try googling "tolerated amino acid changes."  The connection between amino acids, overall structure and function is complex, and not completely solvable.  People can make guesses based on similarity between different amino acids, and can make better ones by consulting the protein structure, if it's known, but it's not possible to predict with total confidence that an amino acid change will be harmless or not.

As others have said, although certain amino acid substitutions are considered to be conservative, the effect of a particular substitution will very much depend upon the context. Here are some examples:
gly>ala can change stability of glyceraldehyde-3-phosphate dehydrogenase
gly>ala mutations in a fungal glucoamylase increase thermostability
asp>glu in a lysosomal α-glucosidase is responsible for a glycogen storage disease
asn>gln will abolish glycosylation at NXS/T sites which can have effects on stability and secretion
ser>thr at the active site has profound effects upon catalytic activity of an alkaline phosphatase

There are twenty standard amino acids, and some of them are structurally/functionally similar to each other, such as aspartate and glutamate, or asparagine and glutamine, or glycine and alanine. In general, mutations that cause these amino acid switches don't change the function of the protein, but that's just a general rule - it also depends on where these amino acids are in the protein structure. These are called conservative mutations.

I think you are referring to the concept of conserved substitution, which tends not to change the property/function (http://en.wikipedia.org/wiki/Sequence_alignment) of a protein although thats not necessarily true if the mutated AA (point mutation) changes a functional residue in an enzymatic domain such as GAP or kinase domains or even certain residues that are important for PP interactions such as tyrosine Y, which can become phosphorylated and thats important at times for its interaction with other proteins or the activation/inactivation status of a protein such as receptor tyrosine kinases (http://en.wikipedia.org/wiki/Receptor_tyrosine_kinase). But in most cases it depends where the AA is and the role of the AA. For example two AA can have the same charge/polarity but if their sizes are considerably different, then that could interfere with the way protein folds (conformational changes) and end up affecting its function. So AA substitution and its effects is not necessarily straight forward and its very much dependent on other factors!


text:
Are insects attracted to near infrared light?
Do insects see near infrared light?  If yes, are they attracted to it at night, as they are to visible light sources?
I am building something similar to a home-made trailcam with a Raspberry Pi camera.  Currently I use an incandescent light source.  Obviously, it attracts lots of bugs.  I was wondering if the same is going to happen when I switch to an infrared light source.  This would be 850 nm or 940 nm, as these types of LEDs are commonly available.

Just to avoid misunderstandings: the insects are not the reason why I'll switch to an IR light source, but I'd like to know if insects are still likely to be a problem after that.

I tried to build an IR light source for my raspberry pi and IR camera board. I used 24 NIR LEDS, and it worked, but I was dissapointed with the range. What light source were you planning to use?

See this.

In general, insects are most attracted to UV light. If you switch to a light source without UV-light, the amount of insects attracted will reduce to almost zero.
It has been hypothesized that this sensitivity to UV-light is because direct light sources (sun, moon) contains more UV than objects that reflect light. In this way, it may help insects to distinguish between open spaces and shelter.
It has long been thought that insects are blind to red and IR light. However, there is evidence that some insects do see, and are attracted to, IR light, at least up till 740 nm. However, red or IR light will attract far less insects compared to ypur incandescent light source.

Mosquitos use it to find warm animals from afar, and then to home in on warm zones with good circulation. I slept on an inflatable water bladder that was at 35 degrees from absorbing sunlight in summer, the 1 meter long water bed type things. the mozzies did not find me. other insects don't.


text:
Specificity of Protein Kinases in Signaling Pathways..?
In most of the signaling pathways the activated receptor when activates Protein Kinase through the action of secondary messenger, then these protein kinases almost always phosphorylate on the specific Serine, Threonine, or Tyrosine amino acid residues? what is the reason of phosphorylating specifically these amino acid residues. why not other than these amino acid residues are choosen for phosphorylation ?

Phosphorylation requires a nucleophile and hydroxyl oxygen acts like one. Serine, theronine and tyrosine get phosphorylated on the free OH group in their side chains.
Nitrogen, in some cases also can act as a nucleophile. In case of histidine, the imidazole nitrogen is phosphorylated during bacterial chemotaxis signaling. As far as I know eukaryotes do not have an enzyme for histidine phosphorylation.
Carboxylic groups in glutamate and aspartate can technically be phosphorylated as it happens in case of phosphoglycerate. Glutamate is phosphorylatyed by the enzyme glutamine synthase during the synthesis of glutamine. Same happens in the case of aspartate during aspargine synthesis. However, this is a reactive intermediate and the phosphorylation is not stable like that of hydroxyls.
Other amino acids do not have such nucleophilic groups to render an attack on the phosphorous atom in phosphate- so they are not phosphorylated.

This is mostly because of the nature of the amino acids. You need to have a Hydroxy-group in the sidechain of the amino acid which is the point where the phosphogroup is attached. Since this process needs to be reversible, this can only happen here. See the image below (from here) about the chemical structure:

In eukaryotes not only these three are phosphorylated, histidine phosphorylation also occurs (and happens more frequently than tyrosine phosphorylation, see this article:"Phosphorylation of basic amino acid residues in proteins: important but easily missed.").

Those residues are phosphorylated because they have a free hydroxyl group available to be bonded to a phosphate.  Many other resides can be modified, like acetylation of lysines, but only those residues are chemically compatible with reversible phosphorylation.

those are phosphorylated because they are the present in consensus sequences and enzyme are specific to phosphorylate the specific target that's why other are not phosphorylated and also because of the OH group of these amino acids


text:
Kinesin-5 / cytoplasmic dynein spatial density distribution in neurons
Is there some way to experimentally determine the density distribution of Kinesin and Dynein in a Neuron?
Fluorescence labeling would be impossible(?) as GFP markers would probably alter the motor dynamics.
Any ideas? Or do any studies exist which looked into this topic?

I have next to no knowledge of this area, but I do know that Peter Baas has done extensive studies of Kinesin-5 in neuronal growth cones during development.  I mention that in the off chance that some of his imaging techniques might be helpful to you.

Are you sure that GFP tagged motors don't function properly in these two cases? I'm almost certain I've seen motors tagged before.

It is possible to tag molecular motors with fluorescent proteins. It may impede with its movement but as this paper describes, a variant can be created that doesn't have cargo binding ability.

Constitutively active kinesin motors can be generated by truncations
  that remove autoinhibitory and cargo-binding regions of the
  polypeptide. For this work, we generated KHC(1-560) (Figure 1A), a
  dimeric motor that has been well characterized in vitro and in vivo
  [16],[18],[19]. KHC(1-560) motors were tagged with three tandem copies
  of monomeric Citrine (mCit), a variant of enhanced yellow fluorescent
  protein (FP) (Figure 1A), and expressed in COS cells (Figure 1B).
  Single Kinesin-1 motors were tracked in live cells using a modified
  TIRF microscope (Figure 1C) in which the angle of illumination was
  varied to enable deeper imaging as described [17]

However, if your objective is just to determine the density distribution of Kinesin and Dynein in a Neuron, you can simply fix the cells and do IHC staining for the motor proteins followed by high resolution imaging.


text:
Heterochromatin binding sites position information
I am working on a project and I'm trying to find data on the position of genes and heterochromatin binding sites such as HP1 in Drosophila melanogaster. Is this information available for the DGRP lines? Would I be able to measure the distance between a gene and its nearest binding site from such data?

Have a look at these ChIP-seq data for HP1 in Drosophila: 1, 2 and 3. From ChIP-seq data you can find the distance between the TFBS peaks and the TSS of the gene.
You can also look for nucleosome positioning and DNAse hypersensitvity regions; for the former, I am sure that data is available for Drosophila.

As the previous answer said, there are some public HP1 ChIP-seq data from D. melanogaster if not from the DGRP, from modENCODE and maybe others. In the case of modENCODE, they've published not only the reads, but also their peak calls (mapping with Eland + calling with MACS).
BEDTools ( https://github.com/arq5x/bedtools2 )is a nice command line tool for manipulating intervals with genomic coordinates, and the bedtools closest command can calculate the distance to the closest feature. It would look something like this:
bedtools closest -d -a genomic_features.gff3 -b peak_calls.gff3

Where the "genomic_features" part would be any subset of genome annotation that you're interested in.
I've worked through a small example with modENCODE data, Flybase transcript annotation and BEDTools:
http://martinsbioblogg.wordpress.com/2014/07/04/finding-the-distance-from-chip-signals-to-genes/
Cheers,
m.


text:
Heterochromatin production limitations
Currently playing with some ideas for a project and needed some guidance. I am wondering, both in Drosophila melanogaster and in general, is the amount of heterochromatin a cell/nucleus can produce limited/consistent or variable?
Does one cell in a D. melanogaster produce a similar amount of heterochromatin as another cell in the same fly or another fly (assuming same conditions - environment etc.) or is the heterochromatin production quite variable? How is heterochromatin production regulated?

Heterochromatin profile is of course different in different cells but I am not sure if absolute heterochromatin content will vary greatly. This DNAse hypersensitivity region data is for human cells but same principles apply to all organisms. If I have to take a guess then I would say that quiescent cells are likely to have more heterochromatin. Heterochromatin production is regulated by different epigenetic mechanisms but I cannot comment (I feel it is unlikely) if there is a mechanism to control absolute heterochromatin content.

Generally speaking, heterochromatin or euchromatin structures mark specific regions to regulate the transcriptional activity and these marks carry the signature of developmental processes as they differ in different tissues (or cell types).
Therefore, we should not ignore the developmental processes if we want to understand how such epigenetic marks are formed. But first, we should reconsider the question as it assumes that the heterochromatin is produced. The assumption is somewhat valid, there are many enzymes responsible to shut the chromosome off thru the histone modifications. On the other hand, heterochromatin strucure comes as a default (or as the factory settings). Before the mid-blastula transition, where no (or negligable) transcription happens, all the genome is heterochromatin due to the excess amount of histones. After certain amount of division, the amount of histone per cell reduces but the genome per cell remains constant which then titrates the histones and some transcriptional activity kicks in.
Then HATs, methyl transferases etc. help to clear up the necessary genomic regions depending on the extracellular developmental signaling. Then for many somatic cells, the ratio of heterochromatin and euchromatin regions more or less remain similar.

Thanks for posting but I don't think this answers the question at all


text:
If I squash an insect and it produces red "juice", does it always mean it is a blood-sucking type?
If I squash an insect and it produces red "juice", does it always mean it is a blood-sucking type of insect? Or do some insects have red "juice" themselves, so the color is red on its own and not caused by sucking higher animal's blood?
I squashed a small fly-like insect recently, it produced a red stain, so I am wondering if the stain come from the insect itself or if it has to be some other animal's blood.

No - invertebrates don't have "blood" though they do have hemolymph. Hemolymph flows around the body cavity, rather than through vessels such as veins and capillaries, and comes in to direct contact with tissues and generally it is not red.

Hemolymph fills all of the interior (the hemocoel) of the animal's
body and surrounds all cells. It contains hemocyanin, a copper-based
protein that turns blue in color when oxygenated, instead of the
iron-based hemoglobin in red blood cells found in vertebrates, thus
giving hemolymph a blue-green color rather than the red color of
vertebrate blood. When not oxygenated, hemolymph quickly loses its
color and appears grey. The hemolymph of lower arthropods, including
most insects, is not used for oxygen transport because these animals
respirate directly from their body surfaces (internal and external) to
air, but it does contain nutrients such as proteins and sugars.
~ http://en.wikipedia.org/wiki/Hemolymph

The red you see from squashing, depending on the insect, could come from blood of other animals or (eye) pigments produced by the insect. For example, in my lab we have some Drosophila melanogaster with red eyes and some with white eyes (they carry a genetic mutation which represses the production of pigments in the eye) - if I squash the red eyed fly red "juice" is left on the desk, this doesn't happen with the white eyed flies.

I edited my question slightly. I knew insects did not have blood, I just did not know how to name the "juice" which they have inside.

Other examples of strongly red non-blood pigments: clover mites, which are abundant, red, and easily squishable; and cochineal bugs, which have been an important source of red dye for hundreds of years.

Some insects do have "blood pigments", namely hemoglobins, e.g. larvae of many chironomid species.

@har-wradim yeah..chironomous larvae are beautiful ! Especially when they undulate. Amazing to watch them under stereo microscope. ..

Very interesting. Does the red pigment from fruit flies look exactly like human blood? Or does it have a slightly different colour/hue?

Insects do not have blood as we know it from the higher animals. They have a kind of, which is called hemolymph and is, compared to human a mixture of blood and the lymphatic fluid. The most important difference is that hemolymph doesn't transport oxygen and thus has no red blood cells. The "breathing" of the insects takes mostly place through passive oxygen diffusion through the "skin" and small openings in it.
The hemolymph is mostly made of water and contains things like amino acids, carbohydrates, lipids and so on and is very important for the distribution of nutrients in the insect. It also contains hemocytes which are part of the insects immune system and play a role similiar to human phagocytes.
The color of the hemolymph comes from pigments and varies quite a lot between insects from green to yellow to red.

I edited my question slightly. I knew insects did not have blood, I just did not know how to name the "juice" which they have inside.

The term beetle juice does not come from the blood of a beetle or bug. There is a type of red dye, carmine, that is derived from the outer shell of a type of beetle. Carmine is a common food dye used in things like punch, soda, Popsicles, and so forth.
See Cochineal.

Hi and Welcome. Would you be able to provide references to the answer you have provided so that if others want to read further they can. Thank you.

@Julianne - I've added a reference. Feel free to edit in your own if you prefer. FWIW, in our family, we called all juices colored with cochineal "bug juice". :)


text:
Why does temperature shock kill fish?
As is advised with most fish you should avoid sudden changes in water temperature (for example by introducing new water that hasn't been left to come to room temperature). I have, however, never understood why that is the case, in particular given that most fish are cold blooded so there is no issue with needing to "ramp up" the metabolism when in cold water.
Say a particular species of fish can survive in water between 20°C and 30°C what causes a fish that was previously in 30°C water to die when suddenly plunged into 20°C water? I understand this effect is called "shock" but I'm looking for the biological reason for it.
To be clear I'm not looking for "chemical x is released and that leads to the fish dying,  I'm looking for why these chemicals are released at all. So to give an example if my question had of been "why does adrenaline shock kill" I'd be looking for "adrenaline release is usually a good thing, it's released in response to a fright and prepares the body for a fight or flight response. However this heightend preparedness can cause additional strain on the body which can cause death in some cases"

As others have said fish can die from an overload of hormones or muscle exaustionn. Mammals are likely to get hypothermia from the dramatic temperature drop killing them.

How fast can a lake or a river change from 20-30 degrees? 2 days. Inevitable thermal shock is not something fish dealt with a single time in the last 300 million years.  Every chemical reaction in the fishes body suddenly goes at 1/2 speed if you cool it from 30 to 20. some fish can go easily from 15 to 25, they can dive for cover one hour and then bask at the top where they can grow faster.

The question that you're posing isn't "why does temperature changes kill Fish", but why these physiological responses exist in the first place. The above answers clearly explained what the effects are of temperature shock, and what biological responses can occur that can harm the fish. I suggest you research and ask people the rephrased question "Why do these processes occur in fish?" Maybe check this article about metabolic rate and oxygen consumption to start your research: http://fishbio.com/field-notes/the-fish-report/fuel-for-thought-studying-fish-metabolism

You might have an easier time if you look at the reverse question, sudden temperature changes are pretty hard on living things, even something as simple as membrane permeability can be drastically changed by temperature. We don't think about it becasue we are descended from terrestrial organisms, and air can and does change temprature quickly unlike water, so our ancestors had to develop defenses against these sudden swings. most fish never had to bother.

This due to a phenomenon called "cold shock". This induces a number of physiological changes in the fishs metabolism and also in its behaviour and can lead to death.
The first paper cites some reasons in table 1:

Brain and central nervous system response: Changes in neuronal
activity
Catecholamine and corticosteroid response: Release of hormones due to
the shock.
Haematological and metabolic response: Changes in red and white blood
cells and lactic acid in the blood.
Protein expression and molecular responses: Changes in the expression
of proteins of the heat shock family.

These changes (especially in brain and nerves and also the hormones) can deregulate the fishs metabolism so much that it can die. Shock is a critical condition. Obviously a lot of research is going on, but I recommend reading the two articles below for further details.

References:

Cold shock and fish
Physiological stress responses in the warm-water fish matrinxã
(Brycon amazonicus ) subjected to a sudden cold shock

So, would it be correct to say in terms of points 1 and 3 that although the fish's overall metabolism isn't ramped up/down (being cold blooded) there are other processes that are ramped up/down to cope with the current temperature so if those "settings" are in the wrong place for the suddenly changed temperature then the fish will die (as it takes time to ramp up/down the processes). Basically I understand that the fish dies because "This process occurs which leads to the fishes death" I'm looking for why those processes even exist in the first place

e.g. A sudden fright can kill people because adrenalin is released which stimulates the heart rate etc to increase. Usually this would be beneficial giving a "fight or fright" response but in extremes can be lethal (in particular to a weakened system)


text:
How can one create images like those in the PDB ‘Molecule of the month’?
I am impressed by the illustrations for the Protein Data Bank ‘Molecule of the month’, e.g. the gorgeous image of DNA Helicase below. Does anyone know how they were made or how one might create something similar?

(source: rcsb.org)

While I don't know what is used, David Goodsell should know it, as he is responsible for this, as far as I can see. Write him a friendly email, my best guess is that he will tell you. And please tell us (you can answer your own questions), I am curious, too.

Me also don't find it cool or impressive, However, Chimera has a visualization preset that makes this image style, just a click of buttons. In the presets menue click on publication 1 and BOOOM here you go the image will look similar like this

Those (really cool) pictures are created by David Goodsell using custom-written software.
From an interview to the artist:

PDB: How do you create the illustrations?
Goodsell: Most of the pictures are created with a computer program that I developed back when I was doing postdoctoral work with Dr. Art Olson here at The Scripps Research Institute. I've been using this style of illustration--with flat colors and black outlines--for about 10 years now. I like the way that this style simplifies the molecule, giving a feeling for the overall shape and form of the molecule, but at the same time you can still see all the individual atoms. On the last page of each Molecule of the Month--"Exploring the Structure"--I always use RasMol, to give visitors an idea of the kinds of pictures that they can create themselves with off-the-shelf software.

There are good tools around if you want to replicate that look. Although it may take a bit of tweaking (and possibly programming) I would surely give PyMOL and Bioblender a try.

I found QuteMol got me closest to Goodsell's look :)

@nornagon: nice, I did not know about QueteMol!

"I always use RasMol, to give visitors an idea of the kinds of pictures that they can create". Oh no they can't! Rasmol does not run on Mac OS X. But you can use Jmol instead, which has a command for saving high res png files that you can actually drag back into the application and modify further.

@David there are Mac OS X binaries for RasMol, although I have never tried them. http://www.rasmol.org/software/RasMol_2.7.3.MAC/index.html

@nico — Not quite. They are Unix binaries that will run under an X-windowing environment. It requires you to set up Unix directories and move stuff there. I tried it years ago and it was a real pain compared with the Mac OS9 version. Now a user would have to install XQuartz before they started. For practical purposes it's dead. One feature of JSmol is that it supports all RasMol console commands, so if you are used to RasMol...

@nico — Just tested the 32bit version on a Mac running 10.9.5 (itself old), although the version on the site is for 10.3.9. When I tried to run it I got "Bad CPU type in executable". No great surprise. Presumably a PPC version that doesn't run on Intel.

I don’t actually consider these pictures either “gorgeous” or “cool” — they are not to my taste — and I’m not really sure that the question is about biology, but when it resurfaced after almost 5 years I thought I’d give an answer which explained how one might create something similar, rather than how they were actually made.
The original 3D-graphics program used was RasMol, but as that only runs on Windows, hasn’t been updated for years, and has no viable web version, I would suggest using JMol/JSMol instead. This is free, and you can either download the application and work with it as described in my answer to a previous question. Alternatively you can just find a web page with a JSMol window (such as a page used in my own teaching material) and use that with the Console available from the JSMol logo. So what I do is:

Get the PDB file I want to work with from the Protein Data Bank.
Drag the file into the JMol window, which causes the protein to load in wireframe mode, as in (A), below.
Give a series of commands such as the following to get a spacefilling image (B) in colours other than CPK (you can specify the colours of the chains if you wish) and without the shiny light patches, which are fine for standard images, but will cause problems. One useful feature of JMol is that it allows you to generate high resolution images:

    restrict protein
    wireframe off
    select protein
    spacefill on
    colour chains
    set specular off
    write pngj 2000 2000 "my.png"

You can subsequently drag these back into a JMol window and make further adjustments, as long they haven’t been edited. (So do graphic work on a copy.)

Next you need access to decent bitmap graphics application. If you are in a University someone will have a copy of Photoshop (old versions are fine), but otherwise you will have to make do with what you can find — GIMP is a free cross-platform altenative. I am almost certain that the original artist would have developed the style he uses with Photoshop. He says he wrote a program himself to automate it, but he could just have well used a Photoshop script (Action) in my opinion. Anyway, for occasional use, you can just do it interactively.

The first thing is to get the outlines on the spheres and make the colours flat. The former is done with a filter that finds the edges, and the latter by posterizing (reducing the number of colours in the image). I used a filter called ‘Poster Edges’ to produce frame C. There are sliders that allow you to change the intensity of the edges and degree of posterizing.

Finally to reproduce the rather washed out feel of the colours I used the ‘Exposure’ tool (Image > Adjustments > Exposure), but I could have used curves (Image > Adjustments > Curves) or, no doubt, other options.

And there you have the final image shown in D. It doesn't have quite the same posterization as the DNA Helicase illustrated in the question, but if you really wanted that you could probably achieve it after a little experimentation.

Four years on, and when this question came up again I discovered some typos and missing links. I've remedied them now. Please flag me if you find anything else wrong.

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


text:
Can insects feel pain?
Insects do have a nervous system, even if it isn't nearly as complex as that of other animals. Can insects or other arthropods sense pain? Does their aversion to harmful stimuli suggest that they can 'feel' pain in the sense that other animals seem to?

This question has been asked in different forums and many of the answers say that there is no nociception in insects. This book, however claims that Drosophila do have heat induced nociception and is mediated by TRPA ion channels. Also, there is a gene called painless whose mutation causes loss of nociception.


text:
Why are men stronger than women?
What are the evolutionary explanations for why women are physically weaker than men (on average), and is this difference adaptive? See figure one here.
I suppose that something puts pressure on men to be physically stronger than women, but I don't see what it can be. Why the discrepancy between the sexes?

You should clarify your question, and your reason for asking. I assume that you are asking about a difference in average physical strength of sexes (and evolutionary reasons for this), but the Q can be read in other ways as well. Also, differences in body size/strength between sexes is common in many animals (see Sexual dimorphism), and this is usually not to "dominate women" but often (when males are larger/stronger) used in male-male competition.

For the record, I don't think the Q should be closed as opinion-based. As currently stated, I find it unclear with poor background, but there is a relevant Q on the evolution of sexual differences in humans hiding in there.

I agree.  this site is so steeped in the jargon of biology that it can't handle questions from the public.  [reopen]  The term they need to hear is 'sexual selection' which was broadly discussed by Darwin.  Its not entirely incumbent upon the question if the readers misunderstand.  Men and women are clear terms that specify human males and females. Fairly precise.

What are the evolutionary explanations for why women are weaker than men (on average), and is this difference adaptive?

All of the theories surrounding this fact are speculative; it would be difficult to prove "why" men are, on average, stronger than women.
One contributing theory is Female-Choice - basically that women had (or has) the ability to be more selective when it comes to choosing a mate. Over time men will reflect the preferences of women (taller than them, stronger than them, facial hair qualities, etc.). This is superficially supported by casual studies like this study from OkCupid where the "attractiveness" curve for men is down-shifted, meaning women think the average man looks below average in attractiveness and implying those who are viewed as average ( actually the top 20% of men or so) would have better reproductive success. Men, in the same casual study, had a nearly perfect bell-curve associated the attractiveness of women, implying that men are excellent at deducing whether a women is below average in attractiveness, average, or above average in attractiveness.
Another contributing theory is Male-Male Competition. Basically men, at some point (and still might) compete with other men to win over women. The bigger, stronger man would presumably win in a fight and eliminate his competition - directly preventing the production of offspring by the weaker male. The male-male competition also holds true in a more speculative theory in that the winners of wars literally raped their way to reproductive success.
It is worth noting that men, on average, are only about 30-40% stronger than women due to the larger muscle fibers in men (as cross-sectional area determines muscle strength, not volume). With training the difference (kg for kg) is reduced to 15-20%.
Ultimately why women are weaker than men (or men are stronger than women - whichever way you prefer to put it) doesn't have a solid answer beyond "because the stronger, taller men have reproduced".

I find your first subanswer somewhat vague. The Q is probably asking if there are evolutionary reasons why men are on average psysically stronger than women (see Sex differences in human physiology#strength). How strong we are in comparison to other animals isn't really relevant for this question. However, sex differences in species closely related to us is interesting to understand our evolutionary history.

Saying 'men have more capacity for strength', 'men never use it' is not relevant either. It still does not explain why both genders diverged, and men diverged to be stronger.

@QuoraFeans - Then ask your question again, and be more precise. You're asking why the genders diverged in capacity for muscle development, and I answered that the theories involve Female-Selection for stronger men and that men acted as the defenders/hunters. What type of answer are you looking for?

@MCM This is a good attempt at an answer. "The male-male competition also holds true in a more speculative theory in that the winners of wars literally raped their way to reproductive success." This is a rather grim prospect, but I would entirely believe it as a driving force in our selection. Is there any citation or study into this?

Moreover, the male-male competition and the success of the stronger man should lead to evolution of stronger humans (both men and women). If it has more effect on males then there is something that pertains to the activity of Y-chromosome. This would finally boil down to whether androgens have a positive role in promoting muscle development (more than estrogens).

@WYSIWYG Not necessarily, selective pressure on one sex does not have to have any effect on the other.

but can you explain WHY all of these possible reasons are sex-specific? Whether it be 'Female choice' or 'Male Male competition', why wasn't it the other way round, like 'Male Choice' or 'Female Female competition' ?

@user1993 - No, and I doubt anyone will ever confidently be able to do so. It could be due to a population bottleneck millions of years ago. It could be down to a few mutations on the Y chromosome. It could be deeply integrated with how we have young. Nobody really knows the 'why', only what's happened since.

@WYSIWYG As this https://en.m.wikipedia.org/wiki/Bateman%27s_principle states(Bateman's principle), Can the reason be "Sperms are cheaper than eggs (ibid). So producing a strong male means they can protect the female and even if while protecting the female,the male by chance dies accidentally,the loss can be compensated by the long surving female who can be able to repopulate effectively with the lesser number of available males"? To conclude,I don't know the exact reason and asking can this be reason?


text:
Convert gene name to uniprot ID
I have a list of gene name in a file
CHRNB2
EGR2
GCK
KRT14
LMNA
FGF3
TK2
ABCC8

How can I map them to uniprot ID ?
P.S I tried Uniprot "ID mapping" (from-"GENEID" to-"UNIPROTKB AC"), but it couldn't map.
Please suggest me what to do.

I guess these are human genes?

yea your are right.

try biomart.. ..

Thats my recommendation, too. Biomart is the swiss army tool for this kind of convertion.

biomart did help...thnx a lot

apologies for the delay.I will do it asap...

for biomart goto below link
http://central.biomart.org/converter/#!/ID_converter/gene_ensembl_config_2
Also there is one more converter which i found pretty useful
http://biodbnet.abcc.ncifcrf.gov/db/db2db.php#biodb

Can you explain what these links do? Just posting links as an answer is bad practice: http://meta.stackexchange.com/questions/8231/are-answers-that-just-contain-links-elsewhere-really-good-answers

its quite self explanatory...its basically for mapping of two identifiers.Please refer question for more details.

The biomart link is broken. Why would you choose biodb.net over Uniprot? (I'm not slamming it, I've just never heard of it and am curious if it has a major advantage)

ID mapping
This is called ID mapping. It used to be a headache as programmatic access was the only real way, but it is pretty trivial these days.
As mentioned in the comments, by far the most popular and easy method is to use Uniprot's list uploader for mapping. The corresponding publication can be found here. You must convert from Gene name to Uniprot KB ID
Programmatic access
The Uniprot web user interface will work for thousands of IDs, but is like to result in errors for queries exceeding 10,000 IDs. In that case, programmatic queries are probably better. I've slightly modified this from the Uniprot docs so that the IDs are queried 1 at a time to avoid any errors in exceeding query size. The python code would be:
import urllib,urllib2

list_to_convert = ["CHRNB2", "EGR2", "GCK", "KRT14", "LMNA", "FGF3", "TK2", "ABCC8"]
url = 'http://www.uniprot.org/mapping/'

print "From To"
for i in list_to_convert:
    params = {
    'from':'GENENAME',
    'to':'ACC',
    'format':'tab',
    'query':i
    }

    data = urllib.urlencode(params)
    request = urllib2.Request(url, data)
    contact = "" # Please set your email address here.
    request.add_header('User-Agent', 'Python %s' % contact)
    response = urllib2.urlopen(request)
    page = response.read(200000)
    print page.splitlines()[1] #Ignores the header line returned by uniprot

The output from this looks like:
From    To
CHRNB2  A0A096MXS8
EGR2    A0A096P554
GCK     A0A021WXA1
KRT14   A0A024R1X6
LMNA    A0A096MQV4
FGF3    A0A096NXI3
TK2     A0A096NJ58
ABCC8   A0A088S7J5


text:
Database of Multicellular and Unicellular organisms?
I'm trying to annotate a list of organisms taken from NCBI for cellularity (unicellular or multicellular). Does any of you ever found a database with association between an organisms' name or taxa and whether it is unicellular or multicellular? Desirably, I would like to get information both on species level and on higher taxonomic level (phyla, classes, etc.), but any information on this is welcomed.
In case it matters, I'm using Perl to do this annotation.
Thanks in advance

I think this might be useful if you are also looking for domain level classification.It has all domain classification.   ftp://ftp.ncbi.nlm.nih.gov/pub/taxonomy/taxcat_readme.txt  File:taxcat.zip. Link:ftp://ftp.ncbi.nlm.nih.gov/pub/taxonomy/  .Thanks.

though that may be useful for refining and curating the taxonomy itself, it does not help with the main issue here: finding an association between uni/multicellularity and specific taxonomic groups.

More like a comment:
It doesn't seem that such a database exists, but I think it's relatively easy to create a list of multicellular taxa and the rest should be considered unicellular. Since you use ncbi taxonomy, you can easily get higher-level parent for any species, so there is no need to define cellularity for individual species.
The challenging groups would be different algal and fungal taxa, but there are some good reference books. You also have to decide, whether to introduce a separate category for colonial/coenobial/filamentous organisms.

Yep, that's the whole thing: even though in some cases you can define multicellulars from higher level taxa (e.g. Metazoa), the problem lies on Fungi and Algae where it's more difficult. I ended up doing this by hand. For Fungi I sometimes had to go to the family level to be able to distinguish these taxa.
It surprises me that no one has ever done this.
However, I understand that in many cases, having this type of separation relying on taxonomic classification is not the best...

Recently i came across this text file which has Kingdom,Phylum etc.              https://app.box.com/s/hsmvie7vgjdj1z3g0iuf

That also exists in NCBI and a bunch of other databases. My problem is not having an association between the several clades - and thus your answer does not answer my question. Please read my question again and, specifically, where I wrote "Does any of you ever found a database with association between an organisms' name or taxa and whether it is unicellular or multicellular?"

I answered only for this "Desirably, I would like to get information both on species level and on higher taxonomic level (phyla, classes, etc.), but any information on this is welcomed."


text:
Does a top heavy population grow, decline or stabilize?
Imagine a population that has a larger proportion of older individuals than younger ones, what could possible happen to it in the future?
I am guessing that if the older individuals reproduce, the population will increase but as the older generation grow older they would eventually perish again decreasing the population. As they form the larger proportion, the net population would eventually grow but decline, but would the population then begin to stabilize or continue declining?

Your question leads to the field of structured population models, and I am afraid the answer is: It very much depends on the exact Leslie matrix!. The population may go extinct, may remain at stable size or may grow indefinitely (theoretically speaking), may increase in size and then go extinct, etc…
This is at least true if you make the assumptions that the rates that govern transitions between age/stage classes (survival, growth, reproduction) are  stable over time. Your scenario is explicitly dealing with transitory population dynamics, i.e. it is asking about the population fluctuations that will happen before the age-structured population stabilizes (assuming it does stabilize at some point).
To understand what will happen to your population you can model your population using a Leslie Matrix.
Leslie matrix
The Leslie matrix describes the age-specific survival and fecundity of individuals in a population. Shortly speaking, a population dynamic model using age-specific survival and fecundity looks like this:

Renaming the matrix and the two vectors you see above it gives: $n(t+1) = M \cdot n(t)$, where $n(t)$ is the vector of number of individuals in the population at each age and $L$ is the Leslie matrix, where the first row gives the fecundity of each age ($f_2$ is the fecundity of the individuals of age class $s$ where the number of individuals is a given time is given by $n(t)$) and the lower diagonal gives the survival probability ($s_2$ is the probability of surviving from age 2 to age 3).
So, basically to answer your question, define your Leslie matrix $L$, define $n(0)$ and iterate (left multiply your vector $n(t)$ several times) to see how the number of individuals change through time.
Leslie Matrix and Linear Algebra
The right leading eigenvector of $L$ gives the stationary distribution and the associated eigenvalue gives the growth rate $R$. If $0<R<1$, then the population size decreases through time if $R>1$, the population size increases through time. $R$ cannot be lower than zero (see Perron-Frobenius theorem to understand why). Many biologically interesting features can be extrapolated from the Leslie matrix such as the average lifespan or wether you'd better to introduce individuals of a age 1 or of age 2 (for examples) in a natural population in order to prevent its extinction. The sensitivity of the population to change in parameter (such as an increasing mortality rate at lower age due to a new predator for example). You will find more information on the Leslie matrix on the wiki article and on many other websites.
Other ways to model using a Leslie Matrix
One can also model age-structured population using right matrix multiplication (unlike the above example) and use row vector rather than column vector. The Leslie matrix may also be a function of various variables such as the population size. One can also extend the Leslie matrix to incorporate different class of individuals in the population (different genotypes or different sexes for examples).
Books
Charlesworth (1994) and Caswell (2001) are both excellent books to go deeper into the subject of structured population models, but may be challenging if you lack some background knowledge in linear algebra or population biology.
Hope that helps!

EDIT - R simulation
It's been a time I haven't programmed in R. So, I took the advantage of your question to have some fun and write a quick and dirty code. Below you'll find a R code that allows you to see how the age-specific population size varies depending on your initial vector $n$ and the Leslie matrix. I also add some instructions in order to change the number of age classes (because my code is not very flexible).
install.packages("ggplot2")
require(ggplot2)

######## Parameters

n = c(2,23,40,300) # initial age-specific population size. MNodify as you which. You can as well change the number of age classes

L = matrix(c(0,0,1,2,0.8,0,0,0,0,0.8,0,0,0,0,0.3,0), byrow=T, ncol=4) # Leslie matrix (Left multiplication). Modify as you wish but make sure it should always be a Leslie matrix. You can modify the number of age classes

nb_generations = 100 # Number of generations you want to compute

############

n_t = data.frame(age1=rep(0,nb_generations), age2=rep(0,nb_generations), age3=rep(0,nb_generations), age4=rep(0,nb_generations), Generation=1:nb_generations) # It is a data frame to keep track of age-specific population size changes through times. You will have to add more `ageX` columns if you want to simulate more than age classes

# print (n)
for (generation in 1:nb_generations){
    n_t[generation,1:4] = n
    n = L %*% n
#   print (n)
}

n_t2 = reshape(n_t, direction='long', idvar='Generation', v.names='Age_Specific_Number_of_Individuals', varying=c('age1', 'age2', 'age3', 'age4'), timevar='age') # Just to reshape the data for convenience!

ggplot(n_t2, aes(x=Generation, y=Age_Specific_Number_of_Individuals, color=factor(age))) + geom_line() + scale_color_manual(values=colorRampPalette(c("black", "grey"))(4)) # change the last number of this line according to your number of age classes.

You can see that there are important osciliations in the first 30 or so generations just as expected. Then, the population more or less stabilizes. You also see that due to a survival probability that is different from 1 for each age class, there is necessarily at equilibrium more individuals in age class 1 than in age class 2 and more in age class 2 than in age class 3, etc...

Made some small additions - I hope this was ok.

@fileunderwater You did very well! Thank you!


text:
Fast standing and the heart's insufficient accommodation of the increased venous return
Assume you are 45 minutes on the supine position. Furthermore: you stand all of a sudden and fast and without sympaticus activity.
The venous return (smooth musculature of vessels) accommodates faster to the change (decrease of venous return) so returns blood to the heart before the sympaticus has accommodated for increased cardiac output.
This creates a significant increase in the blood volume entering the heart.
In pathological situation where systemic vasoconstriction not occurring normally, the heart is not capable of handling the overdistension; resulting in a pain during the second cardiac cycle.
I am interested in knowing which phase the heart is most vulnerable:

filling,
isovolumetric contraction
ejection
isovelumetric relaxation

or more explicitly (from my answer here)

Atrial systole
Isovolumetric ventricular contraction
Rapid ventricular ejection
Reduced ventricular ejection
Isovolumetric ventricular relaxation
Rapid ventricular filling

I think filling can happen normally, but not with the sudden isovolumetric contraction (most sympathetic innervations here, so therefore I think this is the weak link).
When there is too much blood in the ventricles, some of the blood is reflected back from the ventricles into the atria causing a painful sensation and possibly tachycardia (as well as an possible increased risk of atrial fibrillation if such events happen regularly).
Is the isovolumetric contraction (systole of ventricles) of the cardiac cycle the possible weak link in accommodating a sudden increased venous return?

When you stand up suddenly from a supine position, venous return to the heart will decrease, not increase. Moreover, heart chambers overdistension does not cause pain. What will happen when standing up is that systemic vasoconstriction will occur to maintain blood pressure until the venous return can be adjusted.

@Raoul I agree with every sentence of your comment. I used little bit overloading in my language. I made it now more explicit. However, my case is a pathological situation where the musculature is not able to accommodate and thus causing a pain.

If you get retrosternal pain, it means myocardial ischemia is occurring, for whatever reason. I do not think ventricle overloading or blood regurgitation per se can cause pain.

@Raoul You are right again. I added my explanation and answer about the case here. I think prolonged undiagnosed celiac disease can cause symptoms that remind those of retrosternal pain.

Raoul's gives sensible comments:

ventricle overloading not sensible
retrosternal pain $\to$ myocardial ischemia
other cause reminding retrosternal pain such as celiac disease:

Posterior 1/3 of the septum is supplied by the following artery where any ischemia can weaken the isovolumetric contraction (TODO this has to be discussed much more carefully):

ischemia coronariaea posterioris created by problem in ramus interventricularis posterior arteriae coronariae dextrae


text:
can recessive alleles produce codominance?
Maybe I'm confused by the term "codominance", but I wondering if codominance only occurs with two dominant alleles.
Can two recessive alleles produce codominance in an individual?
Likewise, can two recessive alleles produce incomplete dominance?

An allele is not dominant or recessive by itself. It is dominant or recessive compared to another allele. Therefore, if you consider one locus (position on a sequence) that has two alleles (bi-allelic locus), you cannot have two dominant or two recessive alleles. It is like saying that two things are darker. In reality you can either say that one is darker than the other one or that the color is as dark as the other one. So either one allele is dominant (or partially dominant) and the other is necessarily recessive (or partially recessive) or the two alleles are codominant.

Think of a gene that influence a phenotypic trait such as tail length for example. This locus is bi-allelic (two different alleles (=variant of a gene) exist (=segregate) at this locus). We'll call the two alleles $A$ and $B$. An individual that homozygous $AA$ has trait value $M_{AA}$. The homozygotes $AB$ have trait value $M_{AB}$ and individuals $BB$ have trait values $M_{BB}$. Viewing this in a table it gives:
$$
\begin{array}{c|lcr}
\text{Genotype} & \text{Tail length} \\
\hline
\text{AA} & M_{AA}\\
\text{AB} & M_{AB}\\
\text{BB} & M_{BB}\\
\end{array}
$$
The following table gives the tail length of the different genotypes under the different types of interactions (dominance, partial dominance and co-dominance).
$$
\begin{array}{c|lcr}
\text{Interaction} & \text{AA} & \text{AB} & \text{BB} \\
\hline
\text{A is dominant and B is recessive} & M_{AA} & M_{AA} = M_{AB} & M_{BB} \\
\\
\\ & & M_{AA} > M_{AB} > M_{BB}\\
\text{Partial Dominance} & M_{AA} & \text{or} & M_{BB}
\\ & & M_{AA} < M_{AB} < M_{BB} \\
\\
\text{Codominance} & M_{AA} & M_{AB} = \frac{M_{AA} + M_{BB}}{2} & M_{BB} \\
\end{array}
$$
Because, in the codominance case $M_{AB}$ is necessarily between the values of $M_{AA}$ and $M_{BB}$ ($M_{AA} > M_{AB} > M_{BB}$ or $M_{AA} < M_{AB} < M_{BB}$), one can consider codominance as being a special case of partial dominance where neither $A$ or $B$ dominates because they both contribute as much to the determination of the tail length.
Various definitions may exist for such concepts as well as for overdominance (also sometimes called heterozygous advantage) or stabilizing selection for examples. Those definitions differ in the sense that they sometimes apply to the value of the quantitative trait, to the fitness value (which is another quantitative trait) or to genetic polymorphism.

When two alleles show codiminance, they are not described as dominant or recessive relative to each other. They are simply codiminant to each other. The same applies to incomplete dominance.
Note that all these terms are relative to the alleles you're talking about. An allele that is dominant over one allele may be recessive to another and codiminant with yet another.

Shorter answer:
The dominant/recessive paradigm that is taught in middle school and high school is not universally applicable.  It accurately describes only a small number of phenotypes, compared to all the genotype/phenotype interactions which an organism exhibits.  It was a useful place to start when it came to unraveling the relationship between genes and phenotypes, but it is very limited.
So trying to shoehorn all phenotypes into that paradigm is a serious mistake.  Just because all of your homework problems are solved using it doesn't mean that it's applicable to all real-life situations.


text:
How do we know the presence of light when our eyes are closed?
Last night I laid on my bed and tried to go to sleep with the light off.
I closed my eyes (but hadn't gone to sleep). My younger brother touched the wireless mouse (which had laser) for the laptop.  He wiggled the mouse and it's laser contacted my closed eye . I knew some light was thrown on my face, and it's color was red. The laser on the mouse was actually red. So my question is, when my eyes are not functioning (not seeing, closed) how did I come to know that there was a light aimed at my eyes, and it was red?

There are two reasons for light to appear red through the eyelids.

Eyelids get a rich supply of blood which contains iron (in hemoglobin). The iron in blood absorbs all colors of light but reflects red light. (reference)
Our tissue transmits red wavelengths of light very well, but it doesn't transmit blue or wavelengths of light towards the blue end of the spectrum very well. So, the blue light is absorbed by the skin, while the red light travels through. When this light hits our eye through our eyelids, it is mostly red. (reference).

Also, as Rickard Sjogren said, the eyelid is a thin membrane and allows light to pass through.

Short answer, your eyelids does not block all light. Since they are only a thin layer of skin, the light is able to pass through although not completely obviously. Since the eyes are still completely functional when you close them, only covered by the eyelids, you are able to see when light strikes your face.

Most people can see a bright torch (flashlight in US English) or desk lamp through their hand, which is a good deal thicker than eyelids. If anything, the surprising thing is how dark it is with your eyes closed.

@pete kirkham very interesting point ! Why dont u convert this into a question ?


text:
what is the biggest known functional distance between an enhancer and its target gene (TSS) in cis?
since the title seems self explanatory;
It would be nice if anybody could provide a reference. I'm looking for a paper that I belive stated around 1.5 Mb but anything above will be cordialy welcomed.
thanks a lot

I haven't found 1.5 Mb, but 1 Megabase. This is the case for the shh gene in chicken, where the enhancer element is located 1 Mb upstream. The original article can be found here:

"A long-range Shh enhancer regulates expression in the developing
limb and fin and is associated with preaxial polydactyly."

There are two reviews which are also interesting in this context:

When needles look like hay: How to find tissue-specific enhancers in
model organism genomes
Remote control of gene expression.

thanks. I also have encountered 1 Mb and distances slightly above, but I'm specifically interested in the longest known functional distance in cis. it is not as easy as I thought since I have spend now several hours on ncbi/pubmed ...

I can have an additional look later today. Do you have any idea in which organism or for which gene this has been described?

unfortunately i don't. i may belive belive it was in M.m - but then again if I remembered properly I would have found it by now. thanks again anyway

this paper "Extensive Promoter-Centered Chromatin Interactions Provide a Topological Basis for Transcription Regulation" at least states finding interaction-distances in the range of megabases... and leaves it at that.

I stumbled upon a few of these claims but they never show data or have references for it.

i found "On a chromosome far, far away"  and " Extensive promoter-
centered chromatin interactions provide a topological basis for transcription regulation.
". one of the papers claimed multiple Mbp and the other stated a range of 2-3Mbp. they did provide their 'not-fully-raw' data bu I have not yet calculated myself. anyhow, since it was I think you who recomended at least one of these two papers in another forum (what are the chances) I thank you


text:
Soft and Hard selection
Seems to me that these two sources (M. Whitlock, B. Wallace) use different definitions of soft and hard selection.
M. Whitlock: Soft selection occurs when the relative fitness of an individual is calculated relative to the fittest individual of the local patch. Hard selection occurs when the relative fitness of an individual is calculated relative to the fitness of the fittest individual in the whole metapopulation.
B. Wallace: Soft selection occurs when the relative fitness of an individual is calculated relative to the fittest individual in the population. Hard selection occurs when the relative fitness of an individual is calculated relative a hypothetical fitness. Therefore, extinction only occurs under hard selection but never (except eventually when all individuals have fitness of 0) in the soft selection case.
Are there other definitions? What is the most common definition?

I think Wallace (1968) developed the ideas of hard and soft selection, as they relate to genetic load. He further explains the concept in Wallace (1975). As the idea was his, I'd go with Wallace's definition over Whitlock's.  I haven't had time to watch the Whitlock video to see if they are saying more or less the same thing overall.
Consider a hypothetical population of individuals, each with 1000 loci (I'm basing example and ideas on an example given by Ridley 2004, pgs. 162-167). Heterozygotes at each locus has the greatest fitness (heterozygote advantage). Homozygotes at any locus will have reduced fitness. Therefore, the fitness of each genotype is given as:
AA: $1-s_{AA}$
Aa: $1$
aa: $1-s_{aa}$
Even if every individual in the population at time zero was heterozygous at each locus, Mendelian inheritance ensures that no individuals will be heterozygous at all loci after the second generation.  Assume that fitness reduction at each homozygous locus is just 1%. Given that well over half of the loci will be homozygous, fitness of those individuals will be reduced to 0. They will die before reproducing.  This is hard selection.  If hard selection of this magnitude occurred in a population, then extinction would occur. This is what Wallace (in your link) is saying.  This mortality due to the genetic load is added to the normal background mortality.
Soft selection compares the fitness of an individual to the genotype with the greatest fitness in the population, even if that genotype does not the theoretical optimum fitness. Soft selection replaces some of the background mortality with selective mortality, so the population size is not decreased overall.
Literature Cited
Ridley, M. 2004. Evolution. 3rd ed. Blackwell Publishing, Malden, Massachusetts, USA.
Wallace, B. 1968. Polymorphism, population size, and genetic load. pp. 87-108 in R.C. Lewontin, ed. Population biology and evolution. Syracuse University Press, Syracuse, New York, USA.
Wallace, B. 1975. Hard and soft selection revisited. Evolution 29: 465-473.


text:
A question about IPTG induction
I have found the information: `In the absence of lactose, the lac repressor binds to the operator sequence on DNA and bends the DNA by 40 degrees. This blocks access of T7 RNA polymerase to the promoter site and thus prevents leaky transcription of your gene before induction.'
I am confuse about one fact.
When I add IPTG,  the lac repressor protein (from E.coli chromosome) can no longer bind the operator and native E. coli RNA polymerase begins transcribing, the T7 RNA polymerase gene engineered into its chromosome.
So if there is IPTG and lac repressor protein (from E.coli chromosome) can no longer bind the operator standing in front of the T7 RNA polymerase gene, why lac repressor protein still can bind to operator standing in front of the target gene from plasmid?

What makes you think that the lac repressor will still be bound at the target gene?
In strains with this type of regulatory configuration (usually with DE3 in the genotype) the idea is that IPTG induction turns on expression of T7 polymerase from a lac promoter on the chromosome, and then this T7 polymerase then transcribes the target gene on the plasmid. The presence of IPTG ensures that repressor will bind at neither site.
Supplementary:
I think that I understand why you are confused now. Your picture of the way this works is based on the idea that the repressor is locked on to the operator until an inducer such as IPTG comes along. In fact there is an equilibrium between bound and unbound:

repressor/operator <=> repressor + operator

and, in the brief periods when the repressor isn't bound, the E. coli RNA polymerase can bind and transcribe the operon. This is referred to as 'escape synthesis' and it is generally assumed that it is functionally relevant in ensuring that there are low levels of lac permease expression at all times so that lactose can be taken up. If this wasn't the case, how would the natural inducer (a derivative of lactose) ever be able to induce the lac operon?
In protein expression systems it is generally considered desirable to keep escape synthesis of the foreign protein to a minimum so that there is no selection acting on the gene to negate any deleterious effects of its expression. The use of T7 polymerase as an intermediate level of regulation helps to achieve this. Even if there is a low level of escape synthesis of T7 polymerase, the concentration of T7 polymerase will be so low in the uninduced state (compared to the endogenous RNA polymerase) that the amount of escape synthesis of the target protein due to T7 polymerase gaining productive access to the T7 promoter on the plasmid will be negligible.
Read more here.

As I wrote before I have found the information: `In the absence of lactose, the lac repressor binds to the operator sequence on DNA and bends the DNA by 40 degrees. This blocks access of T7 RNA polymerase to the promoter site and thus prevents leaky transcription of your gene before induction.'

Because the T7 RNA polymerase is expressed after IPTG induction, there is no possibility that the T7 RNA polymerase is before the IPTG induction. Right? so how lac repressor protein  blocks access of T7 RNA polymerase and leaky transcription of the gene before induction if there is no T7 polymerase then? I do not understand the second sentence of passage that I quoted

@gucio I have expanded my answer - hope this helps.


text:
The pBR322 convention
What is the pBR322 convention? For example in the description of the pET28a vector we can find information that the sequence is numbered by the pBR322 convention, so the T7 expression region is reversed on the circular map.

Could you please clarify the question? what do you mean by pBR322 convention? do you mean why it was named pBR322? I'm not clear what you mean by pET28a being numbered by the pBR322 convention.

pBR322 is a distant ancestor of pET28a. If you compare the two maps below you will see that they have the same replicon labelled as ori or pBR322_origin.
The map of pBR322 is shown in the conventional orientation: the single EcoRI site is at coordinate 0/4359 and numbering proceeds in a clockwise direction through the BamHI site. The map of pET28a is presented with the pBR322-derived ori element in the same orientation (note the labelling of a pBRrevBam_primer also). Because of the way that the pET vectors were built, this means that in the conventional depiction the expression region runs counter-clockwise.


text:
What is the scientific name of this butterfly?
I have this  butterfly but I don't know its scientific name. I think that it's a common butterfly which can be seen everywhere (btw, I'm in Taiwan.) Thanks for your help :D

Could you give us an indication of the size of the butterfly and the time of year you saw it?

If it's a common butterfly, can you ask locals for the common name? That will give us more to go on.

Your specimen is in very poor shape. did the inner lower wings have have a small 'eye' two thirds of the way down? It may be very insignificant, or difficult to find, on some specimens.

Maybe common in your locality, is it common throughout world?

For a species-identification question, size-mention is a must. At least approximate size.

With the information given, I have to say I think it's a Spangle, Papilio protenor, of the swallowtail family, probably a male.
It also is listed on the butterflies of Taiwan.
See pictures for comparison:

........................Male...............................................female............................................................................


text:
What bird makes this sound?
It sounds like some kind of crow but not really. Here is my recording: https://www.youtube.com/watch?v=4TsKFUugot8&feature=youtu.be#t=06s
This bird always wakes me up at 04:00 and this started in late June. I live in a village in Hungary.
I really need to know and don't know where to ask.

Please [edit] your question and mention 1) where you heard this 2) what time of day 3) what period of the year.

The portion of the bird's voice is very short. maybe less than a second.

It can't be confirmed but it sounds like a pelican.


text:
How does a woodpecker not give itself concussions?
How does a woodpecker go about smacking it's head into a tree without killing itself?

Physical perspective : The motion of a woodpecker's beak is a straight line motion. Researchers believe that concussion occurs in animals when the head is rapidly rotated around the neck (and brain stem), which is less likely in straight line motion.

This does look Quite painful. Ouch!

Various features of brain,skull and beak anatomy help to achieve protection.
A paper was published in PLoSOne in 2011 on this very topic:
Why do woodpeckers resist head impact injury: a biomechanical investigation
There is also a very readable summary on the BBC website. I advise that you read the whole article, but here is a quotation which lists the main findings:

The team's simulations showed that three factors were at work in sparing the birds injury.
Firstly, the hyoid bone's looping structure around the whole skull was found to act as a "safety belt", especially after the initial impact.
The team also found that the upper and lower halves of the birds' beaks were uneven, and as force was transmitted from the tip of the beak into the bone, this asymmetry lowered the load that made it as far as the brain.
Lastly, plate-like bones with a "spongy" structure at different points in the skull helped distribute the incoming force, thereby protecting the brain.
The team stresses that it is the combination of the three, rather than any one feature, that keeps woodpeckers pecking without injury.

Gibson (2006) identified three characteristics that help woodpeckers avoid brain injury:

their small size, which reduces the stress on the brain for a given acceleration
the short duration of the impact, which increases the tolerable acceleration
the orientation of the brain within the skull, which increases the area of contact between the brain and the skull.

Combined with Wang et al.'s findings, maybe that makes six features.
Gibson, LJ. 2006. Woodpecker pecking: how woodpeckers avoid brain injury. Journal of Zoology 270: 462-465