text:
Can viruses protect themselves against restriction enzymes?
Restriction enzymes cut the DNA of bacteriophages. Have bacteriophages evolved any mechanism to protect themselves from it ?

I guess you are talking about the restriction modification system, not restriction enzymes in general (which are used a lot in the lab, for example).
If so, this paper might help answer your question.
I have not read through it totally, but at least some viruses trigger the downregulation of restriction enzymes to make them cleaving their DNA less likely. Restriction enyzmes are also quite selective for the site they cut at, so single nucleotide changes at this site, might, if the phage is lucky, not change the function of the encoded gene, but keep the restriction enzyme from binding (and thus cleaving) at that site. Mutating helps a lot. And it is fast in those little critters.

One of my friends said that they have ligase to join their fragments again , but that doesn't seem correct because then the bacteria could again use restriction enzyme to cut it. What is your opinion ?

A biological system is always fluent. There are several possibilities to "kit" the DNA, especially ligase. But then, as you said, the DNA would be cut again. The main point for the bacterium is, to prevent it from being stable enough to be transcribed.

Do you know an actual virus that  does so?(I tried googling it but couldn't get anything :) )

In the wikipedia article for DNA ligase you'll find an example of a bacteriophage ligase. http://en.wikipedia.org/wiki/DNA_ligase#T4_DNA_ligase Also, even the bacterias own ligase could ligate the foreign DNA. An enzyme has (more or less) specific binding sites, but it does not recognise anything beside that. Ligases need co-factors to bind and ligate, but the cofactors for the bacterium ligase of course will be present.


text:
Non-Ethical Issues with Eugenics
Notwithstanding the obvious ethical issues with the idea of eugenics, I have read in many sources that eugenics has practical issues or otherwise "would not work", but I haven't been able to find an enumeration of the reasons more complex than "genetics doesn't work like that".
From a biological or genetic standpoint, what are the main problems with eugenics, in its broadest sense as "organised, goal-directed human breeding"?

Eugenism is a set of believes on how to improve the "genetic quality" of the human population. There are no set of clearly defined practices that we could discuss here. If you want to question the practicality of a particular practice, can you please clearly defined this practice?

In its broadest sense, the most obvious biological concerns about selective breeding in humans are really sociological in nature. One of the potential issue is related to increase homozygosity and inbreeding depression . But it will really depenss upon the details of the eugenics program suggested.

Well, there can be multiple reasons about why eugenics won't work.
The first problem is related to pleiotropy of human genes. That is, one gene can control multiple traits, although the influence of a single such gene on a particular feature may be small. So eugenic practices will very likely pick out some characters caused by pleiotropic genes and amplify desired alleles in the gene pool, but there may be other anomalous traits linked with the very same gene. Thus eugenics introduces new problems in this scenario.
(Some afterthoughts: These antagonistically pleiotropic genes are not uncommon, and they could be rationalized from an evolutionary perspective. Some traits encoded by such genes may be beneficial to the organism in its early life but not later. Such benefits, if they come before sexual reproduction, confer greater fitness to that organism. An classic example is the sickle cell anemia. Heterozygotes have resistance to malaria while homozygotes suffered from reduced life expectancy.)
Then, it's easily understood that eugenic programs shall proceed slowly in comparison to Morgan's fruit fly experiment, for example, as a result of the extended period between birth and sexual maturity for our species. Therefore, we have to wait for decades to have some real accumulation of beneficial phenotypes.
Finally, critics of eugenics widely believe that it will sacrifice genetic variety. This argument makes sense because those desired phenotypes are chosen by us, not by nature, so they are not necessarily those best assist our survival. Though we live in comfortable environment nowadays, there may be plagues, droughts, and other large-scale natural disasters in far future that select against our chosen traits. If our species is too homogenized then by eugenics, we will probably face a grave situation...
Reference:
1.Carter, Ashley JR; Nguyen, Andrew Q. (2011-01-01). "Antagonistic pleiotropy as a widespread mechanism for the maintenance of polymorphic disease alleles". BMC Medical Genetics. 12: 160. doi:10.1186/1471-2350-12-160. ISSN 1471-2350. PMC 3254080  Freely accessible. PMID 22151998
2.Richard Lynn, The Science of Human Diversity: A History of the Pioneer Fund (University Press of America, 2001 ISBN 978-0761820406).
(Since this topic is really controversial, extreme care is needed to choose evidences to support the answer. For those who may disagree, please put a comment below about your opinion instead of immediately casting a down vote, thanks!)

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text:
Extinction of species with extant descendants
From what I've seen, species such as Homo heidelbergensis which have extant descendants are classified as extinct, which makes sense as far as it goes.
However, given that species exhibit a continuum of development throughout time, does that mean that for any given extant species and their ancestors there is an "extinction line" which moves gradually forward as small changes in the "current" gene pool render the ancestors from a given time no longer capable of producing fertile offspring with the "current" species and thus shunts them out of the current species and into the extinct species immediately proceeding it?
Additionally, does that mean that there might have existed a species (say, for argument's sake, H. heidelbergensis) with a genetic distribution such that some of them would be capable of producing fertile offspring with the "current" descendant species (in this example, H. sapiens) and some of them not, thus rendering half of the species effectively extinct and the other half not (at least, not yet)?

I don't fully understand your question. I think it is less misleading to talk about about lineage than species given that you start talking about half-species. Some lineages get extinct, others don't. The extinct lineage cannot be the direct ancestor of a extant lineage. An extinct lineage however have a common ancestor (and a Most Recent Common Ancestor MRCA) with some extant lineage.

For example, among the "big" lineage that is homo (Genera), you have several lineages (sapiens, neanderthalis, * heidelbergensis*, etc..). The lineage Homo is extant (thanks to the lineage sapiens) but all the non-sapiens lineages within the homo are extinct. I am not sure that this helped...

It is helpful, but not what I'm asking. I understand the distinction you're making, but I'm specifically interested in this particular oddity in what appears to be the common definition of "a species".

The common definition of a species (for sexual species) is based on reproductive isolation. So, if some individuals within a species die (or don't reproduce) , then only the other ones will be left. And if you consider one population (of constant size to make it easier) and look backward in time, you'll see that the number of ancestors of the currently living individuals are much less numerous that in the current time.

Maybe you are interested in coalescent theory. It is a mathematical framework that allows you (among other things) to calculate the expected to the MRCA of a sample of $n$ individuals. Here is a recent question related to this concept. Did I nail down to your interest or am I off-topic?

If any species has descendants, then it isn't extinct. Mating ceased once extinction occurred.

You are right. Consider a population at some point back in time and ask how many of the individuals left descendants that are still alive today?, the answer will be between 1 and N (inclusive), where $N$ is the population size. We call this process coalescence
A tiny introduction to coalescence
Consider a population of constant size $N$ and to the previous generation and ask the question What is the probability of two random individuals to be siblings?. This probability is $\frac{1}{2N}$ (assuming no selection and diploid population). The probability of them not being siblings is $1-\frac{1}{2N}$. We can say that, with probability $\frac{1}{2N}$, two randomly individuals coalesce in the previous generation. What is the probability that 2 random individuals coalesce $t$ generations ago? It is the probability that they don't coalesce for $t-1$ generations and then coalesce, that is $P(t) = \left(1-\frac{1}{2N}\right)^{t-1} \frac{1}{2N}$. In words, the coalescent time follows a geometric distribution with parameters $t$ and $\frac{1}{2N}$.
Because coalescent times are independent variables (and I won't prove it here), one can extend this to not only 2 individuals but $n$ individuals. There is therefore, a point in time where all individuals of the modern day population coalesce into only one individual. At this time, this one individual was not alone in the population of course.
Coalescent theory: Usages and book recommendation
The simple calculations I just made are the very basis of coalescent theory. Coalescent theory is a very powerful set of mathematical tools that one can use to make detailed predictions of the genetic patterns to expect in a population. Statistical test such as Tajima D test is based on results from coalescent theory. Coalescence theory can be extended (through approximations) to structured population (structured coalescent theory), non-neutrality (selection) and recombination.
coalescent theory: an introduction (by John Wakeley) is a good book on the subject. However, it requires from its reader some basic knowledge in mathematics and problem some knowledge in population genetics.
What is the percentage of people living in England in 1500 AD whose lineage is still alive? is a recent post on Biology.SE that is relevant to the kind of question that could be answered with coalescent theory.

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text:
What is the difference between DNA vs RNA Editing in the context of gene therapy?
As a someone with beginner knowledge on biology, I have come across the terms "RNA editing".
Take this paper for example : RNA Editing with CRISPR-Cas13
From my understanding, DNA -> RNA -> Proteins
If we use a vector for delivering a gene to a cell in-vivo, does it mean that corrections aren't permanent for RNA edits?

There are several differences, both mechanistically and functionally.

DNA edits are heritable by the daughter cells and are therefore permanent whereas RNA edits are not.
The type of Cas protein used in the editing process for DNA and RNA are different.
In the paper that you linked the authors have fused an RNA editing enzyme (ADAR) with dCas13 (a variant that does not cleave the target). So the CRISPR-Cas system directs ADAR to the sites on RNA that need to be edited. Usually when editing the DNA with CRISPR-Cas, people rely on the ability of the complex to cleave the DNA. This double strand break may be then repaired using different pathways (NHEJ and HR) during which editing happens. See these posts for more details:       How is the type of genetic manipulation determined in CRISPR-Cas9?       Mutations/deletions with CRISPR       How does NHEJ cause indels?
It is also possible to edit DNA in a way that does not involve cutting of the DNA. These techniques use similar principle as in the case of RNA editing described in the paper that you linked (see the abstract and introduction of this paper). However, if you cut the RNA, then it will be completely degraded instead of being repaired.

+1 on the answer overall, but should probably clarify that only some DNA edits are heritable (whereas RNA edits are generally not). There’re important conversations about somatic (non-heritable) and germine (heritable) gene editing, and both of those are DNA cuts, I believe.

@CalendarJ By heritable, I meant the daughter cells of a cell, not the entire organism.

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text:
Should gene therapy safety protocol include isolation?
In the case of a gene therapy trial where viral vectors are used to deliver genes into mammalian cells, including humans, should biosafety and ethical protocols include isolation of the patient as a precaution post administration that the viral vector may recover its ability to cause disease and harm the environment (more so the patient as the animals tested can be destroyed by incineration)? And how long should that isolation stay be to ensure safe disarmament of the viral vector?

The viral vectors used in gene therapy trials are so heavily modified they can't just start replicating again. Chances are they are a lot more dangerous to the patient than they would be to anyone around them. I don't know what happens if you use a replication deficient lentiviral vector in an AIDS patient though.

But usually there is the delivery vector and the helper viral vector to help promote the new sequence, no?

@user137 you don't use lentiviral vectors in AIDS patients.

@Nederealm no, there's only one vector, delivered with a completely replication-deficient virus. Isolation of gene therapy patients is completely unnecessary.

@Nederealm It sounds like you're confusing the production of viral vectors with their application. The replication deficient viruses must be produced in cell lines that produce the missing proteins, and I think AAV only grows in cells that are also infected with adenovirus, though I don't know much about virus production.

So why is the argument of viral vectors gaining the ability to become a replication virus often brought up in an ethics debate?

I found my answer here > ISSUES RELATED TO PARTICULAR CLASSES OF VECTORS FOR GENE THERAPY http://www.fda.gov/BiologicsBloodVaccines/GuidanceComplianceRegulatoryInformation/Guidances/CellularandGeneTherapy/ucm072987.htm#vi


text:
Niche differentiation in birds of prey
I'm not much of an ornithologist but I know enough to distinguish most Central European birds of prey. To me it is amazing that there are so many species that seem to occupy the same niche. Especially the two native kite species (Milvus milvus and Milvus migrans) and the common buzzard (Buteo buteo) are -- to my impression -- quite similar in terms of size, preferred prey, habitat etc. According to the competetive exclusion principle, these species would not coexist if they would exploit the exact same set of resources. So my question is:
What are the major differences between the mentioned species that allow coexistence? Are there more such examples from other geographical regions?

Note that competitive exclusion states that the species should differ at least according to one axis of their ecological niche. Meaning that if their niche totally overlap in terms of source of food, it doesn't that they necessarily can't coexist theoretically speaking. I might be wrong though!

No, you're right. I'm just asking for the axes that differ.


text:
How to prevent e coli from clumping (for FACS)?
I'm performing FACS on e coli, but the cells are clumping together so each event is multiple cells.
I ran a control where I had one flask of e coli expressing GFP, and one flask expressing RFP. Run separately, I got a clean population of either high-GFP fluorescent events, or high RFP fluorescent events. If I mix 10uL of each population into 200uL TE buffer and immediately run that sample, all the events have high RFP AND high GFP fluorescence, indicating the cells are sticking together immediately upon mixing.
Cell line: ER2566 (NEB)
F- λ- fhuA2 [lon] ompT lacZ::T7 gene 1 gal sulA11 Δ(mcrC-mrr)114::IS10 R(mcr-73::miniTn10-TetS)2 R(zgb-210::Tn10)(TetS) endA1 [dcm]
Host strain for the expression of a target gene cloned in the pTYB vectors.
Carry a chromosomal copy of the T7 RNA polymerase gene inserted into lacZ gene and thus under the control of the lac promoter. In the absence of IPTG induction expression of T7 RNA polymerase is suppressed by the binding of lac I repressor to the lac promoter.
Deficient in both lon and ompT proteases.
Growth media: M9 minimal media
FACS running media: TE
I know there are anti-clumping agents for yeast and mammalian cells, but I haven't come across one for bacteria.
Can anyone recommend:

an e coli protein expression strain that is known to not clump
an anti-clumping agent for bacteria
any other possible solutions
?

Thank you!

Check out the (many) strains and methods in this paper: http://www.ncbi.nlm.nih.gov/pubmed/18926860

If you don't have access to that journal, I put a copy of the PDF in my Dropbox here.


text:
Protein-Bound Drugs in Kwashiorkor
Kwashiorkor is characterised by decreased serum protein (including serum albumin) due to poor dietary protein intake.
What is the effect of this lowered serum protein on highly-protein-bound drugs? Is it substantial enough that administering such drugs (such as warfarin, though it's hard to imagine a situation in which a patient with kwashiorkor would need anticoagulant therapy) is potentially dangerous, and if so, can this be compensated for?


text:
Circadian rhythm in birds

Animals can use their circadian clocks to determine direction from the
  position of the sun. In a particular experiment conducted in Iceland,
  a bird, kept in a cage open to the sky, was trained to seek food on
  the western side. Its circadian rhythm was then phase-delayed by 6
  hours and after phase shifting, the bird was returned to its open cage
  at 12.00 noon real time. It was observed to seek food in the:
a. north.
b. south.
c. east.
d. west.

I think that if its circadian rhythm was phase delayed by six hours, at noon, it will feel that it is still 6 a.m. So, the sun will be located in its "east" and it will try to seek food in the "west" but its"west" will be our south. So, answer should be south. Is my reasoning correct ?

I think it also matters when before the phase delay, the bird was fed.


text:
What is the surface area of the vitreous humour in contact with aqueous humour?
This is a question regarding the anatomy of the human eye, however for my purposes medium sized mammals should do. I am interested in estimating the surface area of the hyaloid membrane of the vitreous humour which has contact with the aqueous humour circulating in the posterior and anterior chamber of a typical human eye.
The surface area in question is highlighted in red in this schematic of the cross section of the human eye.

Area=πr², d≈2cm (less than maximal d) -> r≈1cm,  thus the area in question is roughly
3.14*1cm*1cm≈3.14cm²
UPD by request (ref):
The vitreous body base middle is at ora serrata (+-2mm), so we should calculate the area at this level. Here is the reference of the diameter:

from: Basic and Clinical Science Course, Section 02

Wonderful, thank you very much! I don't suppose you happen to know what the point where the vitreous meets the lens is called?

@Freeman i've already told you - come back to your prev. question

@IIan thank you. Thanks for the reference also, that looks like a great book to keep hold of!


text:
Bird Identification: New Delhi, April 2018
I've looked in Birds of the Indian Subcontinent (BNHS version, not Inskipp) and two phone apps and still can't find this, although I am a newbie tourist so am probably making a basic mistake. Seen today, 2018-04-07, 9:00 local time, in a New Delhi urban garden.

Maybe 25cm long. Uniform grey above, mottled grey below, grey legs with slight orange tinge. Orange-yellow bill, very slim light eye ring. I wondered about a large grey babbler, but all the pictures I can find seem less grey.
Thanks!

It looks like you're on the right track.  Here's a photo of a Jungle Babbler (Turdoides striata).  They are found on the Indian subcontinent.

Source: https://en.wikipedia.org/wiki/Jungle_babbler

I'm no pro at species identification, but being in New Delhi (although I see them everywhere I go), I can pretty much confirm this. +1 for this ;)


text:
What determines the pathway of a neurological signal?
My question is about the neurological signals. In our body when a signal, for example a hearing signal from hair cells, is built, it goes through a lot of neurons and it passes a lot of synapses. I am wondering how it doesn't lose it's correct path and chooses the right way to auditory cortex? I mean what are the features of a neurological signal that shows it the correct way?
In other words, how can a neurological signal be created and sent through a chain of neurons to the brain, how can it 'know' when entering a synapse contacting multiple neurons which is the correct one for going through it?

please, read this section on how to ask good questions and try asnwering: "Have you thoroughly searched for an answer before asking your question?" This is not only about searching through this site, but also googling

@aaaaaa - I must say this question and related ones are understandable. E.g., folks in computer science tend to compare the nervous system with computer commands and don't understand why an isolated '1' (an action potential) enters up in the correct place without proper guiding info.

i have problem of different kind with given question

Short answer
Neuronal signals neither choose where to go, nor do they carry routing flags of some sort to guide them. Instead, neuronal signals are guided by the hard wiring of the nervous system.
Background
Neuronal signals (action potentials) basically follow a one-way path. When they encounter a cross roads, action potentials are simply propagated to all of those alternatives. External effects of neurons, hormones or drugs may alter these signals, for example by inhibiting action potential formation or propagation.
To take the example of the auditory system (Fig. 1):

Fig. 1. Auditory system. Source: New York University.
One can readily see that the signal from the hair cells are routed into the auditory nerve to the cochlear nucleus, from there to the colliculi in the brain stem and further up to the auditory cortex via the medial geniculate. Basically this is a one-way, straightforward route.
There is complexity in the system, however. For example, the fibers of the auditory nerve bifurcate on entering the cochlear nucleus and make synapses on a number of morphologically different types of neuron. Each of the latter sends its axon out of the cochlear nucleus with a distinctive projection pattern that gives rise to further divergence. Specifically, some cochlear nucleus neurons project directly to the inferior colliculus, whereas others project to various divisions of the superior olivary complex and nuclei of the lateral lemniscus, which in turn project to the inferior colliculus (Irvine, 1992).
But even in this complexity the divergence is basically generated by simple bifurcations. An action potential reaching such a junction by default simply gives rise to two parallel signals; there is no choice involved. Regulation is due to other neurons targeting these pathways.
Reference
- Irvine, The Mammalian Auditory Pathway: Neurophysiology Springer Handbook of Auditory Research (1992).

Ok thank you.  Now my quedtion is what are the features of a specific neurological signal?  I mean for making a fake signal .

@Pedram, I do not understand your follow up question and you should perhaps consider asking a new question. The answer comments should be reserved for clarifications only.

I mean our ear collects sound and make signals and it goes to brain and we hear.Now I want to make a fake signal and the brain hear it I mean here the ear doesn't have any role and we give a stimulation to auditory nerve and it take it to the brain.

@Pedram, I suggest asking a new question on this and carefully explain what you mean with a fake stimulus etc. Comments are not ideal for new questions. Thanks.


text:
Can we change the direction of a neurological signal?
My question is can we change the direction of a neurological signal? When a neurological signal is generated it goes to the brain. Along the way it passes synapses. Can we make it change it's pathway to go through another neurone instead of the neurone it was going to ?

With an eye to doing what with the end result?  Theoretically it's possible, but in practicality, it would be extremely complicated (dealing with axon collaterals and convergence/redundancy in higher centers).

When you write "can we"--who is "we"? A neuroscientist administering drugs to an animal? A neuroscientist using some other technology on an animal? A person exerting their will to influence the activities of the brain? I'm trying to understand what you are imagining happening, and who is involved, when this alternate routing occurs.

And do you mean change it on the fly, or permanently? I am inclined to vote for closure when this question is not clarified and/or specified.

OK jonsca you said it theoretically can be done. Can you show me a refrence that describes it with details?

"Neurological signal", or as I would put it, action potential, or activity propagation can be modeled as current in an electrical circuit. Trick is that such a circuit contains a bunch of highly regulated and non-linear and non-static elements. Imaging bunch of potentiometers (variable resistances) in your circuit. And all of them behave depending on something else in the system. So certainly currents will go somewhere, but level of control and complexity is phenomenal.
An example that should let you appreciate possibility of rerouting is simple Pavlovian conditioning. Neutral stimulus (bell) that has no evident connection to stomach, after conditioning elicits response there. Even though circuitry is very complicated and signal propagation is hard to investigate, this is an evidence that changing path of signals is very possible in some way. (Of course, conditioning require changes in higher-than-stomach systems, some intermediate levels).
On more practical note, we can readout neuronal activity in region A (of brain, muscle or else) and rely it via electrical stimulation somewhere in brain or muscle or gland. Both parts of this are available technology. As of drugs, some people report "seeing" sounds while intoxicated, this might be an example of such temporary effects.

How can neural activity being relayed to a muscle or gland? This seems to be at the heart of the question and references are needed. Further, psychotropic drugs alter brain activity not by changing connectivity but by changing synaptic activities within existing connections afaik. Here too references are needed to prove otherwise.

Also, a potentiometer although having a resistance, is a recording device and it's neural representation is unknown to me.

potentiometer is variable resistance, it can be analog or digital. Neural activity drives muscle through NMJ. You can readout muscle activity through afferent cells. I am precisely not talking about connectivity, but about changing final route. You have roads around, but take different route every day, based on traffic. In neurosystem you can do similar things


text:
What are necessary parameters for a tissue scaffold to be biodegradable?`
I am a mechanical engineer with little biological experience, but I have recently been looking at tissue scaffoldings.
My current understanding is as follows, but may be flawed. I would appreciate any feedback: The purpose of tissue scaffolding is to provide a structure where there is none, and to facilitate healing. The tissue scaffolding is typically porous because it must facilitate the transport of cells during the inflammatory phase of healing, while the scaffold also later provides an interface and structure for the growth of new cells. It can essentially replace extracellular matrix.
I understand that these scaffolds need to be made of inert material so that there are no reactions with the body. But I know that some tissue scaffolds are meant to be biodegradable, so that once stronger extracellular matrix is established, the body can go back to doing its job. But, arent biodegradability and inertness mutually exclusive?
I also understand that a major issue with tissue scaffoldings is the compatability of specific scaffold materials with corresponding tissues, and that there are issues with adherence, etc.
I was hoping to gather some more insight as to what types of challenges tissue scaffolds typically encounter, how they are dealt with, and why? I'm also in scaffolding materials' use to deliver drugs, but that may be an issue to discuss on another day.


text:
determine longest poly-purine tract
how to determine/ find the longest poly-purine tract in any genome  and this needs to be on the E. coli genome . is it to figure out the polypurine tract and then figure out the longest chain ? or is it to splice the introns and exons away from the DNA ? since E. coli's genome is 4.6 million BP long, i need some help in breaking this down ?

One comment: Bacteria have no intron/exons, only eukaryotes have them. Otherwise I don't understand your question. For what reason are you looking for the "longest poly-purine"?

i need to find out a longest poly-purine tract in a E.coli genome

Is a sequenced genome on the internet good enough, or do you need to take real cells, extract the DNA, and analyze it directly for polypurines?

yes sequenced genome on the internet is good enough

are you on windows, mac, or linux? Please say linux.

Code Golf!
This is my Python script, avoiding regex and not at all prettified.
def gettract(strand):
    #if strand is 1 then replace C with T and split on T
    #else replace A with G and split on G

    if strand==1:
        print 'top strand purine tracts:'
        aseq=seq.replace('C','T')
        tracts=aseq.split('T')
    elif strand==2:
        print 'top strand pyrimidine tracts:'
        aseq=seq.replace('A','G')
        tracts=aseq.split('G')
    sortedtracts=sorted(tracts,key=len,reverse=True)
    for i in range(5):
        print len(sortedtracts[i]), sortedtracts[i]

f=open('ec_dna.txt','r')
l=f.readlines()
print 'Sequence analysed is %s' % l[0][1:] #the header line
f.close()
seq=''.join([i.rstrip() for i in l[1:]])
print 'sequence length is %i' %len(seq)
print
gettract(1)
print
gettract(2)

And here is the output:

Sequence analysed is E. coli K-12 MG1655 U00096.2 (1 to 4639675 = 4639675 bp)
sequence length is 4639675
top strand purine tracts:
28 AGAGAGAAAAGAAGAAGAGAAAAGAAAA
22 GGGGGAGAAAGGGGGGAAAAGG
20 AAAGAGGAAAGGGGGGGGGG
20 GAAGAGGAAAAGAAAGAAGG
20 AAAAAAGAAGAGAAAAAAGA
top strand pyrimidine tracts:
29 TTTTTCTCTTTCCCTTTTCCCTTCCCTCT
22 CCCTCCTCTTCTCTCCCTCCCC
21 TTCTCCTCCTTCTCTTTTCTT
21 TTTTTCTTCTCTCTTTTCCTC
21 CTCCCCTTTTCCCTTTTCTCC

The longest purine tract is 29 bases long, and is on the bottom strand.
This script doesn't handle the problem that the E. coli genome is a circular molecule, so if the longest tract was split at the origin it would be missed - I leave that and obtaining the coordinates of the longest tract as an exercise.

Since you said an internet sequence is good enough, I will propose a computer programming approach. The basic idea is to enter the sequence as a string of text and then have the program read the text, keeping track of the length of the current polypurine tract, and the longest encountered so far. When it's done, it reports the longest one. I'm not sure if you know any programming, so I'll attempt to write up an example in C++ and post it. There are probably other programs that can do this, but I don't know about them.
Here is the code:
main.cpp
#include <fstream>
#include <iostream>

// this program reads a DNA sequence from a text file and then looks for
// the longest polypurine sequence. Please make sure there isn't non DNA
// text in the text file. Please call your text file "DNA.txt" and place
// in the same folder as this program.

std::string base_complement(std::string in){
    std::string return_me = "";
    for(int i = 0; i < in.size(); i++){
        if(in.c_str()[i] == 'a' || in.c_str()[i] == 'a'){
            return_me += 'T';
        }
        if(in.c_str()[i] == 'g' || in.c_str()[i] == 'G'){
            return_me += 'C';
        }
        if(in.c_str()[i] == 't' || in.c_str()[i] == 'T'){
            return_me += 'A';
        }
        if(in.c_str()[i] == 'c' || in.c_str()[i] == 'C'){
            return_me += 'G';
        }
    }
    return return_me;
}

int main(){

    std::cout << "WELCOME TO POLYPURINE COUNTER" << std::endl;
    std::cout << "WRITTEN BY SAM CROWLEY, SAMUEL-CROWLEY@UIOWA.EDU" << std::endl;
    std::cout << "WILL READ THE DNA IN DNA.txt AND REPORT LONGEST PURINE STRETCH" << std::endl;
    std::cout << std::endl;
    // open the file and read the contents into the string
    std::string DNA;    // this string will hold the entire DNA sequence
    std::string line;   // this will hold one line of the file at a time
    std::ifstream text_file("DNA.txt");

    while(!text_file.eof()){        // read the file until we get to the end
        getline(text_file, line);   // get one line at a time in the line string
        DNA += line;                // add that line to the DNA string
    }

    //std::cout << DNA << std::endl;  // output the DNA string just to check

    int current_tract = 0;          // length of current tract
    int longest_tract = 0;          // length of longest tract so far
    // true = sense strand, false = opposite strand
    bool tract = (DNA.c_str()[0] == 'a' || DNA.c_str()[0] == 'g');
    char c = DNA.c_str()[0];
    std::string purine = "";
    std::string pyrimidine = "";
    std::string longest = "";
    if(c == 'a' || c == 'g' || c == 'A' ||c == 'G'){
        purine += c;
    }else{
        pyrimidine += c;
    }
    for(int i = 1; i < DNA.size(); i++){    // iterate through the DNA string
        if(c == 'a' || c == 'g' || c == 'A' || c == 'G'){
            if(DNA.c_str()[i] == 'a' || DNA.c_str()[i] == 'g' || DNA.c_str()[i] == 'A' || DNA.c_str()[i] == 'G'){
                purine += DNA.c_str()[i];
            }else{
                std::cout << purine << std::endl;
                if(purine.size() > longest.size()){
                    longest = purine;
                }
                purine = "";
                c = DNA.c_str()[i];
                pyrimidine += c;
            }
        }else{
           if(DNA.c_str()[i] == 't' || DNA.c_str()[i] == 'c' || DNA.c_str()[i] == 'T' || DNA.c_str()[i] == 'C'){
                pyrimidine += DNA.c_str()[i];
            }else{
                std::cout << pyrimidine << std::endl;
                if(pyrimidine.size() > longest.size()){
                    longest = pyrimidine;
                }
                pyrimidine = "";
                c = DNA.c_str()[i];
                purine += c;
            }
        }
    }
    if(purine.size() > 0){
        std::cout << purine << std::endl;
        if(purine.size() > longest.size()){
            longest = purine;
        }
    }
    if(pyrimidine.size() > 0){
        std::cout << pyrimidine << std::endl;
        if(pyrimidine.size() > longest.size()){
            longest = pyrimidine;
            longest = base_complement(longest);
        }
    }
    longest_tract = longest.size();
    std::cout << std::endl;
    std::cout << "LONGEST POLYPURINE STRETCH IS " << longest_tract << " BASES LONG." << std::endl;
    std::cout << "LONGEST STRETCH IS " << longest << std::endl;
}

If you're running linux put the file in a folder and use a terminal to go that folder, then run g++ main.cpp -o polypurine.exe Then run it with ./polypurine.exe
The DNA sequence goes in a file called DNA.txt in the same folder. Make sure it only contains a, t, g, c, so remove any header data or other annotations. If it contains an X, N, or other symbol to represent ambiguous bases I don't know what will happen, but the results may not be accurate. I forget which is used for purines and which for pyrimidines, but if you tell me I can modify the code to make it work with some ambiguous bases.
If you use windows or mac this same code should work but compiling it into a working program will be different. I don't program on those machines so I don't know how to make this work on them.
Also, I ran a test on the cDNA for bee venom PLA2 and got a longest purine tract of 17 bases. I think I can post that DNA here:
Bee Venom PLA2 cDNA
atgattatctatccgggtacactgtggtgtggtcatggtaataaaagcagcggtccgaacgaactgggtcgttttaaacataccgatgcatgttgtcgtacccatgatatgtgtccggatgttatgagtgccggtgaaagcaaacatggtctgaccaataccgcaagccatacccgtctgagctgtgattgtgatgataaattctatgattgcctgaaaaacagcgcagataccatcagcagctattttgttggcaaaatgtacttcaacctgatcgacaccaaatgctataaactggaacatccggttaccggttgtggtgaacgtaccgaaggtcgttgtctgcattataccgttgataaaagcaaaccgaaagtgtatcagtggtttgatctgcgcaaatatggatccatggataaagttttccggaattccgcaaaaaagaagagaaaggtagaagaccccaaggactttccttcagaattgctaagttttttgagtccaagcgcggccgca

If you use this program for publications or anything, let me know. I put it here so you can use it, but I'd at least like to know if it's used.

Why do you need to do this?
This is pretty simple with the right computer tools and some knowledge of how to use regular expressions, but the fact that you are daunted by a 4.6 Mbase file suggests to me you don't  have that.
Using an old copy of E.coli DH10B, and Lasergene's SeqBuilder, I found a stretch of 29 Cs and T's, so in the reverse stand, that would be a poly-purine.  I don't see a longer stretch in my fasta.

thank you  for the reply . can you share your code or steps followed ? iam trying to use regular expressions . what are the recommend tools needed ?

Can I get the DNA sequence you used? I'd like to test it against my code.

I used commercial Windows software, just to get the answer fast.  If I was going to do it in Perl, I'd make sure newlines were stripped out, and just search for /[AG/{30}]/ and if I didn't find it, I'd keep dropping the number until it hit.  And the same for CT strings.  You might not be able to search the whole 4.6 million letter string at once, but cutting it into overlapping first 10k long pieces should work.  Grep in Unix might be able to handle the whole string at once.

I meant /[AG]{30}/ or /[CT]{30}/

search for /[AG/{30}]/ and if I didn't find it, I'd keep dropping the number until it hit... I like this method.. It is likely to be fast. But the issue is that it wont be able to find all instances- but a small modification in the code would fix it. Keep removing the part rightwards from the first match position and continue regex search. An awk example here

Just search for /[AG/{30}]/ and if I didn't find it, I'd keep dropping the number until it hit - swbarnes2

Code for swbarnes2's method (will work on Linux terminal, Mac Console and cygwin terminal)
Usually in a genome file a single fasta sequence will represent one chromosome. In E.coli there will be only one. You would need to pop the fasta header (first line) out when analyzing your sequence. (Assuming that you have done so).
This code below will find all polypurine tracts of a given length in the genome. Basically you have to keep dropping the part from the sequence start to the match location and redo the regex search.
cat ecoli_genome.fa | tr -d "\n" | awk '{for(i=30;i>=10;i--){
pp="[A|G]{"i"}"
s=$0
while (match(s,pp)){
       print substr(s, RSTART, RLENGTH)
       s=substr(s, RSTART+RLENGTH)
    }
 exit
}
}'

Regex searches of type /pattern{N}/ may not work on all versions of awk. It does work in gawk >=4.0 but doesn't work in mawk.
This will load the entire genome sequence in the RAM (this is not huge at all). If you have RAM limitations and the genome file is really huge then you can stream read letter by letter (but you can't do regex search in this case). Stream read and regex are two strong features of awk.


text:
If evolution is a gradual and continuous process, how can we say humans came about 200k years ago? What is so special about that point in time?
It just seems arbitrary to me to say "ok, now THIS is officially a human" when you could look at its parents and find no noticeable differences. At no point in the line of my ancestral history is there ever a hard cutoff between one generation and the next. It's a gradual progression. So how can you possibly pick a certain point in time when humans "first came around"? What criteria is used to say what exactly differentiates humans from whatever our ancestors were before 200k years ago? Did we "branch off" from something else at this point?

It seems arbitrary to you because it is arbitrary. Your instinct is to be commended. You've got to draw the line somewhere, and it's drawn about 200kya for mostly morphological/genetic reasons. Mitochondrial Eve and Y-chromosomal Adam lived at about that time, plus minus 100k years.

You're right that evolution is largely a gradual progression, but we don't have the luxury of having that gradual progression in the fossil record. We'll have a fossil from, for example, 350 KYA and another from 190 KYA. The older one is clearly not modern human and the more recent one is. So the age of modern humans is set at approximately 200 KYA, especially since genetic calculations confirm that age.
Now, if we find a 400 KYA fossil that is clearly modern human, then there'll be some 'splaining to do, but so far, nothing like that has happened.

The 200,000 years are the age of the fossils that has been classified as the first modern human. It's not like a magic number and if an older fossil is discovered the age of the modern human will be changed.
The modern human is an anatomical feat. You probably recall the look of the Neanderthals and the obvious differences between them and us, there is a whole list of anatomical feats that differ between them and us.
Somewhere between 200k and 500k years the clade Homini split up into a lot of different hominids. The others have gone extinct.

It would be great if you could add some references/links.

The  question is a dupe if memory serves but in any case your answer doesn't address what is probably a valid point. There probably was no clear distinction and the classification is an arbitrary convenience. That we do not resemble Neanderthals seems not to have any bearing on the question. Why a period in 200000?

@daniel how is the question a dupe? what do you mean?

He means it's been asked before on biology.stackexchange.com, like this: http://biology.stackexchange.com/questions/3304/human-evolution-where-exactly-did-the-first-human-come-from-whose-parents-we/3314#3314 Often duplicates are not exact and may have unique things worth keeping separately, despite the similarity of the questions.

Oh I see. Duplicate. I thought I was being accused of duping people somehow. My mistake.

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


text:
How prominent is the gene-centric view of evolution among professional researchers?
Richard Dawkins famously advocated a gene-centric (as opposed to organism-centric) viewpoint on natural selection, most notably in The Extended Phenotype. However, I have also heard "on the grapevine" that most professionals in biology and related areas do not take the gene-centric viewpoint altogether seriously.
My question is simple: how prominent is the gene-centric view of evolution among professional researchers in biology and related fields?

Okasha's levels of selection might be interesting here

What do you mean by gene-centric view of evolution
I am not totally sure you know what really means the gene centric view of evolution. Everybody agrees that selection (also) acts on genes and that selfish genetic elements exist. I think that what one calls the gene centric view of evolution is nothing but the modern synthesis of evolution (following the work of Ronald Fisher, Sewall Wright and some others such as Motoo Kimura).
Or maybe by gene centric view you refer to the concept of level of selection.
Some people however argue that because of the gene centric view of evolution, we tend to underestimate the importance of some parameters in evolution and some are willing to rename the evolution theory into Extended Evolution Theory according to new insights about how parameters such as developmental bias for example influence the evolution of populations.
Modern snythesis of evolution theory
You will find more information in this recent article that you may appreciate reading if it is not too complicated. I personally endorse the "No, all is well" opinion. It is important to understand that those who criticize the gene centric view in this article are NOT saying that selection do not act on genes neither that selfish genetic elements do not exist (thinks that R. Dawkins talk about in his books). They totally agree with those things. They just argue that the fisherian view of evolution in not enough and that according to recent findings we may want to rename our theory. The "no, all is well" opinion totally agrees with the importance of these new insights that do not come from what one may call the gene-centric view of evolution but they just don't think it is worth renaming the theory for that because our knowledge in evolution is just growing as it has always been growing and it doesn't seem that we are currently living a revolution in our understanding of evolution. I think that the main revolutions that happen to occur in evolution these days mostly have to do with the methodology of testing rather than with the theory itself. These revolutions have to do with increased computer power, better statistical methods and faster and cheaper sequencing.
Level of selection
Now, by gene-centric view of evolution you may refer to the concept of level of selection. To my knowledge everybody agree that selection occurs at different levels. Again, NOT everybody agree on the relative importance of selection acting at different level. The vast majority of research focus at evolution at the gene level, sometimes implicitly only.
To conclude, we all agree on the theoretical principles (I think) but not everybody agree on the relative importance of the different mechanisms. In saying this, I don't mean that everybody agree with everything that is written in R. Dawkins books!


text:
How are sequential patterns grouped into meaningful objects in the brain?
The background how I came up with this question derives from information theory so I am not sure that it will formulate it well.
What I am looking for it is the process how our brain forms patterns.
Lets say I have word “Hello” (It is a complex example, but lets say that our brain is blank and sees it for the first time and somehow it can form only this pattern).
How our brain (neurons, synapse connections) “knows” that certain signals should be grouped and after “H” waits for “e” and “l” and so on.
Why it makes certain connection or just “cuts” and waits for new one.
As our brain is so complex, I am not looking for all scenarios how in could be influenced in terms of chemical neurotransmission, but I am looking for a basic principle of how it is done, i.e., how our brain manages to translate patterns into certain connections inside the brain.

I don't have time to write a full answer, but I'd suggest you look superficially into how artificial neural networks learn new patterns: although the structure of many such networks is not biologically plausible, some of the more general concepts are both motivated by the biology and support our understanding of the biology. The short, simplistic answer is that patterns themselves are associated with more abstract concepts. It isn't likely that the brain processes "hello" as h-e-l-l-o, but as a full word: hello, whether heard or read.

3/1 Well, I want to bridge from the information theory perspective to the biological perspective, but still want to keep biological background. I know that “Hello” it is not that great example as it is already complex structure and looking for very basic principle or lets say very beginning how those patterns are created.

3/2 Scenario:
If we receive different sound frequency or combinations of different light lengths,  somehow our body should differentiate inputs and “assigns” it to neurons (guessing). Based on this assumption I looking for an explanation that could explain how those differentiated and “assigned” signals to neurons, creates a connections between each other.
How those neurons that represents different signal spectrum end up connecting and form certain mirror of that signal complexity.

3/3 Brainstorming:
Is it almost the same timing and chemical released that allows neurons connect together.
Is it near the same location where signals are sent and neurons forms connections there with help of chemicals.

I'm a little confused by what type of answer you are looking for, because you talk about information theory but you aren't using any of the terminology of information theory (except "information" which is pretty broad and colloquial). I think you are also asking for answers at too many levels of analysis: you are asking about information and systems level organization and at the same time asking about neurotransmitter release and spike timing dependent plasticity. Can you try to clarify a bit what you are looking for?

At this case I think I am looking for spike timing dependent plasticity as the first step even though my question asking is complex, as I see now. Your question gave better insight in to mine own question.

The key here is the Gestalt principle formulated in the early 1900's consists of a set of 'laws' describing how perception elements are grouped into recognized objects. The Gestalt laws "prescribe for us what we are to recognize 'as one thing'". Recent data support this view (Pelli et al., 2009).
On a more fundamental level working memory is essential in this process. It is a form of short term memory. An example where short-term memory comes into play is when information is cut up in pieces, like in your example - 'Chunking' is the organization of material into shorter meaningful groups to make them more manageable.
Short-term memory is supported by transient patterns of neuronal communication in the regions of the frontal, prefrontal and parietal lobes of the brain. Long-term memories are maintained by more stable and permanent changes in neural connections widely spread throughout the brain.
The hippocampus temporarily stores information and gates it to the long-term memory. Typically, information is transferred from the short-term working memory to the long-term memory within just a few seconds,
Reference
- Pelli et al., Cogn Neuropsychol (2009); 26(1): 36-49


text:
How do disulphide bonds in hair cause curling?
I understand that there are several characteristics of curly hair which differ from straight hair (such as an asymmetrical distribution of disulphide bonds in curly hair), but really am struggling to understand the root cause of inherent curl on the macroscopic level.
My current understanding of the hair structure is based mostly upon this website
The most relevant part of the hair for our discussion is the cortex, which is made up of many axially aligned macrofibrils, or macroscopic keratin fibers, which are in some filler essentially of lipids/proteins. Inside these macrofibrils are microfibrils. These are also aligned axially and in some filler of lipids/ proteins. Inside the microfibrils are the protofibrils, even smaller fibers which are twisted around each other like a yarn. These protofibrils are made up of 4 keratin chains which are essentially twisted together and connected by disulphide bonds and hydrogen bonds. While hydrogen bonds are easily broken, the disulphide bonds are not. In curled hair, the macrofibril isn't symmetrical but I am unsure as to how this, or what other effects, actually lead to the curling.
I had previously assumed that the reason for curling is that in an asymmetrical configuration of the hair(IE not cylindrical but more oval in cross section), some residual stresses are formed by the disulphide bonds between the keratin, If this is true, it would lead me to believe that it would cause increased buckling of the protofibrils. But, even with straight hair and more symmetrical disulphide bonds, you already have some curling and buckling of the protofibrils, but the hair doesn't curl on a macroscopic level.
As such, it doesnt seem like this buckling due to asymetrical disulphide bonds would necessarily lead to a curled or organized structure on the macroscale, with the macrofibrils. This leads me to believe I am missing something.

Nice question. I must say it took me many hours to get satisfactory answer.
Hairs are made of keratin molecules, which contain cysteine. Cysteine has thiol (-SH) group, by which it can form disulfide (-S-S-) bond with another cysteine of another keratin, causing bending of hair. See this image from here:

Curling of hair can be justified on both microscopic and macroscopic level.

Microscopic level: See this post from here:

Curly hair has to do with the chemical bonds in the protein that makes up hair - $\alpha$-keratin. Keratins, particularly $\alpha$-keratin, have long sequences of amino acids (often more than 300) which forms a helical structure.
Pairs of these helical structures then coil about each other in a left-hand coiled-coil structure. These are then attracted to another coiled coil so two keratin helices will stick together. These four-chain structures then associates with another four-chain structure to form the hair filament. One of the amino acids which make up these chains, is cysteine which has a sulpher group which is able to make connections with other sulpher groups on other coiled coils.
The more interactions a filament has with another filament, the more tightly coiled the coiled-coil becomes. Hence, curly hair has more interactions than straight hair. The process of `perming' hair introduces more accessibility of the sulpher on the amino acid, cysteine, to make these connections. Finger and toe nails have many many bonds between filaments and are thus, very hard.

For example, see how hairs are curled artificially via perming.

Source
This change in location of bonds is what causes curling of the hair (look again at the first diagram and notice the orientation of disulfide bridges). Those vertical strands now get curled due to change in these bonds. Here, the required mechanical tension for bending is provided artificially.

Macroscopic level: Shape of hairs is also determined by its macroscopic structure. Look at this article:

All hair, whether curly or straight, has two major components: the shaft and the follicle. The shafts are the visible, flowing strands that we see on our heads. The follicle is the part of our hair that resides within the skin, or dermis, of our scalp. Each of these structures plays a role in determining our overall hair shape.
Let’s start at the root of the issue (pun 100 percent intended): the follicle. It turns out that the shape of our follicles is a major determinant of our hair texture. If you were to look at the follicle of straight hair, you would find it is perfectly round. The follicle of curly hair adopts an oval shape. The flatter the oval is, the curlier the hair will be.
Another contributing factor to a hair’s curl is the way the follicle tunnels into the scalp. Follicles of straight hair tunnel vertically down from the skin’s surface into the dermis. If the follicle angles into the dermis then the hair will curve as it grows causing it curl. Although, this curving of the follicle can lead to gorgeous curls it causes one major drawback that all curly-haired persons can attest to, dryness. Within the dermis, special glands line the follicle to secrete oil, called sebum, to lubricate the hair. Unfortunately, when follicles curve sebum isn’t able to travel the length of the hair as well leading to dryness of hair that doesn’t get lubricated.

Source
Although how shape of follicle determines structure of hair strand is probably not known, the major contributing factor likely is how hair emerges from the scalp. When it emerges in a bent shape, it faces a lot of tension from the scalp, which causes it to bend in the shape of the follicle to form curls. Since straight-emerging strands don't face such forces, they do not lead to curled hairs.
In this way, hair curls are a consequence of large number of disulfide bridges between keratin molecules and how the hair emerges from the scalp.

Yes, this is an excellent summary of essentially what I had read on the internet as well. However, it fails to fully address the root of the question: why exactly does the disulfide style bonding. We have two obvious contributors to curling: 1) high twisting in the alpha-keratin and 2) asymmetry in the cross section. It seems like 1) may change the elastic modulus of the hair, thus making it more susceptible to bending, while 2) changes the cross section and (assuming the cross sectional area is roughly the same) render the hair more vulnerable to curling.

However, the root cause is still not addressed. There is some cause that is leading to the actual curling. The two factors mentioned previously don't directly cause curling, there must be some residual stress that occurs during the hair growing process. In my mind, this residual stress may occur in several different manners but most likely due to a change in surface chemistry as the hair grows into atmosphere. This change in surface chemistry likely leads to a change in mechanical properties, which in turn induces a mechanical stress and leads to curling.

@user2341 it seems I still have not caught the root of the problem. Apologies, but could you please explain what I have failed to answr here?

As in my previous comment, there is no information regarding the cause of the curling. I went on to speculate as to causes in my previous comment, but I'm not sure that any actual evidence as to the cause or the reason why hair curls.


text:
Why are there splice variants within the same organism? What might contribute to the need for the feature?
I only know splice variants are produced by different combinations of introns and exons. I wish to know why there is a need of such function. Perhaps using the same amount of DNA sequence to produce multiple proteins saves genetic material. Also, I want to know what contribute to the need for splice variants feature (e.g. evolutionary pressure, the need to increase the complexity)
I find that in human, protein CD81 is predicted by Ensembl to have a lot of splice variants (http://grch37.ensembl.org/Homo_sapiens/Gene/Splice?db=core;g=ENSG00000110651;r=11:2398547-2418649;t=ENST00000475945). However, only 1 of them is characterized. Thus, splice variants seem redundant. Any examples of splice variants actually carry different function?

The reason is very simply to provide enough variation in a limited sized genome to produce the repertoire of proteins produced by the cells of multicellular organisms. It is also a matter of efficiency and reduced energy consumption.
Consider that on average there are about 100,000 unique protein types being produced in a human cell [1], but the human genome is estimated to contain only 19,042 protein coding genes [2], then the cell needs some way to vary that limited instruction set.
Also remember that differentiated cell types express certain genes but not others, and produce different proteins that other cells do. So that implies that there are more than 100,000 different types of human proteins, and far fewer than 19,042 genes being expressed in any one cell at the same time.
So without splice variants, our genomes would either need to be far larger than the approximately 3 billion base pairs it is already or our repertoire of proteins would be significantly less. We would also have a lot of redundancy, as many common exons would have to be repeated over an over again. That would require a lot more energy for DNA synthesis, and nucleic acid synthesis, etc. The process would become inefficient rather quickly and would likely make complex multicellular animal life untenable.
There is a bit of an error in your question. Splice variants are identified by the mRNAs that are produced, and exons are defined by the sequence that is in the mature mRNA. Introns are, by definition spliced out of the pre-mRNA, meaning that splice variants are not "produced by different combinations of introns and exons." Splice variants will only consist of different combinations of exons. The only time an intron would be found in a mature mRNA is if a splice site is mutated and it is no longer recognized by the spliceosome, so it leaves the intron in incorrectly. This will generally result in a non functional protein.
EDIT

The collection of components required to carry out the intricate processes involved in generating and maintaining a living, breathing and, sometimes, thinking organism is staggeringly complex. Where do all of the parts come from? Early estimates stated that about 100,000 genes would be required to make up a mammal; however, the actual number is less than one-quarter of that, barely four times the number of genes in budding yeast. It is now clear that the 'missing' information is in large part provided by alternative splicing, the process by which multiple different functional messenger RNAs, and therefore proteins, can be synthesized from a single gene.

-Expansion of the eukaryotic proteome by alternative splicing: Nilsen and Graveley

Alternative splicing of pre‐messenger ribonucleic acid (pre‐mRNA) allows the generation of different mRNAs from the same gene. Evolution of alternative splicing affecting translated regions of mRNAs permits the synthesis of different proteins from a single gene, significantly increasing the diversity of the protein repertoire.

-Patthy, László(Apr 2008) Alternative Splicing: Evolution. In: eLS. John Wiley & Sons Ltd, Chichester.
Also while I am not one to accept a Nobel Prize at face value, they are usually awarded when the field accepts the explanation of the hypothesis. The 1993 Nobel Prize in Physiology and Medicine was awarded to Richard J. Roberts and Phillip A. Sharp "for their discovery of 'split genes'."

Thanks AMR! Do you know any sources to back the argument? I feel like the answer is rather a deduction from the two cited numbers. Or the deduction you gave is widely accepted?

You cannot escape the deduction, but it is pretty much universally accepted.

An interesting application of splicing is in CD45 on T cells. Essentially, effector and memory T cells express a splice variant that is shorter than the CD45 expressed by naive T cells, and it facilitates faster TCR signalling. The splice mechanisms that catalyze this variant are activated during the effector/memory state. In this case we're not trying to fit more genes into less DNA, we're actually increasing efficiency of a system! Some light reading on CD45.

@Kendall, I am not sure I see your point? The entire pre-mRNA of the gene encoding CD45 will be transcribed. The regulation of splicing determines the isoform that the cell expresses and significantly increases the probability of that isoform, but does not change the fact that there are several possible isoforms present on the on the pre-mRNA to chose from. That the isoform expressed is more efficient is a function of the conformation of the molecule that alternate splicing choses. No? Somatic recombination of BCRs and TCRs are more in line with what I think you are trying to point out.

There was no point other than an example of utility, but if that was a poor example I apologize!

@Kendall Not a poor example, just an example of regulated alternative splicing, which is something I did not address in my answer. That is probably worthy of an answer of its own if you are up for it.

Insofar organismal complexity is defined as the number of known cell types, there is a strong relationship between splicing, the repertoire of isoforms and organismal complexity.
See paper here

I personally think that you embark up a slippery slope when you try to qualify or quantify organismal complexity. It is only a veiled attempt at trying to justify ones place in an arbitrary hierarchy of living things. More important than complexity is the study of homology, as it gives us insight into processes and allows us to test hypotheses without having to rely on empiricism. If we can amass evidence by studying flies or worms or yeast that can be translated to humans, then all the better, as the costs are far lower and the time to obtain results is far less.

Also, I want to know what contribute to the need for splice variants feature.

One common function of splice variants no one mentioned is to function as a dominant negative of a longer functional full length transcript. dominant negative splice variants So it allows for additional regulation of post-transcriptional processing.
This is actually quite a common function of splice variants.
In addition, as others have mentioned, it adds complexity at a reduced cost.  Many transcription factor proteins have both transactivation domains (ability to interact with and regulate DNA transcription) and protein-protein interacting domains. With splicing variants, the organism can make different parts of that protein that are functional for only one subset of activity.


text:
Bacteria resistance to natural antibiotics?
It is a known fact that bacteria develop immunity to antibiotics. Why then did not all bacteria develop immunity to natural antibiotics like penicillin in the fungi?
It is for sure that fungi did not care to continue killing all bacteria so that them won't be able to develop immunity (as we're adviced today to use antibiotics carefully, in order not to develop a superinfection)..
Looking at all the time span that bacteria and fungi exist, it seems unlikely that there'd be any bacteria left not yet immune to penicillin at all. However, that's not the case, the antibiotic is still a rather successful one.

As far as my limited genetics background allows me to assess this question, it is population genetics. Let's not close this well-researched question based on a philosophical community question..

@AliceD hi! I am sorry, I think I don't get your second sentence... could you please say it differently? :)

@noncom - that second sentence was addressed to the community at large. Don't worry about it.

@AliceD however well researched question might be, if it is a case of the CW post, then there is no point repeating the same stuff again and again. Newton's law does not change if you replace a "ball" with a "car". Why did all bacteria not evolve antibiotic resistance is clearly an example of the CW question. Just replace "organism" with "bacteria" and "trait" with "antibiotic resistance". Can you explain why this post is different? Also, that post is not philosophical. We created the post such that all possible relevant scientific points are cited to address the evolution problem.

@noncom many bacteria previously sensitive to the antibiotics are becoming resistant.

@WYSIWYG So, basically, you have marked the question as a duplicate of a question on general trait acquisition/persistance and together with that you give a broader answer in the comments that there actually are bacteria that become resistant, but do not mention if you mean natural or engineered antibiotics. Turns out that you have attributed half of the question as a duplicate of another, but marking the whole question as duplicate, and the other half was simply ignored at first and then briefly touched in the comments. Thus, the question was first broken down, and then its parts mistreated

@WYSIWYG Technically, you are right, the "why" of my question is probably answered in the referred duplicate, but there's more to it, and that "more" is being lost.

@noncom Okay. You can edit your question to focus on the "more" part; add more details so that it is no more yet another example of the CW question. We can have this reopened then.

For a natural immunity to evolve, two things have to happen:

The immunity has to actually occur. That means all the necessary mutations will need to be there to grant this bacterium resistance to penicillin. For penicillin, for example, bacteria that evolved such a resistance evolved to produce the enzyme beta-lactamase.
The immunity has to grant an advantage. Penicillin is produced by Penicillium, which is a mold found in environments with lots of oxygen. Lots of bacterial species have never encountered penicillin and the vast majority (for example anaerobic bacteria that don't infect humans) never will. In the absence of this pressure, a resistance to penicillin, even if it evolves, will likely deteriorate within a few generations because the individuals with the resistance do not have an advantage in survival. Producing an enzyme such as beta-lactamase is not without its costs (protein synthesis).

While bacteria van exchange genetic material in the form of plasmids between different species, so not all species would need to evolve beta-lactamase de novo, this is also only "helpful" if the bacteria a) come in contact with resistant bacteria species, and b) if this resistance confers an advantage for the receiving species.
Origins and Evolution of Antibiotic Resistance
Mechanisms of Bacterial Resistance to Antibiotics

Penicillin is made by Penicillium, not Aspergillus.


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Who were the first authors to talk about local adaptation?
I was curious to read about what Darwin had to say about the existance of locally adapted subpopulations. I discovered to my surprise that the expressions and terms "local adaptation", "spatial heterogeneity" (or just "heterogeneity" even) and "environment" are completely absent from On the origin of Species. The expression "local conditions" was found 12 times but I could not find a place where he would suggest subpopulation of the same species could be locally adapted to their environmental conditions.
Who were the first authors to talk about subpopulations being locally adapted to their environmental conditions? Who were the first authors to understand the role that migration plays in reducing local adaptation?

Darwin mentions adaptation and coadaptation ample times in The Origin. All adaptation is local, I submit. The word adaptation comes to us from natural theology as Chambers showed in a later edition of Vestiges of Creation.

“… ‘second, of another impulse connected with the vital forces, tending, in the course of generations, to modify organic structures in accordance with external circumstances, as food, the nature of the habitat, and the meteoric agencies, these being the 'adaptations' of the natural theologian’." 10 ed. Of Vestiges of Creation, quoted by Darwin a later ORIGIN


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Limits of brain neuronal spatial mapping
It is being claimed that brain maps the world space in (roughly) 1-to-1 correspondance of a place to a neuron (link1, link2).
My question is: as the mapping happens in 1-to-1 manner, then is it logical to assume that the brain loses the ability to map space anymore when it already has each suitable neuron assigned to a place?
From these articles, it is clear that the space unit is not very big, and is a sphere of some size not significantly bigger than the body. If the answer to the question is "yes", then what is the approximate size of the world we can map? (any metric would do, be it a volume in liters or surface area in square meters).
Other than that, if the observations described in the articles are lab simplifications, and in real life the mapping mechanism is more complex, then what is it like?


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Would blue light be effective to help average people when sunsets come much earlier in the day?
I know people with SAD (Seasonal Affective Disorder) benefit from blue light in the winter as night-time comes much earlier (in the UK, sunset is around 4pm in December, compared to 9pm in June).
However, during winter (say the UK), would the average person also benefit from more blue light in the late afternoon/early-evening than standard light bulbs currently supply?


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Reasons for the HIV-1 epidemic
So, the HIV-1 jump to humans occurred as early as the 1920s, but the AIDS epidemic didn't start until the early 1980s.
Some things I don't understand about this:

Why the delay?
What is needed for a successful zoonosis transmission in the first place?
If Bushmeat practices (eating meat from non-domesticated animals, in this case HIV-infected fruit bats) have been the same for centuries, why has HIV only really spread in THIS century?

There is probably a decent answer, and aandreev may have touched on some the reasons, but I don't have time to write one right now. I have heard about blood samples taken in the Congo in like 1914 that tested positive for HIV. The advent of european colonialism, easier travel with trains, etc probably allowed HIV to get from remote villages to larger cities. Also, the virus probably had to mutate to grow in humans instead of only chimpanzees. So it probably took both the mutant virus getting into a human at the same time as travel became easy.

As usual, Wikipedia has a long article on this topic. Did you read it?

if Bushmeat practices (eating meat from non-domesticated animals, in this case HIV-infected fruit bats) have been the same for centuries, why has HIV only really spread in THIS century?

We can't really rule out the existence of similar epidemics in the more distant past. In fact, almost certainly they were transmission events from bushmeat (not necessarily of the same virus). The thing that made 20th century different, as the other commenter rightly says, is the mobility. Previously, such transmissions would have lead to local epidemics which would have run their course - leaving super-controllers or individuals with immunity and killing everyone else. And since most of the African cultures haven't left a written record we wouldn't know about such isolated local epidemics. Not to mention that in the unlikely event of such records existing they would hardly be scientific - the disease would be most likely attributed to "evil spirits" or some other supernatural cause.
So, it is really the mobility, the public policies (mass vaccinations by colonial authorities that used the same syringes repeatedly) and the fact that we can retain information in a much better way which make the HIV epidemic different than the ones that almost certainly have happened in the more distant past.


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G>T transversion VS. T>G transversion?
So I'm reading about how mutations in DNA can be caused by oxidative damage. An example of a product of oxidative damage is given: 8-oxo-7-hydrodeoxyguanosine
My textbook says that this product frequently mispairs with A, resulting in a high level of G-->T transversions.
What I'm not understanding is why it's a G-->T transversion. If the 8-oxo-G is pairing with A, resulting an an A-G pair, isn't this a T-->G transversion? Or does the order not matter?

Originally the position had a G:C pair. After the mutation, there is an oxoG:C pair. Upon replication, the strand with C will pair to G and the original pair will be created as expected. However, since oxoG can also pair with A, the strand with oxoG may form an oxoG:A pair. Another round of replication gives the products T:A and oxoG:A. Thus the G in the original strand is replaced by T (ie it is a G$\ce{->}$T transversion).


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Do the right-handed people tend to use the right side teeth of their jaw to chew food more often than the left-handed people?
And vice versa, do the left-handed people tend to use the left side teeth of their jaw to chew food more often than the right-handed people?Or the frequency of food chewing distribute fairly to both sides of the jaw?

Related: https://biology.stackexchange.com/questions/57361/do-animals-exhibit-handedness-paw-ness-preference

Individuals have not only hand dominance but also a dominant foot, eye and ear. There has also been a belief that this sidedness applies to chewing as well. However, the short answer is that no one is sure, but that it may be related to handedness. I only looked at studies done after 2000.
One large study[1] found a questionable to weak correlation, not consistently maintained through different dentition (baby teeth, mixed, and permanent). A slightly smaller study showed a correlation; in 78% chewing side preference correlated with other tested lateralities (footedness, handedness, eyedness and earedness).[2] Another similar sized study found none.[3]
A small 2012 study found that there was a preference for right sidedness when chewing hard food (73.68%) and for soft food (57.89%) but failed to correlate this with hand/other-sidedness.[4] Another small study tested for sidedness, finding that 55% of subjects did not have any side preference, 30% preferred to chew on right and 15% preferred the left side, and this was reproducible in 90% of subjects only with almonds (a medium hardness food) as opposed to jerky or asparagus. Unfortunately they did not measure sidedness. Their findings were that chewing-side preference is not a fixed characteristic, and texture seemed to affect sidedness.[5] A review article determined that a person's dental condition to a large extent dictates how they chew.[6]
The studies were mostly designed very differently, making good comparisons difficult. I think it's safe to say it's possible but not known with certainty.
[1] Absence or weak correlation between chewing side preference and lateralities in primary, mixed and permanent dentition
[2] Chewing side preference as a type of hemispheric laterality
[3] Relationship between chewing side preference and handedness and lateral asymmetry of peripheral factors
[4] Chewing side preference in first and all mastication cycles for hard and soft morsels
[5] Chewing-side determination of three food textures
[6] Adaptation of mastication in response to the characteristics of the individual or the food


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What mechanism prevent Colchicum Autumnale from being affected by Colchicine
Colchicine is a chemical usually used to cause polyploidy mutant by inhibiting chromosome segregation. It is synthesized in the Colchicum Autumnale. But what mechanism prevent C. Autumnale from being affected by the Colchicine?


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Can we influence evolution by teaching primates to control fire? Should we?
Most people with a strong interest in biology will have heard of Kanzi the Bonobo, the ape that has the wherewithal to collect fuel for a campfire and play pac-man.
But is it conceivable to influence the course of their evolution so that it becomes more likely they gain the intelligence to support a civilization in the distant future?
Let's face it: it's easy to imagine that Bonobos are looking superficially like early human ancestors.  They have been forced to become more peaceable and social because they are polyamourous (which is why the human phallus is shaped the way it is).
If we are willing to genetically modify them, we would have to do so so heavily the depend on the genetic modifications, or they might just get bred out again - intelligence may be delicate.
In conclusion, is it conceivable to "enlighten" some groups of primates and send them into the wild, in the hopes they (much) later evolve intelligence?  Their existence would serve as an "insurance policy" on intelligent life in the not unlikely event we destroy ourselves.

are you ready for the ethical issues that come with it?

The ethical issue isn't really one for this Q&A site, and as a side note I think most likely circumstances (global warming etc) in which we destroy ourselves are also likely to wipe out a large portion of complex life, particularly terrestrial due to flooding.

This question appears to be off-topic because it is about ethics

Is it conceivable to influence the course of their evolution so that it becomes more likely they gain the intelligence to support a civilization in the distant future?

No, I don't think so, based on what is known about evolution.
Your idea is in keeping with the opening of Kubrick's 2001: A Space Odessey, where the monolith inspires one of the primates to see a femur as a weapon. He picks it up, hits an opponent with it, and the idea catches on within his group; the implication is that this inspired male's (female's?) group goes on to domination and are the progenitors of the human race.
In real life, that's not how intelligence is passed on. You can teach a gifted bonobo how to build a fire, but if he's not into roasted meat, or really cold, or trying to scare away predators (or if he doesn't realize that's what fire is good for), all you have is one bonobo who can start fires. It doesn't influence his genes.
To actually influence evolution of bonobos, I imagine it would look like this: You capture 4/5ths of all the bonobos in the world (leave the 1/5 for genetic pool variation). You test them for basics of quick-wittedness. Kill all the bonobos that fall below a certain threshold, and release. Repeat several generations later. Keep doing so for 50 cycles. What you will have are a race of quick-witted bonobos - maybe. Because if the quick-wittedness you selected for doesn't provide them with a survival advantage, it (and they) will die out. What if the smarter bonobos all want to be alphas, and all that fun cuddling and sex-as-peacekeeping were to disappear? They might not survive the bonobo-chimpanzee wars, because they won't live in large, peaceful, cooperative groups any more. Maybe you can teach the bonobos to plant crops, assuring a food source. Will they irrigate, too? What would this decrease in roaming mean for pygmies who hunt bonobos for food?
My point is, we can't control evolution very much unless we also control the total environment they live in. That's one way we have been able to have such an impact on a rather extraordinary species: dogs. But in the end, a dog, whether it's a sheep-herding or rat-catching or boar-hunting or bull-baiting or duck-fetching breed, is still only a dog. Invaluable helpers, but after all that selective breeding, they're just dogs. The smartest dog in the world still likes to play fetch more than anything in the world. Even eating, if she's anything like my two Border Collies.


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Can anyone identify this plant?
We found this seemingly ornamental plant somewhere in the midwestern United States; does anyone know what it is?
It's fairly low to the ground.  Thanks!

If you add some more information about this plant for example widness of leafs,  specify the somewhere part of your question and you might get your answer.

From the general appearance, and from the opposite leaves (seen if you look carefully in the enlarged photo) I think this is Euoynmous europaeus (Wikipedia entry).  Specimens I've seen can grow like a ground cover, similar to your picture, but they also get shrubby/woody.  It is not native to the US.  We'd need more details/pictures to be sure, but I'm guessing from how you worded the question these might not be available.

Euonymus europeus has green twigs that are square in cross-section. There are hardly any other species (in Europe) that have this, so it is a very distinctive feature.

It will also climb a vertical surface.

I think it is Vinca minor, or periwinkle. I'm from IL and it is a common landscaped ground cover around me. It is opposite, low growing, and woody. Check out https://www.illinoiswildflowers.info/weeds/plants/periwinkle.htm to confirm, I can't give any more of a detailed answer without a more detailed picture.


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What wavelengths of lights do plants need to grow?
So, I found a list of L.E.D.'s from Cree here (the company seems to be known for efficiency, they power most of the bicycle lights that I know of) is selling a line of lights designed for growing plants.  If you click on the data sheets, you'll find something like this:

Now, I know that plants reflect green preferentially because it is the least useful color to them (energetically speaking) so I assume that this matters.
I know the first few things about electronics, so I would really like to use one of these in something that I build.  However,the question becomes:
What kind of spectrum light and I looking for?  What is the difference between the "vertical farming" lights and the greenhouse lights?  (Viewing angle?
I kind of want to put some plants in a box coated internally with aluminum foil (it can reflect more than 90% of the energy), and hook one of these bad boys up for some inside growing.  Thanks alot.

A simple Google search using the title of your question will give you many resources. The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Unresearched questions may be subject to down-voting and closure.

I'm voting to close this question as off-topic because it seems more suitable for Physics.SE

The main question is also unclear.

I think the question is on-topic but unclear and lacking in effort (exactly what do you want to grow and at what scale? what do you know from before, and what information are you missing?).


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Is it possible to convert nerve signals or electrical pulses into a readable format?
Can we have the technology to recreate the informations (like images, sounds etc.)[as in the form of signals in our mind] from human mind to human understandable format? In short, can we read human mind?

Ist of all, i am posting this question again because i have asked that question but my account was not linked to it earlier, so i m unable to comment on it.

Thus i am adding all the previous comments here

The question is slightly unclear to me. Although we can measure brain electrical activity and do things like fMRI but we can't read the human mind which is why I said the question is vague since the definition of reading the human mind is required. What I essentially mean is mind is the construct of the brain and although we can measure brain activity but mind reading is not yet possible unless we can have a highly exact knowledge of the brain activity to know how it is perceived, which I do not know if we have reached that stage yet. –  Bez Aug 20 at 13:09

For clarity, Let me ask in two ways: Our Eyes sees anything (e.g. an image of a tree) then convert into a signal/electric pulses; to be processed in mind and then stored in mind. Now, 1. Do we Have the Technology or machinery to read that image before conversion? and 2. Do we Have the Technology or machinery to read the signals after conversion? –  Khushhal Aggarwal Aug 22 at 21:23

In between these 2 questions, what happens is -- "CONVERSION" of that Information. That conversion method must be a "TECHNIQUE". Thus if we are able to design a machine to convert the same information by the same "TECHNIQUE" as used by the human mind, then it will be helpful to understand the signals after conversion. In short, can we define/design the mechanism to convert the the informations into signals/electric pulses? –  Khushhal Aggarwal Aug 22 at 21:47

for 1, I would say no. For 2 I would say fMRI is addressing this and it is at its infancy but the problem is an image, which produces lets say fMRI machine data analysed/visualised by a computer, is usually associated with many things in the human brain such memory and experience and one image can provoke another depending on the individual so its not as easy as signal A equals object A. Don't know much about fMRI but it measures neuronal activity. Apologies if i cannot be of further help. –  Bez Aug 22 at 22:51

This is what researchers are trying to do with machine learning algorithms. There have been certain successes but the field is still in its infancy. Typically one tries to decode ("read the mind") between few simple classes, e.g. does the person see a happy vs. sad face. The input to the algorithm can be EEG, MEG, fMRI, etc.
See e.g. http://www.nature.com/news/brain-decoding-reading-minds-1.13989
Things like decoding content of dreams, visual imagery, or moral judgements have succeeded this far.

I think the researchers are trying to understand/develop the converted informations (i.e. signal/electric pulse) but i am asking from a different view; i am focusing on the method by which our mind converts it. I am symbolising it as "TECHNIQUE" to convert the informations into signals/electric pulses. Thus, i want to understand/define/design that "TECHNIQUE". –  Khushhal Aggarwal Aug 22 at 22:00

Mr. Bez, Ist of all Thank you for all your support and no appologies are required but please look again at the matter with a different view. I am actually trying to understand the method to convert images into signals which i think no one else has thought of. Everybody is trying to read the signals already converted and stored into our mind. But what if we developed the Technique  by which our mind converts the informations.

This is the third post that asks exactly the same question.

Dear WYSIWYG sir, This is actually the 2nd post because i posted it again due to account problems. Please do continue to answer here. And i request you to please take a look at all the comments. Thanks

I would suggest that you edit your question to add the details that you mention in the comments.

I will follow your suggestion in all the next questions but since i had copied this question from my older post i have to mention these comments separtely because these are the comments posted by others like Mr. Bez etc. But i sincerely thanks for this kind suggestion. Now if you can give some views on the question, i will be obliged.

Sorry Mr. Bez, I am unable to understand what you are trying to say by the comment "possible duplicate of ...".


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Does bioluminescence communcation occur on macroscopic level?
Some bacteria are known to communicate using bioluminescence (quorum sensing). Do we observe the same phenomena in any macroscopic species?

don't know about bacterial light speech, but fireflies find their mates that way; or is your question specifically about quorum sensing?

Almost certainly. In the deep-sea, some species of laternfishes (Myctophidae) show sexual dimorphism in their light organs. Males have large light organs. The females are much smaller. Here is a brief summary, based on an interview with Dr. John Sparks at the American Museum of Natural History.
Sparks is discussing his recent publication with colleagues (Davis et al. 2014) that suggests that bioluminescent communication may actually facilitate speciation in some deep-sea fishes.
There are probably more instances of communication using bioluminscence in deep-sea organims but, to my knowledge, the Davis et al. paper provides the best evidence so far.

Davis, M.P. et al. 2014. Species-specific bioluminescence facilitates speciation in the deep sea. Marine Biology 161: 1139-1148. (open access)

On land, Stoltz et al. 2003 has demonstrated that positive selection has acted on bioluminescent color in Jamaican click beetles. The male beetles use the flashing to attract females for mating. Some males emit yellow light while males in a separated area have orange light.

Stoltz, U. et al. 2003. Darwinian natural selection for orange bioluminescent color in a Jamaican click beetle. Proceedings of the National Academy of Sciences USA 100: 14955-14959.

Some species of fireflies (Lampyridae, Coleoptera) synchronize their light patterns during the mating procedure. link


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Alleles notation in SNPPedia criteria
I can understand the allele notation when is in the form rs8176719(T;T) or rs8176719(G) but recently i found this ones rs8176719(T;-) or rs8176719(-;T).
So im confused, rs8176719(T;-) is the same as rs8176719(T)? or is the location is important ?
Thanks .

The '-' means that that allele has a single base deletion.


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Calculating the frequency of a recessive allele in case of three segregating alleles
Is it correct to say:
A. f(A) = p; f(a) = q
B. p = f(AA) + ½ f(Aa)=$\sqrt{f(AA)}$?
Also,

For a gene locus segregating more than two alleles, the frequency of
  each allele is the frequency of its homozygote plus 1/2 the sum of the
  frequencies of all heterozygotes in which it can occur.

For example, I have this data on blood-types from a population: 42,4% type A, 8.3% type B, 1.4% type AB, 47.9% type O. Plus we know that p(A)=0.250, p(B)=0,050, p(O)=0,692.
When I try to calculate p(O) in different ways, I get p(O)= $\sqrt{0.479}$=0,692
If I calculate p(O) as:p(O)= 0.479+½*0.424+½*0,083=0,7325
 As the result, I am getting two different frequencies for p(O). What am I getting wrong here?

Welcome to Biology.SE
A few issues about your post
You should always limit your post to a single question.
Make sure to define what the function f() and p() mean.
Use points (.) instead of comas (,) for the numbers.
You should show how you made your calculations otherwise we can't tell what is right and wrong.
Your question

is $p = f(AA) + \frac1{1}{2} f(Aa)=\sqrt{f(AA)}$ correct?

$$f(AA) = p^2$$
$$f(Aa) = 2pq = 2p(1-p)$$
$$f(Aa)/2 = pq = p(1-p) = p - p^2$$
, therefore
$$f(AA) + f(Aa)/2 = p^2 + (p - p^2) = p = \sqrt{p^2} = \sqrt{f(AA)}$$
So, yes you are correct