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If we sequenced the genome of every species, would all phylogenies agree?
The Tree of Life is still up for debate. Most of this debate seems to be due to a lack of genomic information, but that deficiency is decreasing rapidly with advances in technology and sequencing power.
Hypothetically, if we knew the genome of every species, would we resolve all phylogenetic debates? If not, what would still be up for debate?

Horizontal gene transfer
Don't expect to have a tree! Horizontal gene transfer happens and therefore we would end up with a network, not a tree.
Gene trees
Different DNA sequences have different evolutionary histories. See, in particular, the question of incomplete lineage sorting. This means that one may compute a tree for a given DNA sequence that must disagree with the tree of another sequence. So, don't expect a perfect species tree where all sequences will agree on.
Note that the two points "Horizontal gene transfer" and "Gene trees" are highly related. So much so that they could fit together.
Not all individuals have been discovered
If by saying of every organism, you meant "of every organism that we encounter", then we still have the issue of organisms that we have never encountered. If you meant "absolutely every individual that exist", then this is a non-issue. It also matters as to whether you mean every individual of every species or just one individual per species.
Also, it is slightly unclear whether, in your hypothesis, we can sequence all dead individuals! Extinct lineages would still not be resolved if we cannot sequence them.
Massive mutational events
It is possible that very large mutational event could prevent us to see the exact relationship between individuals. But that would only interfere on an extremely fine scale phylogeny (intra-species level).
Methodology
If we really sample all the individuals, the detail of the methodology may not matter much. It will still need to be decided whether we want to consider AATC closer to AA.C or to AGTC (where . indicates a deletion). Again, this will likely only matter on a very fine scale (intra-species level).
Computational power
Of course, if we sequence every nucleotide that exists on earth, we would never have the computational power to even store the data. Not talking about actually processing it. We would not either have the computational power to process the sequencing (nor the necessary amount of products to allow for the sequencing to happen).
If you meant to fully sequence only one individual per species (and then again the arbitrary nature of the concept of species will complicate things up), then we might have the computational power (see @KonradRudolf's comment)

The concept of species can often be misleading. You might want to read the post How could humans have interbred with Neanderthals if we're a different species? for a discussion on the concept of species.

You could compress the data. Lots of it is similar; I'm sure that somebody would come up with a data compression algorithm that works better than the existing ones on groups of genomes.

“we would never have the computational power to even store the data.” — I’m not sure how you got there. Even uncompressed, genomic data isn’t that big. The human (haplotype) genome is a measly 3 GiB. Assuming this is representative (it’s actually rather on the high end!), and assuming estimates of 8.7 million distinct species, this would result ~26 PiB data. That’s peanuts. Modern sequencing efforts routinely produce as much data each month!

@KonradRudolph He was not talking about merely sequencing any (however defined) species but every distinct genome - which is basically every life form on earth. So at least a few billion times what you calculated.

@Nicolai Fair point but given the text of the actual question this is probably just an inaccuracy in the title (OP means “organism” = “species” rather than “organism” = “individual).

@KonradRudolph Yes, that's why I said if we sample every nucleotide that exist on earth. I edited this part to make it even clearer.

@Remi.b I think "sample" is the wrong term then because it means that you don't look at each one individually.

I am not sure I understand why sample is not a good term. I replaced "sample" by "sequence". If you have a better alternative, please feel free to edit the answer. Thanks

Assuming he meant every species, it's within range of a DVD jukebox.

@KonradRudolph Do we really produce ~26PB per month? You might want to try an answer to the question How much Open Access Data is there in genetics?

@Remi.b Not "we": Multiple individual institutes/companies each. Thanks for the link, I'll try to find some official statistics. Most of this is unfortunately neither Open Access nor public in any way.

@Nicolai Due to heavy redundancy in many species genomes (all those conserved regions especially), a "billion times" is really not all that much. You could quite easily store a large number of genomes in a radix tree or another highly compact data structure. SNPs and such do not need to be explicitly specified for each individual creature.

A quick (but not quite glib) answer (having worked in the field): Given identical sequences of DNA from well-known species with likely close relationships - in other words, comparing beetles with other beetles, rather than snakes or bananas - respected researchers almost never arrive at the same phylogenetic trees, especially with very large sequences of DNA, even if they are working with exactly the same DNA samples.
There are several reasons.

Researchers have differing opinions about the weight to give the likelihood of different possible mutations that could have resulted in the differences between the DNA sequences. This automatically results in different phylogenetic trees. This leads to:
There are innumerable paths that could lead to the differences in DNA sequences. This means that there is no way of knowing the actual path that in fact led to any given difference, much less all of them that make up even two different species. This then means that there are innumerable different phylogenetic trees describing the possible ancestry of even two relatively similar species. Computerized tree generating and sorting algorithms are used to make sense of the huge numbers involved, but they cannot and do not list all of the possible trees, as that cannot be done. The list is infinite in size. Instead, they stop generating trees once they reach a pre-set limit (by the researcher, based on heuristics) of likelihood, then sort the ones they have. It's not as random as it sounds, but there is a degree of guesswork in any phylogenetic tree. This could only be mitigated by knowing the DNA sequences of every single ancestor of every single organism so that we could see how the DNA changes at every base pair in each sequence in each generation. It is a little like asking for time travel, but the math is harder.
There is fundamental disagreement, from species to species, about which changes in DNA make for different species and which merely represent variation in a single species. In reality, there is approximately one mutation for every cell division (see this article on mutation rates in humans for a look at the scale of the problem1) across most known species, most of which are meaningless or are spontaneously removed via cell or (often, in the case of germ cells) organismal death. This is a real issue, discussed at length by systematic taxonomists.
Because the DNA of different species is actually different, it is not possible to achieve a one-to-one match of the DNA sequences between two species. Researchers make a best guess,  based on what they think is most likely (and gets more difficult the more species are used).
Statistical methods (which are required by the infinite size of the data sets, even with (relatively) small amounts of DNA and numbers of species) only tell the likelihood of a particular tree. They cannot predict the actual phylogeny. This can only be known if all (or at least most) of the ancestors of each of the representative organisms' DNA can be examined for the mutations that resulted in speciation.

In short (because this answer really was not, despite what I originally said), DNA sequences of every extant species would not be enough to resolve phylogeny. DNA sequences of every extant individual organism would not be enough. Only knowing the DNA sequences of every organism that has ever lived would be enough to resolve phylogeny completely.

No, but it would help. First, though, let's talk about limitations. The limitation you speak of is not rapidly disappearing. The barcode initiative (attempting to sequence a small fragment of mt DNA from every organism on Earth) has been going strong for almost 20 years now and is not even close to covering every species on Earth. Many species have only been encountered once, and have not been seen since their description. Most species remain undescribed. Then there is the issue of computing power. To analyze the data for 10 million species (one ballpark estimate for the number of species on Earth), or even 1.8 million (current number) would not be possible. In addition, phylogeneticists are an argumentative bunch. It is likely there would be debates over methodology. There would also likely be errors in the handling of the data. There would be contamination issues, and labelling errors.
However, as you said, your question was hypothetical. A carefully, error-free analysis, assuming complete coverage and perfect models, and assuming we had the computing power to do it would resolve most of the debate. It would still not resolve species with reticulate evolution or hard polytomies (groups that simultaneously split into more than two lineages). For that, you would need more than one individual to represent a species, and even with say 10 per species, it would be difficult.

Also the vast majority of species are extinct thus have no DNA left to sample.

"[T]hus" seems to be a bit rash. DNA can be preserved in and extracted from all sorts of media, e.g., amber. The amber doesn't care much whether the species embedded in it is extinct or not.

This question is a lot like asking "if we found every fossil there is, would we know everything about life in the past?" or "if we found every ancient manuscript that exists, would we know everything about history?". The answer for both of those is "no", because fossils and manuscripts are an inherently incomplete record. Not all organisms fossilize; not everything is written down; not all fossils or manuscripts survived until today, and those that did suffered various levels of decay; the longer it's been, the more they've decayed.
The same is true of the phylogenetic signal one can infer from genes. The reason we can infer ancestry from genes in the first place is that everyone gets their genes from their parents, and those genes are slightly modified each generation. This means that siblings have very similar genes, cousins have slightly less similar genes, and so on so forth until you have every living thing's family tree.
Except that several factors mess this up. Here are a few:

Everyone doesn't get their genes from their parents. Animals mostly do, but bacteria swap genes such that each gene can have its own family tree, independent of that of the bacteria it's in. This is extremely relevant to the origin of life in particular because it involved bacteria and archaea.
The "very similar, less similar, etc" ranking works if we have infinitely large genes, containing infinite information. If we don't, then at some point you get two individuals whose every base of DNA is different from one another, and from that point on they can't get more different, however distantly they're related. Also, with finite DNA you get mutations on top of mutations - you might have two distantly-related lineages that get the same mutation by chance, or an old mutation gets reversed, or a new mutation happens on top of an old one, looking like only one mutation. All of this can blur the "signal" of relatedness, and it's the reason phylogenetic trees are calculated using statistical methods and as much DNA information as is practical. We (most of us) have huge genomes, which is the reason we can make phylogenetic trees as good as the ones we do, but there are genomes small enough that they can have been completely shuffled since life began, and it's harder to build phylogenetic trees there. On the opposite end of the spectrum, organisms that are so closely related that there are few differences to work from can be hard to sort out too, simply because a single event like mutations overlapping or being reverted can have a bigger impact when it isn't drowned out by thousands of other differences.
The theory also relies on the mutations being random; every individual is different from their parent to a predictable extent because no factor makes some mutations more likely than others. This is the case for many parts of the genome, and that does make them pretty good for phylogenetics, but many other parts are selected for or against. Meaning some mutations are more likely to stick around because they're beneficial at some point, and others are more likely to get weeded out quickly because they're harmful. This is why, even in organisms with small genomes that could be entirely shuffled since life began, they aren't really entirely shuffled: the parts of the genome that are necessary for life stay the same. This can be good for examining deep phylogeny, because it means those sequences change a lot more slowly. It can also be bad, because now family relationships aren't the only reason they change: fitness also affects that and you can no longer be sure that two organisms have similar or different DNA because of their relatedness, or because they've adapted to the same or different functions. This depends on the DNA in question, whether the function can be done by many different DNA configurations or only one, but at the end of the day, it's another factor to muddle the relatedness signal. And while the slower rate of change in conserved sequences makes it possible to separate very deep phylogenies, by the same token it won't do so at a very high resolution, because there are fewer differences to work from.

So essentially, like fossils and manuscripts genomic information is an imperfect signal for building family trees, and it's a decaying one - the longer it's been, the more time there's been for the various factors that make it imperfect in the first place to work their magic. So to answer your question, having the genomic information for all species or organisms would help a lot with resolving the Tree of Life, and might even resolve all the current debates on it. But it might also not. Hard to know without actually resolving the debates. And even if it does, there would still probably be outstanding questions; the general outline of the picture would be clear but there would still be all kinds of details that weren't filled.

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Please name this plant

What is the name of this plant? It was found in a village in Bangladesh, in the month of February.

Where was this plant found and what time of year?

From a village of  Bangladesh, in the month of February.

@FaysalAhmed Add this info (and as much else you can think of) to the actual question (use the edit button).

@FaysalAhmed Don't copy the posted answer(s) to the question. It makes the Q-A pair impossible to understand for future readers.

I believe this plant may be Rotala rotundifolia
Quoting from Wikipedia,

It is a common weed in rice paddies and wet places in India, China, Taiwan, Thailand, Laos, and Vietnam, and has been introduced to the United States.

This makes sense, as Bangladesh is located near both India and China.

The emerse form has rounded leaves, the submerse leaves are narrow lanceolate. It is very variable dependent on light and environmental conditions. Under strong light, the leaves can become almost wine red. It has pale pink flowers.

(source)

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sort: votes


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Are there cannibalistic k-selectors?
My understanding of r- and k-selectors does not go deeper than the wikipedia article. I understand k-selectors to be creatures that put tendentially more effort and energy into rearing their offspring, but produce tendentially less offspring.
With cannibalism I don't mean eating their own on rare occasions, like after a plane crash in the Andes, but exibiting cannibalism outside of extreme situations.
My gut feeling tells me that expanding much energy into raising an offspring and then eating her does not make much sense, but the world is big, there's lots of different species of animals and most of them are weird once look closely enough.
A good answer explains why one species is a rather to be seen as a k-selector, and in what contexts the cannibalism happens. Since we are talking about a sliding scale of behaviours, the question might as well be read as: What cannibal is the strongest k-selector?

pleas add tags, I don't know what this field of biology is called.

Cannibalism can also help a k-selector. If the female spends a lot of time caring for her offspring and is not eager to have another, why not kill somebody else's offspring to have the mother bear yours. Bears do this. Lions as well.

Interesting question. I am not sure I understand it though. Is it "What are all the possible reasons for killing babies of its own species in a k-species?" or "What are all the possible reasons for eating individuals of its own species in a k-species?" Or is it "Why does a species that practice cannibalism might evolve to be a k-species?", or  "Is it more likely to observe canibalism in r-species rather than k-species?"

"What are all the possible reasons for eating individuals of its own species in a k-species?" is closest.

@mart So it doesn't have to be specific to eating its own offspring? Or does it?

no, not specific to own offspring

My answer is messy and incomplete! I very welcome editing!
As soon as an individual is killed, on might as well eat the dead, but the act of killing might not be for the purpose of eating. We might even say that eating a dead might not only be for the purpose of getting energy and matter but only to clean the living place. And killing might appear in many circumstances. The best way to consider such issue is certainly by using the quite fundamental model of kin selection theory. It fits as much to species that gain energy by eating the dead or not. The difference imply just a minor change in the payoff matrix.
The decision of one (the actor) to kill (and eat) another individual (the recipient) depends on:

the relatedness of the actor to the recipient (note a relatedness is not necessarily symmetric)
The competition this recipient causes on the actor
The cost (energy cost, risk of being injured or killed) of killing

Many species (ants, wolves) might kill or injured individuals of the same species, when for example there is competition for reaching a status in the hierarchy.
I think that the definition of k-selected species is not very accurate. First because there are limit cases. But also because r and k can relate to the function that describes the population growth of a species or might describe the amount of energy the parents spend into one offspring which is not necessarily the same thing. If we think of the parental care, we can think of the lions. When a male win the right to access to the females of another male, he will kill the babies that might be potential competitors to his progeny (because they take energy from the females or because females are not fertile before having lost their babies).
Killing its own offsprings is certainly not less common in k-selected species. You might think it is such a big cost to kill one of its own offspring when one has few offspring but what is important is to think in percentage. Killing 50% of the progeny has the same cost of an r-selected species than for a k-selected species.
If one has a probability of 10% to be able to raise its offspring to adult age. But this probability raised to more than 20% if it accepts to kill an offspring to save energy for the next offspring, then it wins by doing so. THen we might ask: "so would one make an offspring if it intends to kill it?"
Well it does not necessarily intend to kill it. It might need to decide late in the season whether or not it has better to kill its own offspring.
Then, maybe offspring might be used as a reserve of energy and matter for its siblings or for its parents.

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Structures of cyclodextrin complexed with small ligands
For some structural study I am looking for cyclodextrin strucutures (in 3D format such as pdb, mol2, etc) complexed with small molecule ligands, such as cholesterol and even smaller. Right now I could only find on the PDB database some proteins complexed with cyclodextrin, but no structure of cyclodextrin with small ligands, could you help me?

I looked for relevant publications at Web of Science using 'structur* AND cyclodextrin' in the Title field. For the period 2011-2012 there were 56 hits including:

Racz et al (2012) Structure of the inclusion complex of beta-cyclodextrin with lipoic acid from laboratory powder diffraction data. Acta Crystallographica Section B 68: 164-170
Ali et al (2012) Structure determination of fexofenadine-a-cyclodextrin complex by quantitative 2D ROESY analysis and molecular mechanics studies. Magnetic Resonance in Chemistry 50:299-304
Lula et al (2012) Interaction between bradykinin potentiating nonapeptide (BPP9a) and beta-cyclodextrin: A structural and thermodynamic study. Materials Science & Engineering C 32: 244-253

I looked at some of the papers but I didn't find any specific case where a structure has been deposited in a database. There were, however, several mentions of the Cambridge Crystallographic Data Centre  as a source of small molecule structures.

this is great! I will check whether the structures have been deposited somwhere


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Experimental techniques to measure protein-protein and protein-ligand structure and dynamics
We would like to compare our simulation results with experimentation. When one wants to follow experimentally the dynamics (and possibly structure) of protein-protein or protein-ligand docking (involving both small and large conformational changes for the complex), which are the most useful hydrodynamic techniques? If not hydrodynamic, which others?

NMR would be a method to get structural and dynamics information, but that is not a quick and easy method. Are you looking for atomic-resolution data, or for simpler methods that only give you some global information on the shape and dynamic of the protein?

I am interested in both, atomic resolution data, and/or "coarse grain" model data


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A question about gag reflex
If left glossopharyngeal nerve and right vagus nerve are intact, but there is a lesion at left vagus nerve, would stimulating the left side of pharynx elicit a gag reflex?

The sensory and motor components are  required (GP and vagus respectively). Similar to the corneal reflex and cranial nerve 5 and 7, if a lesion exists in either the sensory or motor component there will be a defect. In your case, there is no motor innervation on the left due to the lack of the vagus nerve so there is no vagus nerve response.


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Why do glial cells of the retina become more abundant the closer they are to the optic nerve?
I am doing a project on expression of GFAP in the zebrafish retina. GFAP is a marker for glial cells.
I have found that the glial cells are more abundant the closer they are to the optic nerve at the middle of the eye. This may just be because the cells are more tightly compacted here than at the edges of the eye...
But I am wondering if it may have something to do with the glial cells being involved with neuornal processes, and the optic nerve being the transmitter of signals from the eye to the brain?

Any particular glial cell you're noticing this with?
I know that Astrocytes modify Calcium concentrations in the synaptic cleft. Perhaps at places where there are more synapses, more Astrocytes must exist to regulate such thing? Here's an interesting paper on a possible role of Astrocytes on associative networks:
http://www.antanitus.com/

Glia serve the classic support role in the retina, similar to that served by neuroglia elsewhere in the CNS.  That role mostly consists of taking used neurotransmitters and recycling them such as in the glutamate-glutamine cycle.  As Preece suggested, glial cells are a heterogenous group, and with a general marker like GFAP you could very well be observing two different types of glial cell, one with a uniform presentation and one specifically in the central retina.
That being said, the most familiar type of glial cell in the retina is the Muller glial cell.  It is particularly interesting in zebrafish, where it has been shown to act as a neural progenitor cell upon tissue damage in adult animals  As you can see from that article, it fits your requirement of being GFAP expressing, although I couldn't find any good flat mount pictures showing whether it was preferentially expressed in the central retina.
So that gives us two potential roles for glial cells in the zebrafish: as potential multipotent retinal stem cells and as housekeeping neurons present to clean things up.  You could come up with reasons either of those might be important in the central retina, but for my money the arguments are all pretty hypothetical: "the central retina is more active and therefore has a higher requirement for removing neurotransmitter" or "the central retina needs to be protected from potential damage more than the peripheral".
One thing I think we have a good basis to rule out is that it's the optic nerve.  From a retinal point of view, you refer to the point where the optic nerve passes through the rest of the retina as the optic nerve head or optic disc.  Axons from ganglion cells all across the retina stretch out from their soma toward this single point.  By the time they reach the optic nerve, the vast majority of axons are far from their axon hillock.  That means that they're being propagated from one node of Ranvier to the next.  Because that process requires voltage gated ion and not neurotransmitter gated channels, there is no neurotransmitter release associated with that process and consequently no additional reason for glial cells to be present to clean up.
Reference:

 Bernardos RL, Barthel LK, Meyers JR, Raymond PA. 2007. Late-stage neuronal progenitors in the retina are radial Müller glia that function as retinal stem cells. The Journal of neuroscience : the official journal of the Society for Neuroscience 27: 7028–40.


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Isoprenoid Diphosphate Concentration in Yeast saccharomyces cerevisiae
Isoprenoid  Diphosphate(IPP) is an important metabolites which is precursor in lot of secondary metabolites like Dolichol diphosphate, ubiquinone, prenylated proteins and carotenoid (not synthesized in s cerevisiae).
What is the average concentration of IPP present in yeast per gm ?

Although this information doesn't provide a direct answer to your question, I hope that it sets the scene for what is achievable in metabolic engineering from IPP. It should also provide a jumping off point for further literature research.
This is a fairly recent review of metabolic engineering of relevant pathways in various microbial systems, including Saccaharmoyes:

Ajikumar  PK et al. (2008)  Terpenoids: Opportunities for Biosynthesis of Natural Product Drugs Using Engineered Microorganisms. Molecular Pharmaceutics 5:167–190

The review refers to:

Ro, D. et al. (2006) Production of the antimalarial drug precursor artemisinic acid in engineered yeast. Nature 440, 940–943.

In this work, the introduction of a pathway-specific gene led to the production of 4.4 mg L-1 of product. This was increased to 153 mg L-1 by several manipulations including:
Increasing flux through the pathway by expressing a modified HMG CoA reductase
Decreasing flux into sterol synthesis by downregulation of the ERG9 gene combined with expression of a dominant negative allele of the transcription factor Upc2.
UPDATE
After posting my answer I found this paper:

Huang, B. et al. (2011) Metabolite target analysis of isoprenoid pathway in Saccharomyces cerevisiae in response to genetic modification by GC-SIM-MS coupled with chemometrics. Metabolomics 7:134–146

The paper includes a detailed discussion of methodologies, which I won't go into here.
Although there are no measurements of IPP, in Table 7 they present this result: geranyl pyrophosphate 32 ng ml-1 in a 48 h culture, A600 ~ 2.3. ERG9 disruption increased this to 56 ng ml-1
As far as I can tell these values are presented as ng ml-1 original culture. Using 1 U of OD600 corresponds to 0.41 g of dry cells liter−1 taken from here I calculate a value for GPP of 34 µg g-1 dry weight in the wild-type strain.


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fibroblast cells and fibers
I am interested in fibroblast cells in human arteries. Here are the things that I am not clear at the moment and I could not find any answer from the literature:

What are the dimensions of these fibroblast cells? How big are they in terms of diameter and thickness? How big are they if they are comparing with the collagen fibers in the artery?
I think they have to attach themselves to the fibers in order to proliferate or differentiate. However, I do not know, do one fibroblast cell attach itself to one fiber and then "crawl" to another? Or do they "sit" on a network of fibers?

I will appreciate your help on this and will be even more grateful if you could provide me with some literature that I could find the answer to these questions.

Regarding dimensions:

As per this image the length and breadth seems to be ~30-50 μm (area should be roughly around 900 μm²). The third dimension (thickness) as per this article can be assumed to be around 3-7 μm.
Regarding cell attachment:
Cells attach to extracellular matrix via integrins, which attach to ECM proteins like collagen and fibronectin. The matrix is a net of fibres and the cell is not specifically attached to a single fibre but rather "sits"(as you said) on the matrix [see the below image]. A single cell also simultaneously interacts with two different types of ECM proteins such as fibronectin and collagen.

During migration they move along the matrix using lammelipodia (actin filament polymerization in the direction of motion).
Fibroblast express ICAM1/VCAM1 (Inter/Vascular Cell Adhesion Molecules) under certain conditions such as inflammation and bind to T-cells and endothelial cells.

somehow the second image is not showing in the answer.. this is the link

I dont know exact references for these but you can find these info in cell bio books such as Molecular Biology of the Cell by Bruce Alberts

Hi WYSIWYG, thanks very much for your explicit answer! This really helps! Do you mind if I ask you another question: what are the large thick fibers and small very thin fibrils in the second image? Are they collagen matrix?

Also, note that the width and height of the second image is about 0.5 μm. So if a normal fibroblast cell is 40 μm in length, then this means a fibroblast should be 80*80 times of the size of the fiber network showing in the second image? Then How does it attach itself to such a complex network of fibers? Merely via integrins?

mostly integrins as I understand. But integrins are diverse.. some bind to collagen some bind to fibronectin some bind to laminin etc.


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DNA preparation for sequencing

In shotgun sequencing method or some related method that DNA is break up into random fragment. The fragment that have about 3kb in size is inserted into plasmid by enzyme ligase and then plasmid transform to E.coli using electroporator. As i understand, the goal is amplify the fragment to be sequencing.
At this time, i have a question :

After the e.coli growth up, we have too many different type of miscellaneous DNA strand with same size in a colony. How to purify a type of fragment to be sequencing ?

For example, i have 20.000 different DNA strand with the same 3kb in size after break up into random fragment :
-- AAAAAAAAAAAAAAAAAAAA...AAAAAAAAAAAAAAAAATTTTTTT -- (3kb fragment of chromosome 1)
-- GGGGXXXXXAAAAAAAAAAA...AAAAAAAAAAAAAAAAAAAAAAAA -- (3kb fragment of chromosome 2)
-- 19998 DNA fragment left ............................. -- (3kb fragment of random chromosome)
So after amplify them i have :
1000000x of -- AAAAAAAAAAAAAAAAAAAA...AAAAAAAAAAAAAAAAATTTTTTT --
1000000x of -- GGGGXXXXXAAAAAAAAAAA...AAAAAAAAAAAAAAAAAAAAAAAA --
1000000x of -- 19998 DNA fragment left........................ --
These DNA strand is mixed together in a colony. We cannot run sequencing them together as mixed, so how to have the only one for sequencing :
1000000x of -- AAAAAAAAAAAAAAAAAAAA...AAAAAAAAAAAAAAAAATTTTTTT --

I hope I understood your question correctly.
I think what you are missing is that after you break up the DNA, you dilute the concentration so that each bacteria will incorporate ~1 DNA molecule. Then, you dilute the bacteria on a plate and spread it so that they each single bacteria is far from other bacteria. Finally, after they grow you get one genetically identical colony per DNA fragment.

You understood my question exactly and have a quick response, thank you so much !


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What is the potential function of ultra-conserved elements in the genome?
If selection pressure results in conservation of DNA sequences, what is the most plausible explanation for the existence of ultra-conserved elements (refs here and here) given that there hasn't been any significant validation of the functional significance of these elements other than a lot of bioinformatic analyses across different genome datasets? If these are of such high significance, does this mean that there is still some significant gap in our understanding of fundamental biology or is there another explanation? The second reference in particular show that there are UCEs shared between plants and animals, but are not syntenic (which is not necessarily a surprise) so it might suggest that at least a class of UCEs are associated with structural rather than functional elements.
It appears that there are at least several different 'classes' of ultra-conserved elements, based on the number of matching/identical bps, their spatial distribution across the genome and the species in which they exist. Even though there is probably no single explanation that would account for all the possible functions they can have, it is surprising that they are difficult to test functionally. This is again probably due to a lack of understanding about their properties and therefore no real method to validate their function. I think this is where we need to think outside the box to come up with the answer.
What would be the most obvious (and possibly not so obvious) function for UCEs?

What is the question? The papers you linked to already talk about the "most obvious" function for them.

I am also interested in the not so obvious functions as well.

Probably development, in particular transcriptional regulation.  To quote each link in turn,

They are found in clusters across the human genome, principally around genes that are implicated in the regulation of development, including many transcription factors. These highly conserved non-coding sequences are likely to form part of the genomic circuitry that uniquely defines vertebrate development.

and

[Highly conserved non-coding sequences] are significantly associated with transcription factors showing specific functions fundamental to animal development, such as multicellular organism development and sequence-specific DNA binding. The majority of these regions map onto ultraconserved elements and we demonstrate that they can act as functional enhancers within the organism of origin, as well as in cross-transgenesis experiments

Additionally,

Here we report that 45% of these sequences functioned reproducibly as tissue-specific enhancers of gene expression at embryonic day 11.5. While directing expression in a broad range of anatomical structures in the embryo, the majority of the 75 enhancers directed expression to various regions of the developing nervous system.

These regions tend to be highly clustered in around 200 areas, and most of them are non-coding.  ncRNA is often regulatory, and those UCE clusters are associated closely with developmental genes.  That being said, not all of them are clustered near known genic regions, which might be a good indicator that there are heretofore unknown genes in those areas; UCEs might be useful for discovery.  And here's a paper trying to give a role to one in cancer.

I definitely like to think that it is involved in development or some type of regulatory control. However, if it is unique to vertebrate, then why are they also found (exactly identical) in other branches of life? I think we also have to be conscious that sequence location proximity doesn't necessary indicate its association with particular genes. Unfortunately some of the knockout experiments haven't really provided any definitive answers, but this is a mystery that has definitely proved to be intriguing to say the least.

@MichaelLai Because that study looked at humans and pufferfish; removed enough to draw conclusions about vetebrates but not instructive beyond that.  The third link I posted deals with non-vertebrates as well.

Conservation might indicate selective pressure as a general rule, but this isn't a given; you can delete some ultraconserved elements and still get viable mice...
http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.0050234

Does this also suggest that there are different types of ultraconserved elements? Or that they have a function that is not directly related to structural or signaling?

It suggests that high-degrees of conservation might itself not imply selective pressures - at least from a proximal perspective the deletion events should have resulted in loss of fitness if the preservation of those elements was under strong selective pressure.


text:
What kind of mushroom is this?
I picked it this evening beneath an oak, in France, Nantes :

I tried an image search with Google, and it seems I picked a finger of a dead hand :)

What is its name, and is it edible?

Did you try the image search after cropping the fingers out of the target!

@DavidLeBauer No I didn't, I'll give it a shot!

@DavidLeBauer Interesting!

:-) a dog! No, I suspect Coprinus comatus or similar. Did you keep them around? Did they turn black and inky?

@DavidLeBauer I forget it in the fridge, a black juice came out of it and turned all of my roommates crazy. So yes.

The shape, colour and scales on the hat suggest something in the genus Coprinus.
Some species are edible, but it is not recommended to have them with wine.
I would not advise you to eat them without further live identification by someone knowledgeable. Photo identification is not reliable.

Coprinus comatus gills will start to turn pink then to black liquid in a couple days . That would confirm identification so next time they come up in the same area you will know what they are . Certainly looks exactly like them ; I have eaten many pounds of them.


text:
What causes drone bees to die?
... when not killed by other members of the hive.
Is it always a consequence of exile (denial of some resource, etc) or does some organ fail regardless of circumstances?

The number of drones in a colony may be hundred-thousand , i.e 15 % of the total population. The drones lack wax glands, pollen collecting-appartus and sting which is present in worker bees which make them completely dependent on the workers, transferring its genes to the next generation is the only contribution of the drone bees. Usually the drones do not mate with the queen of the same hive. The drones that are able to mate with the queen die shortly after mating due to breaking of bulb of endophallus(penis) inside the queen.

The rest, the survivors of the mating flight (mostly drones that could not participate in  mating) are not allowed to reenter the colony. They remain in the vicinity of the hive and eventually starve to death.
In hours of crisis when the colony needs to drop the expenditure of resources(food) the workers eat up larval drones or drive out the matured drones from the colony that eventually die due to the same reason.
Information taken from:

Wikipedia
Bees
The Backyard Beekeeper

But don't most drones never mate? Do the ones not mating have a normal lifespan or also die of some reason earlier than their sisters in the hive?

Thanks for pointing out I have edited my answer. @skymningen

@skymningen  I did write "when not killed or exiled".   As for "the only contribution", though, I am told that drones, when still welcome, do help with hive temperature regulation (shivering of fanning) same as workers do. I guess that would also make them no less useful than a worker against a hornet.

@kaay: You wrote "when not killed by other members of the hive". In my understanding you asked exactly what they die of in exile. Because even those who mate are in exile after they leave for the mating flight.

@skymningen (not killed) -> (exile) was not obvious to someone who did not already know the answer to the question. In my last comment I did not mean I wrote "when not killed or exiled" word for word, I meant that I did mention two other known reasons for death - being killed and exile-caused denial of resources (which, again, did not obviously need to be starvation - for all I knew they may have just dropped dead in the prolonged absence of some pheromones, etc).


text:
Skull mystery on beach
The skull was found on a beach on the Sechelt inlet on Canada's pacific coast. A marine environment.

What species is this skull from?

There's no question?

It is a species identification question. I is obvious enough to not a fully phrased question.

Can you provide a side view picture? It could be a couple things, but seeing the width of the zygomatic arches (~eye sockets) would be helpful.

The z arches are 13 cm wide. Just trying to figure out how to load another picture.

We found a very similar skull on a beach near Richardson Bay, Lasqueti BC. Decided it was a seal skull (locals agreed)
See harbor seal skull: http://www.skullsunlimited.com/record_species.php?id=4726

I agree with Mark it is a seal, specifically the rear half of the skull.
That low flat profile of the skull combines with with a wide robust zygomatic is indicative of seals. The triangular and yet flat sagittal crest is also a dead giveaway. The orbits are high, large, poorly defined, and deeply recessed with only a narrow band between them that is indicative of seals. Check out a these seal skulls for comparison.

In the last one you can even see how you end up with only the rear portion as you do, as the rest is only weakly attached and the zygomatics are weakly fused at the center and tends to separate as well.
I can't tell you the species but you definitely have a seal.

I know guessing is frowned upon but given the small size of the skull and the relatively small inlet you've cited as a location, my best guess is it's the back half of a dolphin's skull. Probably Pacific White-Sided Dolphin (Lagenorhynchus obliquidens)
Compare:
Sorry for the watermark. From Skulls Unlimited

^ The cheek-bones look pretty similar, but the snout and the pit on the side that superficially resembles an eye orbit have been broken off or caved in on your sample.
From cetacea.ca

^ I can't find pictures of the underside of a skull without the mandible, but the hole in the bottom of yours might match the one on the very far right here, though I'm not sure about the bulges on the underside.
I can't be sure if its a complete match but my best proposal is that it's a juvenile dolphin skull.

@SabelGear can you add some links for those pictures?

Added links to original pages. Sorry, didn't realize Stack hosted through imgur.

the zygomatic is all wrong for a cetacean, far to wide and robust, and the orbits are in completely different place, even the auditory bulla are in the wrong place.

"Dwarf Sperm Whale" Scientific name: Kogia sima

Please provide a citation or 2 and additional information. Right now  this looks like a guess,  not an answer.

Skull is not 'peaked' as seems typical of cetaceans. Skull has no eye socket 'dents' . Assumed eye sockets are forward facing and close together.


text:
Fatty Acid Synthesis

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

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

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

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

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

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

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

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

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

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

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

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


text:
Are Lambic beers the product of quorum sensing?
Lambic beers are a Belgian specialty which is still made by open-air "inoculation" by airborne microbiota first, followed by additional yeasts, LAB bacteria and more joining in at the time of transferring to used wine barrels. (No yeast is "pitched" or added intentionally.)  As many as 200 organisms may play a role, and they seem to take turns, partly regulated by rising acidity and alcohol probably, but with some such as Brettanomyces seeming to simply wait their turn compared to what they will do in a single strain fermentation.
Lambic (or American Coolship Ale hereabouts) fementations can take up to 3 years.  Often a thick fluffy "pellicle" or "film" forms on the top of the barrel, like "flor" on sherry, evidently in response to and protection from oxygen. (Sure seems like a bio film.)
(There have been a few studies tracking the staggered blooms of various organisms, including one done 2 years ago at Allagash and one this year at Cantillon, but no discussion about how the sequence is orchestrated. So this is a speculative question about the evolution of these beers.)
Could interspecies quorum sensing be at work?    How could that be confirmed?

First it is important to identify the species that co-habit the fermenting malt.

That's the part that's been done. (The numbers of different yeasts and bacteria are high.Each fermentation allows wind borne contributions and differing communities in second use barrels, so there are differences between batches.) Actually, I just thought of something from watching a Bonnie Basler video: Could anything be learned by looking for one of the sensing molecules? And found a paper about Acyl homoserine lactones found on surfaces in a modern brewery not trying for ambient brewing. I so want to state that these fermentations are timed by Quorum Sensing. Almost certainly, right?

can you add that information. What are these microbes?

ok, two studies.  The newest one, which I am struggling to grasp, is http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3991685/

That Belgian study showed "diverse members of the Enterobacteriaceae" (month 1), Saccharomyces cerevisiae and S. pastorianus (mos 1-3) then Saccharomyces spp. decreases and Pediococcus damnosus increases from 3 mos, followed by highly acid- and ethanol-resistant Dekkera bruxellensis, (aka Brett) which dominated from 6 mos onwards together with P. damnosus. (plus N. castellii, Hanseniaspora spp, Kazachstania spp, Acetobacter spp, Etc.)
The earlier study, from the US: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3329477/

Almost certainly not. Species occupy different niches due to their differing growth rates and tolerances. Interspecies quorum sensing and the symbiotic relationship that implies do exist(see: lichen), but open-air inoculation is unlikely to produce them.
Why would the Brettanomyces simply kill time waiting for 'their turn'? It's likely they don't grow as fast as S. cervisiae or other early fermenters, and as a result they're outcompeted until alcohol content rises enough to slow or stop other species. Brettanomyces isn't 'waiting', they're eating and growing as fast as they possibly can.
Many microorganisms form spores or simply hibernate until conditions are favorable for growth. For highly acid and alcohol-tolerant species, perhaps they sporulate until the mix is acidic enough to guarantee them habitat. This is a form of quorum sensing, but the transmission medium is pH and alcohol concentration.


text:
Why do cell membranes have a lipid bilayer instead of a monolayer?
Many cells have a cell membrane composed of two layers of lipids. Why is it that they have two layers and not just one?
What purpose do this arrangement serve?

Why use membranes?
Compartmentalising the cell has lots of advantages and purposes. In Koshland's 2002 essay, compartmentalisation was described as one of the seven fundamental pillars of life. Broadly speaking, membranes create different sets of conditions (chemical and biological) inside the cells. This allows more efficient functioning and advanced catabolic and metabolic processing. More complex and adaptable systems were thusly achieved by the evolutionary process.
Why a bi-layer?
There have been several molecular dynamic simulations such as this one carried out to investigate the biophysicochemistry of spontaneous bilayer assembly. There, lipids start in random orientations. The ordered bilayers we know and love spontaneously assemble in under 100ns. What's actually happening at a molecular dynamics level is the self-association of the hydrophobic lipid tail groups driven entropically by water. In other words the polar (hydrophilic) head-groups "prefer" interacting with the water (called the interfacial region) and the the hydrophobic tail groups "prefer" not interacting with the water. With those two preferences in play, the lipid bilayer forms.

On a smaller scale, micelles also form spontaneously, but this doesn't offer the compartmentalization required for biological functions.

It would appear that the conditions for an ordered bilayer are so favorable that they take precedence over any other orientation or combination. One apparent exception is the archael monolayer. Do see @WYSIWYG's answer that refers to the exceptional extremophiles that use a monolayer. Their comment summarises the monolayer succinctly:

They are technically monolayer but resemble bilayer. Like bilayer connected via a covalent bond. These membrane lipids have two hydrophilic heads and a hydrophobic "torso".

Image sources

Image 1: http://www.perkepi.com/cell-membrane/
Image 2: https://en.wikipedia.org/wiki/Lipid_bilayer

Why Bilayer and not a Monolayer
Lipid monolayer vesicles are possible as you mentioned (for example micelles). However, you have to understand that the cellular interior i.e. the cytoplasm, is aqueous and therefore a monolayer vesicle like micelles would not work. In micelles, the two compartments - interior and exterior, have to be of opposite nature for the stability of the micelle. In other words, you cannot have an aqueous environment inside a regular micelle. Conversely, you cannot have a non-polar environment inside an inverse-micelle.
Since both the exterior and the interior of a cell are aqueous, both the membrane surfaces have to be hydrophilic. This is possible only in case of a bilayer of usual amphipathic lipids with a hydrophilic head and a hydrophobic tail. However, monolayers are possible in lipids which have two hydrophilic "heads" at both ends and a connecting hydrophobic "torso". Such lipids are found in certain archaea such as Thermoplasma and Ferroplasma, like Miguel mentioned (see this article for more details). As you can notice, these monolayer membranes would be more rigid than bilayers which may be the reason why they evolved in extremophilic archaea.

 Albers, Sonja-Verena, and Benjamin H. Meyer. "The archaeal cell envelope." Nature Reviews Microbiology 9.6 (2011): 414-426.

Actually there are monolayers in some extremophilic archeon, wich have both layers of the regular membranes attached by covalent bonds.
However, the main reason is that membranes are formed by virtue of hydrophobic interactions. Phospholipids are amphipathic mollecules wich have a polar "head" (given by the negative charge of the phosphate group) and an hydrophobic "tail" (usually two alliphatic chains).
The mollecule tries to avoid the state of minimal entropy, wich in this case would be to "swim" freely in the water. In this hypothetical state, water mollecules would need to orientate themselves in order to minimize the contact with the hydrophobic tail (wich are very big mollecular gropus who doesn't atract the polar water mollecules) and to maximize the contact with the polar head. If this mollecule finds more mollecules of their kind they will stick together by their hydrophobic tails, because that will reduce the urge to organize water mollecules, and by so, raising the entropy of the system. There are some posible conformation wich allow to do this, and one or other will produce depending of the composition of the lipid mix.
Lastly, membranes serve mainly as selective barriers wich separate the internal cell, whose conditions are regulated, and the outside. Membranes can have embeded enzymatical systems, such as photosystems, respiratory chains or some key metabolic paths. Also, they usually contain sensitive proteins who respond to the external condictions and regulate the behaviour of the cell. Other functions can be found, but those are the most important.

Could you add a citation for the extremophilic archeon that use monolayers? It sounds impossible (as much of the extremophilic stuff does)!

@GoodGravy is correct, it sound impossible to get 'living' organism inside single lipid layer. References will be good.

@James and Dexter. They are technically monolayer but resemble bilayer. Like bilayer connected via a covalent bond. These membrane lipids have two hydrophilic heads and a hydrophobic "torso".

@WYSIWYG Thanks for the clarification. A quick Google scholar search provides some interesting papers on this also.


text:
Is there really a clear distinction between dinosaurs and birds?
Traditionally, birds are classified as a class of dinosaurs and the term non-avian dinosaurs is introduced to refer to the rest.
As recent discoveries suggest that some dinosaurs may have been warm-blooded and that some dinosaurs had feathers, the distinction between birds and dinosaurs seems blurred.
I have often heard statements like "Birds are the only dinosaurs that survived the Cretaceous–Paleogene extinction event.". With recent discoveries, isn't this how the clade of birds is defined rather than a fact about the extinction?
// not sure if this question belongs in biology, sorry

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

The question relies entirely on a definition. There is no right or wrong when dealing with definitions. Anyone is free to define birds and dinosaurs as (s)he likes. The question of weather the definition is accurate or very arbitrary with loads of limit cases would be of interest though. Of course a lot of dinosaurs lineages went extinct. One lineage did not, they became bird.

Related: Why do the ancestors of birds still exist?

Dr. Thomas Holtz wrote a full chapter on it in "Dinosaurs: The most complete and up-to-date encyclopedia", Random House, 2007.

The placement of the bird clade within the dinosaur clade is based on much more than just "having feathers and being warm-blooded"; paleontologists have discovered many, many ancient bird and theropod fossils, and as a result their understanding of what the theropod clade was like overall and how the bird clade developed within it is precise enough that discovering another group of dinosaurs was warm-blooded or even had feathers won't result in the conclusion "wow that dinosaur was closer to birds than we thought", but "wow feathers were a much more common feature among dinosaurs than we thought".
If you look at the Wikipedia page you can see there are many "bird-related" clade names that cover different levels of similarity to modern birds. From "Neornithes", which is defined as the clade containing all modern birds, to "Paraves", defined as the group containing all organisms closer to modern birds than to Oviraptors, which are all within Maniraptorans, which is itself pretty deeply nested within the Theropod clade...
So basically what I am trying to say is, our understanding of where birds fit within Dinosauria is precise enough at this point that no discovery about a single trait is going to "blur the distinction between bird and dinosaur"; it might change our idea of dinosaurs in general to be more bird-like, meaning that traits we thought were bird innovations might have been standard-issue in dinosaurs for a long time before, but it will not necessarily change our whole understanding of how birds and dinosaurs are related.
As for this :

With recent discoveries, isn't this the definition of what a bird is rather than a fact about the extinction?

It isn't; the paleontological definition of what a bird is is not at this point an ad-hoc definition related to "whatever survived the K/Pg extinction". Even Neornithes, the crown group of all living birds, originates to before the K/Pg extinction. For example, the splits between ostriches and other birds and within that latter group, of ducks and geese from other birds are thought to have happened during the Cretaceous. And there are some researchers who argue that a few fossils indicate that some non-avian dinosaurs survived the extinction; the consensus view is that those fossils are dated wrong, but that this position exists shows that "non-avian dinosaurs went extinct at the K/Pg boundary" is a fact-based question, not a definitional one.

Also note that several major groups of "birds", like the enantiornithines and hesperornithiforms, didn't survive the K-T extinction.

Right; these aren't in the crown group of modern birds, and enantiornithines in particular are way upstream of modern birds, but they're definitely animals that if you saw them you would think they were birds (in fact the first fossils of these animals were misidentified as belonging to modern bird groups). They are one reason why "bird" can refer to many different paleontological groups; the crown group of modern birds, a higher-order group like Avialae to include those archaic forms, etc. Which further illustrates that the definition of "bird" doesn't hinge on feathers or the K/Pg boundary.

Yes.  I think the problem is mostly linguistic, in the distinction between "are" and "evolved from".  I mean we all evolved from fish, but if someone said you are a fish (or expected you to breathe under water :-)), you'd look at them somewhat askance, no?

@jamesqf not quite; there is a linguistic issue but also a substantive one. People would look at you askance if you said you were a fish, but nobody would disagree if you said you were a mammal. The relationship between evolution and the nested hierarchy that life by and large falls into is that the nested hierarchy is the result of evolution - groups diversify, spawning subgroups etc, so all descendants of one group are still more like each other than they are like descendants of other groups, meaning that "is descended from" and "belongs to this group (based on overall similarity)" coincide.

Exactly my point.  Saying that humans are mammals conveys one set of information; saying that humans are synapsids conveys a different (and generally not very useful) set, which is less confusingly conveyed by saying that humans are mammals, and mammals evolved from synapsids.  Likewise saying that birds are dinosaurs conveys different information from saying that birds evolved from dinosaurs.  (And at least two very different groups of dinosaurs, and other creatures like pterosaurs & dimetrodon that people think are dinosaurs.)

@jamesqf well for one thing that's a strange point you're making, because "synapsid" isn't a vernacular term it's a technical one, a technical field where clades are accepted as a salient concept, and cladistically "humans are synapsids" and "humans evolved from synapsids" are exact synonyms that convey the exact same information. More to the point, the fact that "are" and "are evolved from" mean the same thing in certain contexts is itself a very important set of information (about how evolution works and how today's life results from it) that gets conveyed when one uses them as synonyms.

One modern definition of birds, due to Gauthier, is the smallest clade containing all extant dinosaurs. However, this is not equivalent to the dinosaurs that survived the Cretaceous-Paleogene event, as these are not a clade. The bird clade dates back about 150 million years, and the Cretaceous-Paleogene event was also a mass extinction for birds, although after that they became much more diverse.


text:
Where can one find completed and processed Hi-C datasets?
I and a statistics graduate student at UCR, and I am working on Optimal Binning schemes and peak detection in Hi-C data analysis (a dataset that conveys information about proximity of a DNA strand with itself within the nucleus).  I am not a bioinformatician, so I am looking for someone that already has some complete data, or a website that may have these available for download.  The more datasets, the better.
Can anyone help me?  If you provide the data yourself, I will be sure to mention you in the foreword to my dissertation.
Thanks!
P.S.  If someone can find data generated specifically by the program "Hi-C Pro" with "allele specific analysis," I would be doubly grateful.


text:
Are there examples of animals that adapt to their environment very quickly? The phenomenon is called Phenoptic Plasticity
Evolution and speciation may take millions of years. This made me wonder if there is an animal that adapts itself relatively rapidly to its environment? I don't mean a simple adaptation like a change of a color by chameleons, but a real evolutionary change.
I've heard that some animals can adapt quickly to the environment like snakes (I am not sure they do). When they have a lot of water (e.g., a big river), they grow big, while the same species does not grow as big in a smaller water tank (small body of water). And when you take this animal to a bigger water it starts to grow quickly.  I want to be sure it is a snake or there is some other animals that evolve change like this...

What do you mean? All of them do. Every single one.

I've heard that some animals can adapt quickly to the environment like snakes (I am not sure). When they have a lot of water (big river ie) they grow big and the same species do not grow as big in smaller water tank (small body of water). And when you take this animal to a bigger water it stars to grow.  I want to be sure it is a snake or there is some other animals that evolve change like this...

First of all, that also happens with all animals. If you have enough food, you grow big, if you don't you remain small. Please [edit] your question and clarify.

Given your snake example, I think it is unclear whether you are interested in evolutionary change or phenotypic plasticity.

If phenoptic plasticity means changing the size due to better environment and opposite: not growing or changing (evolving) due to bad ones - I am interested in that. Thanks

@Arcadio Phenotypic plasticity is dealing with phenotypic differences in between individuals in different environments that are not the result of differences in genotype (so that the same genotype can result in completely different phenotypes). The body size differences that you describe are often the result of this. Phenot plasticity does not involve evolution, since the genotype doesn't change. However, also the plastic response (the reaction norm) can be the target of selection and evolve.

@Arcadio You're welcome! You can edit your question to narrow down the answer set (focus on either rapid evolution or plastic responses), so that it is more well-defined and can be reopened.

The snake example you provide is a single animal that adapts itself to its surroundings. Adaptation is similar, yet very different from evolution. Adaptation happens on a short timescale (as little as seconds, to perhaps years, but within a single life time, without substantial changes in DNA other than, perhaps, epigenetic ones), while evolution may occur over the course of millions of years or more, and likely involving gross changes in appearance and hereditary material. I am not entirely sure what you are exactly after.
A striking example of adaptation is the fish Tilapia, an invasive species of fish (Fig. 1) that is capable of sustaining fresh water as well as sea water environments. The transition from one medium to the other is mediated by gross changes in endocrinology. Your specific snake example on size adaptation seems, however, unsupported based on non-scientific websites at least.

Fig. 1. Nile Tilapia. Source: Sea EX
If you are after examples of swift evolution -There is a nice example of the Waterlily Beetle, Galerucella nymphaeae (Fig. 2), that shows striking host-race formation, i.e., the same species of beetle shows clear adaptations (on an evolutional scale) dependent on which plant it has been found. It has been shown that these beetles extracted from different plants (Nymphaeaceae versus Polygonaceae) showed strong morphological and ecological differentiation to their different host plant families. Beetles from Nymphaeaceae were significantly larger and had disproportionally larger mandibles than beetles from Polygonaceae. It is argued that these differences are adaptations (on an evolutional scale) to the tougher leaves of the Nymphaeaceae, which has been linked to genetic differences. In addition, females showed a strong oviposition preference, and all beetles showed distinct feeding preferences for the host family from which they originated. Moreover, these host preferences resulted in clear differences in survival: survival was 2 to 11 times higher on the natal host family than on the alternative host family.

Fig. 2. Waterlily Beetle. Source: Wikipedia.
Exactly how fast these beetles have adapted I am unsure of, but the interesting thing is that these beetle races are not geographically separated by a natural barrier like a sea, a mountain range etc. Instead, they live side-by-side, but have adapted to a specific host plant.
Reference
- Pappers, Evolution in action: Host race formation in Galerucella nymphaeae. PhD thesis (2001), Radboud University, Nijmegen, the Netherlands

Thanks for that answer ! Do you know the name of that snake. Is it Anaconda?


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Does increased cell turnover cause cancerous mutations?
If a certain set of cells or tissue are undergoing a lot of reproduction and repair cycles for some reason, does this inevitably lead to cancerous growths? If the mutation rate exceeds the normal 'background' mutation rate for the tissue will these extra mutations eventually cause cancer?
As user Luke said below; does an increased rate of replication increase the rate of mutations.

This is too broad. Can you please narrow your question down?

If with any type of cells a 'group' of them in a tissue or an organ, say; if they all go through a lot of dividing and reproducing , more than they would if 'healthy' would more mutations occur than 'expected if 'healthy' cells. If a culture of cells in a petri dish are 'made' to reproduce a lot more than they 'usually would ,would more mutations occur as the reproduction rate increases?

it is desperately unclear what you are trying to ask

Why do I bother trying?

So is your question "Does increased replication rate lead to a higher likelihood of mutation?"

You might want to clarify whether you're interested in the mutation rate per division or per unit time, or if it's the cancer-causing aspect of it that you're really asking about. I've assumed the latter, because a good answer to that should encompass the former.

@201044 I voted to reopen your question, because I think it deserves an answer. However, answering aggressively ("Why do I bother trying?") to users likely to be the only ones who may help you is not a good idea. We are a small community, so there are few specialists on a given topic, and if they ask you to clarify, either comply or get closed.

Increased cell turnover indirectly leads to cancer. Below is a direct quote from Human Molecular Genetics, 2ed. Chapter 9: Instability of the human genome: mutation and DNA repair.

Mutations can be induced in our DNA by exposure to a variety of mutagens occurring in our external environment or to mutagens generated in the intracellular environment. In the case of radiation-induced mutation, for example, Dubrova et al. 1996 reported that the normal germline mutation rate for hypervariable minisatellite loci was doubled as a consequence of heavy exposure to the radiaoctive fallout from the Chernobyl accident. However, under normal circumstances by far the greatest source of mutations is from endogenous mutation, notably spontaneous errors in DNA replication and repair. During an average human lifetime there are an estimated 10^17 cell divisions: about 2 × 10^14 divisions are required to generate the approximately 10^14 cells in the adult, and additional mitoses are required to permit cell renewal in the case of certain cell types, notably epithelial cells (see Cairns, 1975). As each cell division requires the incorporation of 6 × 10^9 new nucleotides, error-free DNA replication in an average lifetime would require a DNA replication-repair process with an accuracy great enough so that the correct nucleotide was inserted on the growing DNA strands on each of about 6 × 10^26 occasions.
Such a level of DNA replication fidelity is impossible to sustain; indeed, the observed fidelity of replication of DNA polymerases is very much less than this and uncorrected replication errors occur with a frequency of about 10^-9 to 10^-11 per incorporated nucleotide (see Cooper et al., 1995). As the coding DNA of an average human gene is about 1.7 kb, coding DNA mutations will occur spontaneously with an average frequency of about 1.7 × 10^-6 -1.7 × 10^-8 per gene per cell division. Thus, during the approximately 10^16 mitoses undergone in an average human lifetime, each gene will be a locus for about 10^8-10^10 mutations (but for any one gene, only a tiny minority of cells will carry a mutation). In many cases, a deleterious gene mutation in a somatic cell will be inconsequential: the mutation may cause lethality for that single cell, but will not have consequences for other cells. However, in some cases, the mutation may lead to an inappropriate continuation of cell division, causing cancer (see Chapter 18).

Here is another great paper that specifically addresses your question, linking increased cell division with the accumulation of both significant and insignificant mutations, which over time, lead to an accumulation of mutations needed for cancer to develop.

tl;dr answer: The probability of mutation for each cell division remains more or less the same. So the absolute number of cell divisions will determine the absolute number of mutations. So higher cell divsion rate - higher turn over - means higher risk of mutation - which translates to higher chance of cancer

Yes, essentially, until repair mechanisms have mutations that make them less effective in which case more absolute number of mutations would accumulate per future cell division.

Could a lot of acquired mutations in a cell's genome somehow 'distort' the cell's ability to 'self-destruct'? ( thereby 'making it 'non-mortal')

Yes, that is essentially a cancer.

Would mutations in the repair mechanisms of a cell make it 'noticeable' to the immune system?


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RF Cautery DNA damage?
I'm concerned about the safety and mechanism of RF cautery. The frequency of the radio waves used is 4Mhz so normally there should not be any DNA damage BUT the thing you read everywhere is that only UV, X-rays and Gamma rays have enough energy to pop an electron from the orbit. Can't the same energy be reached with radio waves (higher amplitude instead of higher frequency). After all the RF cautery evaporates the cells why wouldn't it damage the DNA of the remaining cells?

Please read the basics of electromagnetic radiation.

This might be better suited to physics, but I've answered it anyway from a biological point of view.

The thing about DNA is that it's very durable, compared to the rest of the cell. It's not too difficult to extract DNA from cooked and processed food, even though the definition of "cooked" is "denatured and broken many of the proteins in the cell". The long DNA strands may be broken into long pieces, but overall the DNA holds up very well to heat. There's no risk of DNA damage to neighboring regions with RF radiation because the primary way RF energy destroys DNA is through heating, and at the temperatures where DNA starts to accumulate damage the cell around it is cooked/destroyed.
The quantum explanation for why ionizing radiation can destroy DNA is that high-frequency radiation is powerful enough to zip through the surrounding tissue and break/damage individual DNA molecules. Individual radio photons can't "gang up" on a DNA strand to do the same thing because of how quantum mechanics works, so you won't be able to break the strand or damage the bases without high-energy ionizing radiation.
Metaphorically speaking it's like trying to get at a peach pit. Ionizing radiation is like a knife, it zips through the flesh and can get at a peach pit without damaging the peach much. RF radiation is like a belt sander. You can definitely get at the peach pit, but you'll cause a lot of collateral damage doing it.
Mutations or DNA damage that might cause cancer can only happen to cells that are alive that receive DNA damage. If the DNA is damaged by heat, the cell around it is dead, and that DNA damage doesn't really matter.
I encourage you to read about ionizing radiation and the photoelectric effect.

Excellent answer. What you say does make sense. But the thing is that some (turned into a lot during the years) studies do show DNA damage in the microwave range. Quote: "The early studies showed that DNA tended to absorb microwave radiation “in the kilocycle range” (Takashima 1963, 1966, Grant 1978, Grandolfo 1983), but no biocidal effects in the range of 1 MHz to 60 MHz were observed." (http://www.rfsafe.com/dna-and-the-microwave-effect/).

I don't trust RFsafe (they're trying to sell me something). There have been no conclusive studies linking RF or microwave radiation to nonthermal damage of DNA, and several studies showing no effect. Either the effect is ridiculously hard to find, or it doesn't exist. Long story short: it doesn't exist.

Excellent response. I especially like the knife vs. belt sander example :)

@AlBundy interesting that the page you linked to doesn't indicate where the study was published. Anybody can run a study and publish on the internet, citations and all, but unless it's peer-reviewed and approved by a group of independent scientists in the field, it's meaningless.

The EMF/RF doesn’t directly damage the cell. It just deranges cellular metabolism.
The free radicals that are produced by this change in metabolism are what causes the damage.
OXIDATIVE STRESS AND DAMAGED DNA
In contrast with Xrays and gamma rays, Microwave radiation does not have sufficient power to directly break covalent bonds in DNA molecules. But microwave RF can produce resonance interactions with ions and with charged macromolecules, and such interactions can significantly alter biochemical functions. A large body of research has shown that microwave RF causes an increased production of free radicals and reactive oxidant species in living tissues, and that this increased oxidant stress damages DNA. This damage can and does occur at power levels well below those levels that could produce damage by thermal mechanisms. Any chronic exposure to conditions that damage DNA can lead to an increased risk of cancer.
Evidence of increased risk of certain types of cancer has been demonstrated in groups with occupational exposure to microwave RF, including radio technicians in private industry, military personnel, commercial airline pilots, and ham radio operators. Elevated levels of cancer have been demonstrated in populations with increased residential exposure to radio transmission towers. And in the last ten years, studies fro Israel, Germany, Austria, and Brazil have documented significant increased in breast cancer and other cancers in individuals living less than 500 meters from cell phone towers, with measured exposure levels much lower than those permitted by current FCC guidelines.
Research has also shown that RF exposure levels well within current guidelines can cause DNA damage and reduced fertility in insects, birds, amphibians and mammals, and can lower sperm counts, sperm motility, and sperm motility in human beings
http://apps.fcc.gov/ecfs/document/view?id=7520940898

Thanks for your detailed answer. Though you provided a reference it would be great if it is an actual peer-reviewed article as they are considered more authentic than reports and monologues.


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What level of cellular radiation is harmful for humans?
What level of radiation at the frequencies used by the cellular network(1-2 Ghz) is harmful for human health?

This cellular network means mobile phone? Is it electromagnetic radiation?

Yes, I mean it, mobile phone network, like gsm, CDMA, LTE and all...

Addition to the previous answer

First you need to understand how radiation causes cellular damage.
EM waves like γ-rays, X-rays and high-energy UV (in certain molecules even visible light) can knock out the electrons from the atom and create an ion and free radicals by breaking chemical bonds. This term — ionizing radiation is not used for low energy UV and visible light because these waves can only ionize a few types of molecules and are not ionizing in general. Moreover X-rays and γ-rays can dislodge even inner electrons which UV and visible light cannot (High energy γ-rays can also lead to the nuclear reaction of pair production). These ions that are formed are reactive and can attack other molecules (DNA/proteins etc) around them. DNA absorbs UV and this can cause DNA lesions such as dimerization of adjacent pyrimidines (via a cyclobutane bridge). Both reactive ions and pyrimidine dimers can cause cancer; the former is most frequent in melanomas which happen because of solar UV. Since UV cannot penetrate very deep, they affect mostly the skin (See here).
IR, with energy lower than visible light does not have sufficient energy to cause electronic transitions. But it can cause vibrational transitions such as bond stretching and bending. Microwaves have even lower energy and can only cause molecular rotation. Both IR and microwaves because of their property to make molecules move, generate heat.
Continuous usage of mobile phones can cause discomfort but only because of their heating effect. They can by no means cause cancer and even though mobile phone radiation is classified as a potential carcinogen (IARC Group 2B) perhaps because of the pressing allegations of certain factions, they do not have sufficient energy to cause DNA damage.
If you ask me if mobile phone radiation can be harmful to human health, then I would say yes, they can be potentially harmful with prolonged usage but in no way as harmful as to be causing cancer. I would say that it is as harmful as wine :P

One thing to note is that close proximity to cell tower microwave transmitters can and will give you radiation burns, due to the wider range of harmonics. The GSM band runs at 1800MHz, from which the first subharmonic sits inside a range (~915MHz) that is known to excite water molecules in the same way that an industrial microwave does.

Afaik. radio waves don't have enough energy to cause anything similar to the damage ionizing radiation (gamma rays) does.
What it can cause is probably heat damage similar to microwave ovens.

According to the United States Food and Drug Administration's Center for Devices and Radiological Health, a U.S. Federal Standard limits the amount of microwaves that can leak from an oven throughout its lifetime to 5 milliwatts of microwave radiation per square centimeter at approximately 5 cm (2 in) from the surface of the oven.[52] This is far below the exposure level currently considered to be harmful to human health.[53]

http://en.wikipedia.org/wiki/Microwave_oven
Advanced Measurements of Microwave Oven Leakage - http://www.arpansa.gov.au/pubs/emr/microwave.pdf

According to the article referenced by wikipedia a 35 W/kg SAR level (caused by a 30 mW/cm2 leakage) can raise the tissue temperature with 1.5°C, which probably does not any serious damage. I guess from this you can count the radiation intensities - you are interested in - to any frequencies.


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Are missing limbs hereditary?
So with my basic understanding of biology, DNA can change over time.
Does this mean that if one (or both) parents have something major missing (like a limb), the kid will come out without a limb?  Does it matter if the parents had limbs amputated or were born like that?  If someone got melanoma from laying in the sun a lot, would their kid have a higher risk of getting it?

Sun lights do not play a role in transmission of risk of melanoma development from parents to their children because melanocytes are not a germ line.

Human genetic makeup doesn't change just because the parents are missing a limb. The kid will be fine

Does this mean that if one (or both) parents have something major missing (like a limb), the kid will come out without a limb?

Unless there is a genetic basis to the missing limb, no. Even for people born with missing limbs, this is usually not caused by genetics, but by a problem during limb formation in the womb (for example, through medication taken by the mother). A genetic condition associated with missing limbs is tetra-amelia, which is indeed heritable; however, it is very rare, a recessive trait and people actually showing it rarely have children.

If someone got melanoma from laying in the sun A LOT, would their kid have a higher risk of getting it?

No, at least not in the way you seem to think from the way you phrased this. There are people who are more susceptible to melanoma due to genetics. For these people, their offspring can also be more susceptible to skin cancer. However, this is passed to the next generation whether or not the parent has melanoma.

DNA can change over time

Yes, it can. DNA even in adults can change over time, but either this is your germline cells, so it will be passed to the next generation, but won't bother you, or it's in the rest of your cells and may or may not have an effect on you, but won't be passed to the next generation.

So you can't a(e?)ffect your offspring by what choices you make (to a degree)?

@CodyJHeiser most choices won't have an effect, no. At least not genetically.

DNA can change over time

This is a terribly misleading thing to say. You don't have "your DNA", you have a few billion copies of your DNA, one for each cell 1. Within an individual, there are events (called mutagenic) which can change the DNA in an individual cell. The change is practically random. It is like having a pile of DVDs and tossing them around, so some of them get scratched a bit. If one event hits many cells at once (for example a strong dose of ionising radiation), the cells will likely get different mutations each. There is no event during adulthood which will lead to having the same mutation across all DNA copies of an adult organism. 2
A second point: most events which change something in our body don't change a single copy of our DNA. Amputation of a limb is such an event. All (remaining) cells of an amputee have the same DNA as  before.
Having cleared up that, the implications for your question are simple, YviDe already mentioned them.

If two humans experience a non-mutagenic event in their adulthood, their DNA will be the same as before, and the consequences of the event will not be inherited. Thus the child of two people with amputations will be born with all limbs present.
If two humans experience a mutagenic event in their adulthood, it will change the DNA in a very small part of their cells. If they get a melanoma due to UV damage, it's only the DNA in the tumor cells that's different (and probably the DNA in other skin cells which got changed, but not enough to turn them into tumor cells). The DNA copies in the rest of their body, including the DNA of their egg cells and sperm cells, stays the same. Therefore, their child is born without a melanoma.
If two people were born with the same mutation which causes a visible symptom like a missing limb, their child will be born with it too, and will also be limbless. In this case, parents and child have the exact same mutation in all cells throughout their bodies. This is however not due to an event which "changed their DNA over time". Also note that not all birth defects are genetic.

1 This is not exactly true, but true enough for this explanation.

2 I shortly pondered whether a retrovirus can do it across the body, but all the ones I know of only work on certain cell types.

Does this mean that if one (or both) parents have something major missing (like a limb), the kid will come out without a limb?

If the parents are born without a limb, it could have a genetic reason or from external factors such as medicines and radiation. If the baby was born with gene mutations, he may come out without a limb.
So if mutations have taken place in the parents, they may have the chance to be passed on to following generations. And the condition you have presented may be caused by mutations.
This is also suitable for you second question.

I think, that for this answer, you really need to provide references for your claims. They can be case control studies, but I don't think that you just infer this by stating what you think is the case.


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Which of the following is NOT a type of tropism?
Which of the following plant movements is NOT a tropism?

Plant stem growing toward light
Plant structure growing away from light
Plant roots growing in response to gravity
Vines coiling around tree trunks
Leaflets folding after losing turgor pressure

Please help, I am stuck!  Thank u :)

Is there anything you can rule out definitively? Some thoughts about what you've tried will help us fill in what you're missing.

First two are ruled out for sure. I'd rule out the third, considering "Gravitropism", but some people are telling me it's the answer... So it's probably one of the last two.

The answer is #5, Leaflets folding after losing turgor pressure. This refers to a phenomenon called plasmolysis.
1 - positive phototropism, incorrect
2 - negative phototropism, incorrect
3 - gravitropism, incorrect
4 - thigmotropism, incorrect