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Alternative plant taxonomies to Linneaus
In addition to Linneaus-inspired taxonomies of the botanical world, I suppose there are some other proposals for different kinds of taxonomic accounts, perhaps for specific sub-domains of botany or perhaps historical. I'd be keen to learn about those.
Additionally, if any of you know there are some other alternative non-taxonomic approaches to botanic classification that are widely-used in sub-domains or in the early days of science, I'd be keen. I guess there are still some "common sense" classification to be made between use (ornamental/non-ornamental; medicinal/edible/poisonous), but perhaps there's more.

The most common alternative to taxonomic classifications are functional classifications. Emphasizing ecological similarities rather than similarities in relatedness, they can be regarded as complementary approach to, but not as a replacement of taxonomy. Why do we need this? Because species often perform very similar tasks, exhibit very similar characteristics and, most importantly, are very, very numerous (there are ~ 300,000 vascular plants). Reducing this redundant complexity is crucial for decision-making in conservation politics or the projection of vegetation change under future climatic conditions (Woodward & Cramer, 1996).
The idea behind this is to use functional traits, such as seed size, height, photosynthetic pathway, root density, etc., as a surrogate of a species' ecological 'role' -- its response to environmental factors and its impact on ecosystems. Seed mass for example (functional trait), is a proxy for the dispersal ability of a plant (function, performance). You should have a look at Lavorel et al. (2007), there is a nice table (too big to include here) that links specific traits to the actual ecological functions they describe. But look at this figure from the same paper:

By applying multivariate statistics like cluster analyses or ordination methods, species can then be classified into functional types. To make up one example, a functional type that might emerge from species with the following traits

height: > 20 m
seed size: > 0.5 cm
woody: yes
Specific leaf area: low

would certainly represent climax forest trees. This classification does not distinguish between individual species, because, from an ecosystem perspective, they all are functionally roughly equivalent.
For further research google 'Functional trait', 'Plant functional type' or have a look at refs 3 and 4.

Citations:

Woodward, F. I. and Cramer, W. (1996): Plant functional types and
climatic change: introduction. Journal of vegetation science, 7(3):
306–308.
Lavorel, S., Díaz, S., Cornelissen, J. H. C., Garnier, E., Harrison, S. P., McIntyre, S., Pausas, J. G., Pérez-Harguindeguy, N., Roumet, C., and Urcelay, C. (2007): Plant
Functional Types: Are We Getting Any Closer to the Holy Grail? In: Canadell,
J. G., Pataki, D. E., and Pitelka, L. F. (editors): Terrestrial Ecosystems in a Changing
World, Global Change—The IGBP Series, pages 149–164. Springer Berlin Heidelberg.
Halloy, S. (1990): A morphological classification of plants, with
special reference to the New Zealand alpine flora. Journal of
vegetation science, 1(3): 291–304.
Leishman, M. R. and Westoby, M. (1992): Classifying plants into groups on the basis
of associations of individual traits–evidence from Australian semi-arid woodlands.
Journal of Ecology, 80: 417–424.


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Up to date, extensive documentary about dinosaurs?
I just finished reading the Wikipedia page about dinosaurs, and I very much enjoyed it. I knew that much of what I learned in the 80's as a child is (and was) incorrect, and now that I am a parent, I am excited to finally make some time to learn about this stuff.
It seems that a lot is known about ecosystems, socialization, and interactions between different species, herd behavior, and other interesting things.
Before I start reading books, I want to watch a good documentary.  A quick google search turned up some suggested documentaries, but in general they seem to be either old or focused on a particular dinosaur, and not on the era in particular.  All are short.
I watched the 10 hour documentary "The Life of Mammals" by David Attenborough a few years ago, and developed a much better understanding of how we as humans evolved, and how we are related to other mammals. I'd love it if there was something as extensive about Triassic/Jurassic/Cretaceous era dinosaurs. Is there something recent, extensive, and mostly correct?

Doesn't have to be in English either

David Attenborough I stay away from. Since his Aquatic Ape hypothesis. Do read books - and until you do check out the work of a much more modern and better educated evolutionary biologist, Neil Shubin, who discovered Tiktaalik and wrote the Your Inner Fish book. There's a three-part documentary, Your Inner Fish - Monkey - Reptile. http://video.pbs.org/program/your-inner-fish/ Now that's a serious documentary by a scientist. The dinosaur documentaries are usually for kids, and are usually very wrong.

Try Planet Dinosaur (2011) or Dinosaur Revolution (2011). Neither is as good as the original Walking with Dinosaurs trilogy, but both are relatively informative and entertaining at the same time.

source: Stack Exchange

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

sort: votes


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Do Parasaurolophus have hands with fingers to grab?
http://en.wikipedia.org/wiki/Parasaurolophus#mediaviewer/File:Parasaurolophus_cyrtocristatus.jpg
I cannot tell if the hands have fingers strung together to form a hove, or fingers to grab. I have seen so many pictures of Parasaurolophus standing up, suggesting possible other functions of the arms and hands. I think their arms are long enough to reach their mouth. Ironically, I have yet to find any literature talking about their hands, but lots of literature talking about their resonating chamber. Do Parasaurolophus have hands with fingers to grab?

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


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Can memory be improved with mental training?
I am a man in his mid thirties, but I already have a pretty bad memory. (I have always had a bad memory.) I can remember certain kinds of facts and music very well, but when it comes to words or even random  stuff like how did I fix a particular issue when I last encountered it, my mind goes blank. Lack of sleep aggravates it even more. Lack of sleep also severely retards my language skills because I can't recall any vocabulary. Other than the memory issues I am a healthy person. Is there anything I can do to improve my memory?

Welcome to Biology.SE! This post would be a better fit on CognitiveSciences.SE.

I'm voting to close this question as off-topic

You are not alone.
I think most people do not use the memory capacity of the brain optimally.
Some people use it more optimally than others though.
The researchers who wrote the book "Make it Stick" researched exactly this problem.
Of their many excellent findings, I think the most important was that most people did not convert the knowledge that they accumulated in working memory into long term memory because they did not do spaced repetition of recall practice.
When we learn something new those synaptic connections are weak unless we strengthen them.
The brain seems to let go of information that it deems to be less important in this fashion.
Everybody forgets a little.
But if you practice recalling what you've learned at spaced intervals, that seems to greatly improve the ability to convert working memory to long term memory.
Its important that recall involve actually struggling to recall the information.
Its the struggling that seems to strengthen the synaptic connections.
Just rereading some material wont work.
I put everything that I learn into Q&A documents that I use for recall practice.
This seems to have significantly improved my ability to commit new knowledge to long term memory.


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How to measure heat loss in Tardigrades
I want to measure metabolism in tardigrades (a jar of 30 tardigrades). I know that an easy way to measure metabolism is heat loss; I can just measure the temperature of the water before and after a certain period of time and take the difference. I have a few questions:
1) Is this a viable way?
2) Do I need to put the tardigrades in a controlled system (or is the outside environment a constant)?
3) Will the measurements be really really small (so I would need a very precise thermometer?)
4) How long should I wait between the two measurements?

1 and 2) You need to build/use a calorimeter : http://en.wikipedia.org/wiki/Calorimeter
Different types exist, depending on your constraints.
3 and 4) It will depend on the size of your system.
If you decide to use an adiabatic calorimeter: First have an estimate of their metabolism (see e.g. [1]), then divide the energy spent over the duration you think you'll use by the heat capacity of the water volume you have, you get the temperature elevation.
If you use a flux calorimeter, then you don't multiply by the duration but check that the calorimeter will be sensitive enough.

Do these cold-blooded critters emit heat at all you think? +1 for your calorimeter idea. Nice one.

@ChrisStronks: they cannot live and emit no heat at all. Any process will generate some heat, be it only by molecular friction in flows. "Cold-blooded" is misleading, as it rather means that they have no thermal homeostasis target that they'd maintain by internal metabolic processes.


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Why I have to pee more often in low temperature?
I realised that I have to pee more often in winter or simply the temperature is low. Is there any scientific explanation, or just simply psychology?

This question, and its answer, are surprisingly fascinating.

@blackcornall when you notice this are you experiencing symptoms of hypothermia?

@rob No, I am not. Just simply feel the cold.

This phenomenon has been demonstrated in studies [1][2] which show a significant increase in urine output in the cold. The latter study shows the biggest increase is when a person is initially exposed to the cold rather than when they continue to be exposed or rewarmed up. In the study, the average urine out was 157 mL/hour when a person was initially exposed to the cold, 103 mL/hour when they were being maintained at that cold temperature and 70 mL/hour when they were being rewarmed.
The mechanism however is unclear. This study showed that the mean arterial pressure increases. It is well known that the cold causes our blood vessels to constrict (in order to keep the blood and therefore heat inside our core body). The thought was therefore that our kidneys try to lower our blood pressure by taking more fluid out and emptying it into the bladder. This is called cold-induced diuresis.
Other thoughts include that we lose the water we ingest by sweating (perspiring), pooping (defaecation) and peeing (micturition/urination). In the winter, we don't typically sweat as much, which ISN'T counterbalanced with a lower water intake, so we need to pee more.
Another possibility is that aquaporins (the pores that water comes out from our kidneys) are inhibited by the cold. This means more fluid would be filtered out. However there isn't really much research in this area that I am able to find.

Interesting possibilities, but some references would be awesome.  It would also be interesting to know whether the premise posed in the question is actually true or if it just seems true (perhaps because it's less pleasant to use the bathroom when it's cold, or for some other reason).

The last paragraph would be especially nice to have a reference for. In warm-blooded animals, it’s not obvious how a cold environment affects the temperature sensed at the level of the aquaporins. I guess you’re positing some more elaborate mechanism via CNS thermoregulation/ADH? (And minor point: aquaporins don’t affect filtering (glomerulus) but reabsorption more distally (collecting duct).)

@rob, as requested I have added two references which demonstrate this effect.

Cold-induced diuresis, where kidneys relieve blood pressure by increasing urine production.
http://en.wikipedia.org/wiki/Cold-induced_diuresis
The blood pressure is thought to be increased by vasoconstriction due to the cold. One source that supports that theory: Sun, Z. American Journal of Physiology -- Regulatory, Integrative, and Comparative Physiology, February 2005; vol 288: pp R433-R439. American Heart Association: "High Blood Pressure."

Could you elaborate this answer a bit more (e.g., why is blood pressure higher in the cold?). As of now it is more of a comment and comments should not be posted as an answer.

@ChrisStronks the poster doesn't have comment privileges yet.

@dustin - I know, that is why I ask for a little bit of elaboration.

This is the reference @rob was asking for. +1


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How does the molecular machinery choose where to cut a chromosome for recombination?
I'm wondering about a few technicalities of crossover in meiosis. The point of crossover is to create new chromosomes that don't have the same allele combinations as the original two chromosomes. Usually, the chromosomes are cut at the same place on both chromosomes, and each piece is then stitched to that place on the other. This is to avoid unequal recombination, a scenario in which one chromosome has several instances of a gene and the other no instance at all. I'm wondering how the molecular machinery knows where to cut.
So here's my question: How does the molecular machinery choose where to cut a chromosome for recombination?
This question has two parts: At what type of place does it occur (does the machinery choose a completely random place, regardless of where genes start and end, does it just cut at the start of genes, or does it do something else)? Given that it happens at this type of place (e.g. start of a gene), how does it decide that it will cut here (the start of this gene) and not there (the start of that gene)?

Presumably you added a bounty to this question because you're not satisfied with the answers already given. If that's the case, could you explain what else you're looking for?

The question is very broad and complicated, since the situation may differ in prokaryotes and eukaryotes. Nevertheless, I'm citing a good paper that is closely related to your question:

Studies in yeast show that initiation of recombination, which occurs by the formation of DNA double-strand breaks, determines the distribution of gene conversion and crossover events that take place in nearby intervals. Recent data in humans and mice also indicate the presence of highly localized initiation sites that promote crossovers clustered around the region of initiation and seem to share common features with sites in yeast. On a larger scale, chromosomal domains with various recombination rates have been identified from yeast to mammals. This indicates a higher level of regulation of recombination in the genome with potential consequences on genome structure...
  ...DSBs (Double Strand Breaks) occur in highly localized regions and spread over 70–250 bp. DNA sequence analysis reveals no unique conserved consensus sequences, although a degenerate 50-bp motif partly correlates with DSB sites. However, one common feature is that DSBs are located in accessible regions of the chromatin next to either promoters or binding sites for transcription factors. Based on two studies, DSB activity does not correlate with local transcriptional activity, but depends on transcription-factor binding (HIS4 in S. cerevisiae and ade6-M26 in S. pombe).

Bernard de Massy, Distribution of meiotic recombination sites. TRENDS in Genetics Vol.19 No.9 September 2003
I'll sum that up into a more answer-like form. Seems like the process is not random, because the double strand breaking events are clearly not evenly distributed across a genome. As the paper says there are no specific consensus motifs found as of yet, though there clearly is something special before promoters and TF binding sites, which makes them more likely to be a breaking site. How the machinery choses the place? Once again, as the paper says the breaking event depends on TF binding. But that is for S. cerevisiae. There are 17 hot spots found in human and mice genomes some of which are intergenic (they occupy introns or 5'/ 3' flanking regions).
Here is the distribution of recombination frequencies across one chromosome (the figure is taken from the paper).

Here is a list of recombination sites in humans and mice

Great! I gave you the bounty for pointing out where recombination occurs with respect to the gene (intragenic or in intron/exon), even though Ankur pointed out how the molecular machinery chooses which hotspot it will cut this time.

In humans and mice anyway ,a lot of it boils down to the recognition of a specific sequence that marks recombination hotspots by PRDM9.
http://www.sciencemag.org/content/327/5967/836
Edit - I'm expanding in response to the comment below...
Meiotic recombination occurs at vastly greater frequencies in some locations in the genome than others and these are called Recombination Hotspots. For example, the figure here, sourced from http://www.sciencemag.org/content/327/5967/876/F1.large.jpg

shows the recombination rate at the hotspot and further away from it for Chimps and Humans.
These hotspots are recognised by the cutting machinery thanks to the binding of PRDM9, a zinc finger protein, to a DNA sequence that it specifically recognises and is present at hotspots. The DNA sequence varies from species to species (as does the sequence and the function of PRDM9) but in humans is a well-characterised motif 13 base pairs long and of the sequence CCNCCNTNNCCNC (where N is any one of the 4 bases in DNA) , and accounts for the activity of nearly 40% of known hotspots.
The first link I posted has evidence to suggest that variation in composition of PRDM9 is a determinant of which hotspots get used. PRDM9, it appears, stimulates the formation of a specific histone modification - H3k4me3 (DNA is wrapped around histones, there are five histones - H1, H2A, H2B, H3, H4, and each of them has a tail that can be chemically modified, and eight of these (2 of H2A, 2 of H2B, 2 of H3 and 2 of H4) form a nucleosome - in this case the fourth lysine residue of the tail of Histone H3 is trimethylated as regulated by PRDM9, and facilitates crossing over and recombination initiation.
Edit Summary

I've now updated the answer with an extended explanation, cheers Chris.

Thanks Ankur! It was hard for me to choose to whom to give the bounty. You suggested how the machinery chooses which hotspot to use. But GrayFall9 showed at what type of place hotspots exist in the genome, which was an important part of my question.

In meiosis, homologous recombination occurs. Two Spo11 proteins utilize tyrosines to induce a double-stranded break in the DNA. Spo11 has no specific cleavage site. However, cleavage by Spo11 lead to the discovery of Spo11-Oligonucleotide (Spo11 w/ attached oligonucleotide post-cleavage) complexes which could be mapped to 'hotspots' which the linked study finds a number of discriminating factors to Spo11 cleavage in meiosis:

From the precise locations of the 2.2 million Spo11-oligonucleotide sequences, Pan et al. [1] showed that local DNA composition also influences Spo11 cleavage sites. As expected from previous studies, Spo11 does not have a specific recognition or cleavage site. However, sequence biases were detected: the 10 to 12 bp surrounding the cleavage site and predicted to be bound directly by Spo11 is relatively AT rich, predicting relatively narrow and deep helix grooves facing the bound Spo11 dimer. Cleavage favors sites immediately 3' of a C and disfavors G in the same position. Also, within a 32-bp core surrounding the Spo11 cleavage sites, a twofold rotational symmetry for complementary dinucleotide composition can be discerned, suggesting separate contributions of the flanking 'half sites' to Spo11 binding and/or cleavage. In addition, cleavage sites are negatively correlated with positioned nucleosomes. Similarly, Spo11 is generally occluded from cleaving sites where transcription factors are bound, even though the binding sites of several different transcription factors positively correlate with hotspot sites.

While all the answers above are correct and insightful for the process of DSBs formation, recombination has another layer of complexity.
 Mediating proper chromosomal segregation is more likely the real point of crossovers since crossovers still happen in inbred genomes, which do not result in novel haplotypes.
 CO create a heteroduplex structure between DNA strands, Holliday junctions. This structure creates tensions forces which are needed to pass the spindle assembly checkpoint before the meiotic cell can progress into anaphase (see papers by Nicklas work on grasshopper chromosomes and Hirose et al 2011).
In most* organisms, at least one CO is needed per chromosome arm to pass the spindle assembly checkpoint and mediate proper disjunction. Lacking COs or misplaced COs can result in non-disjunction and increased risk for aneuploidy  (Hassold, Hall, Hunt 2007).
(*an exception are male Drosophila melanogaster, which have a CO independant chromosome segregation pathway).
Additionally it should be noted that DSB =/= COs that is, not all DSBs are converted into COs. In all organisms, DSB outnumber the resulting COs. The majority of DSBs are resolved into non-crossovers (NCOs). There is new evidence (in mice at least) that these numbers are not proportional. That is, if total DSBs in the genome are reduced, the total CO number is unaffected. (Cole et al 2012).
I think a more interesting phrasing of your question would be, How does the genome choose which DSBs to resolve into COs vs NCO?


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What fish (and/or shellfish) species with a multi-year life-cycle, besides salmon, die after spawning?
Most species of salmon die after spawning. Are there any other types of fish that spawn once and then die after a multi-year life-cylce? Is this a rare life history strategy among our human exploited marine species? Googling this question only yields articles about Salmon.

Many species of Eel (order Anguilliformes) have a semelparous life history (most species? all?), i.e. they only reproduce once and then die (as opposed to an iteroparous life history). Many species are now threatened by extinction (e.g. American eel and European eel), since they have been heavily exploited by fisheries and they are also vulnerable to habitat modifications (e.g. hydroelectric dams) and pollution. The nature of their life history was also unknown for a long time, since they migrate and spawn in the Sargasso Sea after living many years in fresh water (so the opposite migration path compared to Salmon), which is called a catadromous life history. However, there are also many species of eel that are strictly marine, for instance the very large Conger conger, but many of these species still migrate long distances before mating.

(American eel, Anguilla rostrata, picture from Wikipedia in public domain)
As a fun sidenote, captive eel can become very old, and earlier this year a more than 155-year-old European eel that was kept in a well died (see newsstory) - the oldest known eel from what I know. Eels were often put in wells because they were believed to keep the well water clean.
Semelpary is also found in other fish species, for instance in the Smelt (Osmeridae) family, where many species are fished commercially. Some (most?) species in the family have multiyear life histories, but some, e.g. the Delta smelt (Hypomesus transpacificus) only live for a single year. Similarly to Salmon, Smelt also migrate from sea to freshwater to spawn, i.e. an anadromous life history.
Overall, less than 1% of teleost fish are semelparous according to Finch (1994) - see link for more examples of semelparous fish species and background. However, this figure is most likely uncertain, given that we know very little about the life history of many marine species. In some cases, you can also find a range of life-history strategies from semelparous to partially or totally iteroparous within the same species, depending on ecological context. Nevertheless, the low overall proportion of semelparous fish means that semelpary is generally a rare life history strategy in human exploited fish species.

(Delta smelt, Hypomesus transpacificus, picture from Wikipedia in public domain)


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How to name such grouping behaviour?
Under which keyword would you try to find out more about the grouping behaviour which looks like this? Does anybody recognizes such behaviour, or know an animal species which uses it?
My tries: threshold group behaviour (threshold here is the group size - if bigger than 5 individuals == stable), or gravitational group behaviour?

After step 6 the group disintegrates (for example due to foraging) and mechanism starts by step 1. Important thing is that the location of forming stable group is always different.

You can check this paper out. I used the keyword "pack size threshold"

Hi @WYSIWYG! Close, but no cigar. Did you know any other examples?

While I don't think it's precisely the behaviour you are asking about, you might also be interested in slime molds (e.g., Dictyostelium or Myxogastria). They start out as motile single cell organisms, have limited 'vision' (chemical cues), coalesce into a large multicellular structure when resources become limiting, and then disperse from (usually) a fruiting body.This is an example of "emergent collective behaviour".
Other searches you may want to try are "Biased random walk models" and "Shoaling behaviour".
Although pretty heavy, these papers may contain a formal mathematical description of the model you are after:

Akira Okubo, 1986, doi: 10.1016/0065-227X(86)90003-1
Angela Stevens and Hans G. Othmer, 1997, doi: 10.1137/S0036139995288976

After reading about emergent behavior and previously shoaling(aka schooling), I don't think those apply. When I answered this question, I original did some digging into schooling as well but concluded it doesn't fit. A discrete agent based model can be represented as a random walk so you didn't add anything new.

I believe it is a type of fission-fusion society or even some hybrid with agent based modeling.

In ethology, a fission–fusion society is one in which the size and composition of the social group change as time passes and animals move throughout the environment; animals merge (fusion)—e.g. sleeping in one place—or split (fission)—e.g. foraging in small groups during the day. For species that live in fission–fusion societies, group composition is a dynamic property [fission-fusion society].

A classical example is the Bonobo or pigmy chimp.

Bonobo - Pigmy Chimpanzee
Sociobiology
The Social Behavior of Chimpanzees and Bonobos


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How are we able to find the specific sites at which DNA binding proteins bind?
We know that some DNA binding proteins are site specific, that is they recognise and bind to a specific nucleotide sequence. My question is how can we precisely tell at which sites they bind? Is it the amino acid sequence of the protein? Or is it the repetitiveness factor in case they bind to multiple locations on the chromosome?

Do you have antibodies agains your DNA binding protein?

If there are no antibodies for ChIP, DNA footprinting + sequencing can work too.

I will try to answer the question in the title: how can we know the sites where DNA binding proteins bind?
I'll explain two experimental methods to identify binding sites on DNA.

DNase footprinting
ChIP-seq (Chromatin Immuno-Precipitation with sequencing)

DNase footprinting
We can locate proteins bound to DNA by their ability to protect DNA from some degradation. DNase I cleaves DNA in an almost-random manner and is inhibited by proteins covering ('protecting') the DNA backbone.
In order to locate a site which is protected from DNase I cleavage, we need to take some genomic DNA and treat it. We need separate, short lengths of DNA to examine - we can obtain these from genomic DNA by PCR amplification of different stretches. We need to label these amplicons at one end only, beta radiation is a good choice of label.
Taking one labelled amplicon, exposing it to DNase I for a short time - not long enough for complete digestion - produces cleaved DNA of all possible lengths, which looks like a 'ladder' after separation by gel electrophoresis. Digestion time must be short, such that many DNA are only cleaved once, to have a complete ladder.
Repeating this digestion with your interesting protein present gives a ladder with a missing segment. This is because your protein protects a length of DNA from cleavage.

Important points: DNA is labelled at one end only. Hence we only see the label-end-piece of DNA after cleavage: if DNA is labelled 5' and cleaved in half, we only see 5' halves. Thanks to this, we can estimate the position of the binding site: if our DNA is 100bp and our ladder has lengths 0 to 70bp, a gap, then more from 85 to 100bp, then our binding site is somewhere inside 70-85bp from the labelled end. We can sequence the piece of DNA and read the sequence of nucleotides 70-85.
ChIP-seq
This is a more recently-developed method, which is more suited to studying where a protein binds all over the genome or all over a chromosome. It requires an antibody which specifically binds your interesting protein.
First, a 'snap-shot' of global protein-DNA binding is taken by irradiating cells with UV light, causing covalent cross-links between DNA and binding proteins. Chromatin (DNA with associated proteins) is isolated from cells and chopped up to smaller fragments; the cross-links preserve our 'snap-shot' of proteins and short lengths of their bound DNA.
This mixture is incubated with an antibody (immobilised on beads) which binds our protein of interest. We can separate the antibody-covered beads and hence our protein along with it.
Finally we can sequence the DNA fragments caught in this way. It's like "fishing for binding sequences". The end result is a distribution of where our protein was bound across the genome at the time of our snap-shot.

Ideally the DNA fragments should be long enough to place them uniquely in the genome. There are advanced PCR and sequencing methods which separate DNA fragments in to 'bubbles' in an emulsion containing one molecule of DNA each. In this way, we can sequence all the variants that are present and by counting the number of sequences ('reads') of each type, we have a measure of the abundance of each sequence. This abundance is interpreted as the occupancy of the protein at different binding sites.

Genome-wide studies of DNA binding have shown us that proteins are distributed around the genome. They have preferred binding sites but also have some affinity for similar sites, and spend some of their time bound to non-functional bits of the genome.
Especially in mammals, a 'true' binding site isn't only (and isn't always) determined by having the highest affinity sequence, but also by being clustered with binding sites for other co-factors. This is because, in mammals, proteins often bind DNA, not solo, but as parts of large complexes which can interact with nucleosomes and which allow regulation of transcription or whatever else.

My question is how can we precisely tell at which sites they bind? Is it the amino acid sequence of the protein? Or is it the repetitiveness factor in case they bind to multiple locations on the chromosome?

So, we can tell at which sequences (and where in the genome, even with what relative occupancy) proteins will bind to DNA by experiment. You could try to guess where they bind from their structure, but the way we precisely tell, is by experiment.
The amino acid sequence of a protein ultimately determines its folded structure, and there are many DNA-binding motifs or domains which appear in many different proteins. Some motifs bind the DNA backbone regardless of the sequence of bases, others bind specific sequences.
Let's take zinc fingers as an example. The best-known class of zinc fingers basically inserts an alpha-helix in to the major groove of the DNA double helix, where certain amino acids on the appropriate side of the alpha-helix make contacts with the nucleotide bases. These contacts can be hydrogen bonds, or van-der-Waals contact. (E.g. Histidine and serine tend to hydrogen bond guanine; phenylalanine 'ring-stacks' between As and Ts; and threonine contacts the methyl group of thymine.)

Zinc fingers are often found in arrays in proteins, as you might have been suggesting by "repetitiveness factor". Meaning, a single finger might recognise a specific 3 or 4bp sequence, which isn't very unique. A protein will usually have 3 or more fingers held with regular spacing, so that this string of motifs: ZFa-ZFa-ZFb might recognise the DNA sequence: GCTAxxxGCTAxxxCCAA which is a much more unique site (this is imaginary.)
So yes protein sequence and (thus) structure determines what sites a protein can bind (you can imagine a distribution of affinity for sequences, there will be a 'peak' sequence) - but again some proteins bind the DNA backbone non-specifically, and in mammals they often don't bind alone but within complexes.
People have studied protein-DNA binding by engineering their own arrays of zinc fingers or TALENs, and also by engineering their own DNA binding sites, through a process of 'artificial evolution': selecting the strongest binders, mutating them, and repeat. These kinds of studies might come up with a sort of optimal 'binding code'.

If you have taken the picture from an article then it is good to cite the reference.


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Blood circulation - How to expand blood capillaries?
Do blood capillaries expand? If yes, through what means can it be done? And can warm water also be used to expand blood capillaries?

It's considered a requisite on biology.se that at least some reading/research is carried out and presented with your question. For example, have you read about vasodilation and capillaries? Otherwise it will be closed as homework. The site tour and the help center  provide guidance on how to use this site. Please take a few minutes to read about the kind of questions which are on topic here

@paul What do you mean by "expand"? Do you mean "increase the number of capillaries by angiogenesis" or "vasodilate"? Given the warm water example, I'm guessing it is the latter?

Capillaries are the smallest blood vessels. They are unique in that:

They don't have any muscular component like arterioles or venules do.
They are lined by a single layer of endothelium  (cells lining blood vessels are called endothelial cells) overlying the basement membrane.

Due to these reasons the capillaries are very permeable facilitating nutrient and gas exchange.
The capillaries don't expand as they do not have muscular or elastic components. However exposure to heat do increase the circulation. This is due to the following facts:

Exposure to heat dilates the pre-capillary arterioles - this would inevitably cause improved capillary circulation in capillaries that are already open.
Increase in pre-capillary flow opens up collapsed capillaries. In the human body roughly only one-fourth of the capillaries are open during rest1. As the pre-capillary arterioles dilate, the collapsed capillaries open up thus further improving circulation.

To improve capillary perfusion:

Temporary improvement can be achieved by activity (exercise), exposure to warmth, emotions (flushing is due to vasodilation), even exposure to cold causes vasodilation after the initial vasoconstriction
Permanent improvement of capillary circulation can be achieved by increasing capillary density. Capillary density refers to the number of capillaries present in 1 cm2 area. Capillary density can be increased by consistent anaerobic (isometric and to some extent isotonic) exercise.

References:
1: Boron and Boupaep text book of medical physiology, 2nd Edition, p.467
For more:

http://corporate.dukemedicine.org/news_and_publications/news_office/news/6597
http://www.ncbi.nlm.nih.gov/pubmed/8852622

Yes, some blood vessels change their diameter, they dilate or constrict. This is termed 'vasodilation' and 'vasoconstriction'. Large and mid-sized vessels contain smooth muscle in their walls. The walls of arteries tend to be stiffer than those of veins, to withstand high pressure coming from the heart.

Smooth muscle, when stimulated by the nervous system, can sustain contractions for long periods of time, and often with fine control. When smooth muscle in the walls of your blood vessels relaxes, those vessels will dilate.
Small capillaries do not have smooth muscle in their walls, but the flow of blood through them can be controlled by the larger vessels that feed them. When arterioles constrict, the capillaries they feed can have reduced flow.

Our nervous system takes in a lot of signals relevant to controlling blood pressure and flow, and controls these smooth muscles. Flow can be increased or decreased to individual organs when needed, like the intestine (after a meal), the muscles (during exercise), the skin (for heat exchange).
The question about warm water is actually quite interesting. Placing your arm in warm water will cause vasodilation in your other arm (the one not in the water), in order to lose some heat to the cold air and maintain your core temperature. Normally, the blood vessels in our 'extremities' (our hands and feet) are kept quite constricted to reduce heat loss with the cold air.
If we exercise or take a hot bath our core temperature will rise, some people will notice their skin gain a red hue after these activities, due to vasodilation.

Very little of this answer addresses the OP's question. Can you expand on what, exactly, increases capillary flow and how?

OP asks "by what means [can capillary expansion] be done?". As C Rags says capillaries don't have muscular or elastic components to their walls, but I (and he) have answered that the flow through them is controlled by contraction and relaxation of the smooth muscle of the arterioles that feed capillary beds. Flow resistance is inversely proportional to the diameter to the power 4 - decreases of diameter increase resistance steeply.
Are you asking what environmental stimuli & nervous input causes increased capillary flow? I can't answer that - there's many (google), and OP didn't ask that imo.

As I said (I did not miss the above), very little of your answer was a direct response to the OP's question. That remains a fact.

You're right. Honestly, I don't see much point in improving it: OP ought to read a textbook, as you commented. I tried to give some background since it can't be assumed from the question.

On 2nd thought, I disagree with you. All paragraphs of the answer contribute, having assumed OP knows little:
-Larger vessels have smooth muscle
-This smooth muscle changes their diameter
-Precapillary vessels control capillary flow
-Circulation is influenced by many things
-Warm water is one
The issue is purely that the question lacks any background awareness of vasodilation. I think the answer is an appropriate one for a bad question, but is not a good read for yourself. :)


text:
How can I isolate live Wolbachia endosymbionts from Drosophila
I am interested to culture Wolbachia bacteria in cell line.

Welcome to Bio.SE! Could your add some details on what kinds of approaches you are thinking? Perhaps some more info on characteristics of Wilbachia?

If I had to close then I would vote to close this as homework because a simple google search fetches relevant answers. I am not voting to close, however, because Wolbachia is not such a common topic. -1 for lack of effort

You can see this protocol for Wolbachia isolation:
See this protocol for infecting cell lines with Wolbachia.
In this study the authors have established a cell line from a Wolbachia infected tissue of Aedes albopictus. You can have a look at that too.

Why downvote ??

I downvoted because I thought it to be somewhat of a link-only answer. Removed. If you add some details I am totally happy to upvote, but likely the question needs work before a proper answer is possible.

@ChrisStronks Cannot paste the protocol here. Since the OP is asking only for the protocol, I provided the link (all links are to published articles and are not likely to be broken in future). To add anything more, the question needs to be refined

Agreed, totally. Again, after question refinement I am happy to upvote.


text:
Why do we get 'bags under our eyes'?
Why do these circles form around the eyes if somebody is tired? And why does fatigue express itself around the eyes this way? Can I get eye bags very quickly in another way?

http://www.todayifoundout.com/index.php/2014/06/causes-dark-circles-eyes-sleeping-people-really-tired/
http://www.top10homeremedies.com/how-to/how-to-get-rid-of-dark-circles-fast.html

It's considered a requisite on biology.se that at least some reading/research is carried out and presented with your question. Otherwise it will be closed as homework. The site tour and the help center  provide guidance on how to use this site. Please take a few minutes to read about the kind of questions which are on topic here

I edited your wording. I wasn't entirely sure what you meant with your last question "How can I get it really fast?", so I re-worded that sub question as best as I could. If you are unhappy with the edits, feel free to change or roll back.

I'm sorry I had to change the title from 'why do we get eye bags'

I know that dark circles and bags are two different things with different causes, the dark circles are mostly related to breathing problems while the bags are related to fluid retention, although these answers don't satisfy me which is why I'm still researching.

A possible answer for the first image may be that if you sleep badly you release more of the cortisol stress hormone, which breaks down your skin collagen across your entire body, which makes your skin thinner and reveals the blood behind the dark circles with a dark blue tint.

According to the Mayo Clinic website:

As you age, the tissue structures and muscles supporting your eyelids weaken. The skin may start to sag, and fat that is normally confined to the area around the eye (orbit) can move into the area below your eyes. Also, the space below your eyes can accumulate fluid, making the under-eye area appear puffy or swollen. Several factors can lead to this, including:

Fluid retention due to changes in weather (for example, hot, humid days)
hormone levels or eating salty foods
Not getting enough sleep
Allergies or dermatitis, especially if puffiness is accompanied by redness and itching
Heredity — under-eye bags can run in families

Of the list above, the most common reason is likely heredity.
Sources:

Mayo Clinic, as linked above
http://www.allaboutvision.com/cosmetic/puffy-eyes.htm

http://health.howstuffworks.com/skin-care/problems/beauty/what-causes-bags-under-eyes.htm Good answer +1

@CRags Thank you! I appreciate the feedback-- good or bad! I read that article as well, it was helpful.


text:
How to set threshold in ImageJ for quantifying relative fluorescence?
I have taken images from two different samples that have uptaken EdU during DNA synthesis (S-phase). The experiment setup is to find which condition had uptaken more EdU. Therefore I am detecting EdU with fluorescent to be able to quantify them in two conditions and compare them. The images are taken under same exposure. However in ImageJ when I want to adjust threshold I am not sure if I need to have the same threshold for both images or they can be different? Any tips are appreciated and let me know if I need to provide more info.
cheers!

Presumably your image is either a blot, or of cells. You're going to use some software to measure the density of the blots or cells - what software? You can use ImageJ if you haven't another way. Either way you need to have the original images in a lossless format for the quantification. I think if you adjust levels and click 'apply', you stand to change pixel values.
I've used an old program called OptiQuant to get numbers, and separately adjusted the images for ease of viewing.

I'm voting to close this question as off-topic because questions regarding software use are off topic on BioSE. I understand the need of bio researchers for protocols, but your question is still off topic

@Raoul you have a good point but image j framework is very specific to biology. I think seeing these sorts of questions here is within scope.

You definitely need to have the same threshold for both images because you want to make comparison between them. Do you have a control condition (the condition which is not supposed to uptake EdU)? if yes, then use it to set your threshold and keep the same threshold for the tests conditions. If not, you can either make a experiment control, or select a region of interest (ROI) in one of your 2 tests where there is no coloration (no uptaking of EdU) and set the threshold in this ROI.
Cheers

You need to normalize both images to the background. This can be done in many softwares including photoshop.
When I was learning this starting to do it with something more simple like SDS page protein bands helped me a lot. The principles are the same you are still subtracting background. Look at this tutorial:
http://m.youtube.com/watch?v=JlR5v-DsTds
However, when analyzing intensity values in fluorescent microscopy the most important parameter is area of your analysis. This needs to be an objectively applied as much as possible, and that can be by increasing the number of replicates whose area you analyze. Your going to look at pixel intensities for many many cells and average those intensities. Using the imagej cell counter plug-in is helpful to see how to determine cell area.


text:
Was Earth's atmosphere more buoyant in the prehistoric era then today?
The mass and size of the dinosaurs and prehistoric insects continues to amaze me. I read from an earlier post that oxygen was more abundant during the prehistoric era. However supporting the weight for me is still a mystery. Is it possible that the air was denser, allowing slight decrease in weight from greater buoyancy?

How much denser should the air be? Unless it's not becoming a liquid, you can forget about this.

@Chris - actually this is a question pertaining to the flight of large reptiles as well, isn't it? So it's not far fetched. Not that I buy that the atmosphere was significantly different then from now.

@anongoodnurse If you go up to 10.000m the air is getting considerably thinner. Yet still birds can fly over the Himalaya without much problem. To have a real impact, the atmosphere had to be much thicker.

@Chris - agreed. I read a couple of papers on this, and the thought was (not mine) that there was more CO2 then, maybe twice as much, which might be enough. In any case, I don't know about aerodynamics. I agree the atmosphere was not likely so very different once sources of CO2 were being sequestered and the oceans were sucking it up out of the atmosphere.

At least for arthropods, the reason for those large species during the mesozoic was simply that their maximum body size scales with the partial pressure of oxygen in the atmosphere. This is due to their relatively simple respiratory system -- they have no lungs but tubular structures that reach into each segment for passive gas exchange.

This belongs at SE Earth science

While it seems difficult to me to imagine any mechanisms that would allow significant changes to the total amount of atmosphere (and therefore density) in geologically recent times (< 100M year), it's quite difficult to find direct evidence about it.
In 2012 Nature published a paper that calculated the air pressure (and therefore the air density) by noting the distribution of sizes of puddles formed by raindrops in 2.7 billion year old ash. The conclusion was that the air was no more than twice as great as it is today.  This amount would be quite a bit for flying creatures, but would be almost completely insignificant for  supporting the weight of large creatures.
As an example, a large elephant has a volume of slightly more than $10m^3$, and a mass of over $5000kg$.  The buoyancy of the air only takes off the equivalent of about $12kg$ of that mass.  Even an atmosphere 10 times the modern density would be little help in supporting its weight.

Is the loading bearing problem still in question, or is it resolved?

This question has an answer with some references.  http://biology.stackexchange.com/questions/1018/how-did-the-huge-dinosaurs-cope-with-gravity-and-loads-on-bones-etc


text:
How to get a pdb file of a single atom?
I am trying to get a pdb file that contains a single atom, it doesn't matter if it's Hydrogen or another atom. How can I obtain this? Are there any pdb files with just a single atom available to download? Or do I have to take an existing molecule and remove the atoms manually?

How do you want to make a crystall of a single atom?

I have no idea why you would need sth like that, but you'd have to cut existing one

I'm currently working on a problem on molecular modeling and our software is having problems. I was told that a good way to debug this is to run the program using a pdf file with just a single atom

you'd have to cut existing one can you explain how?

@user4352158 In the PDB file you can remove every other entry except an atom. You can also view a single atom without altering the file itself(at least in swiss-pdb viewer)


text:
First documented beneficial mutation?
I've been reading up on beneficial mutations, and am curious when we discovered and documented the first one.
Can anyone point me to the first documented beneficial mutation?

Per request, let me try to clarify my answer a bit.
I know that we've been aware of mutations perhaps as long ago as the 1930s (I believe it was R.A Fisher who was one of the first to talk about them??).
I have read various documented beneficial mutations since then, such as lactase example in humans, or cit+ in E.Coli.
What I'm curious about is when it was that we first identified and documented (scientific paper or article) an observed beneficial mutation, in any organism (not just humans).
So yes, Remi.b, your wording would have been what I was looking for:
"what is the first article that has documented a beneficial mutation, in any organism"
Does this clarify it enough?

You think about things like the mutation which activates lactase in people of european ancestry permanently?

Do you mean the first documentation (no matter if mutation was earliest exactly known), or earliest exactly known such mutation (which has been documented at any time)?

I am not really sure what kind of observation you are interested in? If we see a sweep just like for the lactase example in humans? Or are you looking for a mutation that appeared in a lab and that has directly been shown to be beneficial? And as Hyde said did you actually mean "what is the oldest beneficial mutation we know" or "what is the first article that has documented a beneficial mutation". In both case, the question needs editing I think, to make clear what kind of observation you are interested in.

I'm not even sure if you mean in humans or ever. This question is unclear. As others have said, it really needs to be narrowed down in its scope. This could mean nearly anything.

E. coli using citrate might be the best document beneficial mutation.

@user137 - there are many examples of beneficial mutations. The problem is that it's unclear what the OP is asking.

It's a valid question, just needs refinement and then it can be re-opened for sure

Earliest beneficial mutation discovered by humans is what I guess OP is interested in, which I think is of no great relevance. Mutations happen all the time and beneficial mutations are selected in the evolutionary process. Which was the first example in the textbook doesn't make any great sense to me.

What search parameters have you tried to find the paper?

Good Gravy:  I didn't save my exact search text, but a lot along the lines of 'history of beneficial mutations', and 'first discovered beneficial mutations'.  I was getting no-where.  I figured I'd turn to a place like this, hoping someone here could point me in the right direction.

I found a list of documented beneficial mutations by typing in google "beneficial mutations". It was the fourth link. (http://www.gate.net/~rwms/EvoMutations.html)
Check the years and find the one which interests you. All of them are very well vulgarized and all their sources are cited.


text:
How does beta branching stop alpha helices from forming?
I am told that beta branching interferes with alpha helix formation.
Problem is that I don't see how beta branching has anything to do with alpha-helix formation. Beta-branches are on the outside of alpha helices and internal hydrogen bonding holds the helix together.
My book (Lehninger) also doesn't say anything about beta branching interfering with alpha helix formation.

Beta branched amino acids are bulky and can sterically clash with neighbouring atoms, forcing the backbone to adopt torsion angles which don't favour helix formation. Does that answer your questions? If it does I can expand on it and post it as an answer.

Also it shouldn't be said that they stop alpha helix formation outright, it's really contextual. Generally, though, they are favoured in domains where the back bone is more extended than in a helix.

@canadianer can you expand

@canadianer can you post this as an answer. You may also add an picture of helical wheel or Ramachandran plot for these residues.

@WYSIWYG Yes I will when I have time. Feel free to answer if you wish

The answer to this, as said by @canadianer in comment, is that beta branched amino acids are bulky and can sterically clash with neighbouring atoms, forcing the backbone to adopt torsion angles which don't favour helix formation.
I couldn't find reference for these exact words, but similar one here:

amino acids such as Valine, Isoleucine, and Threonine all have branching at the beta carbon, this will cause steric clashes in an alpha helix arrangement... valine, threonine, and isoleucine will often destabilize the helix because of branching of the beta carbon. These three amino acid residues are more often found in beta-pleated sheets, where their side chains will lie in a separate plane than the main chain.

Also, for torsion angles, from same source:

The torsion angle is the measure in degrees in bonds between atoms. Folding of proteins are influenced by the degree of rotation amino bonds can hold. There are two different types of torsion angles existing in polypeptide bonds. Psi, ψ is the angle between the α-carbon and the nitrogen atom of a peptide bond. The other bond is called phi, φ which is the angle between the α-carbon and the carbonyl group.

See this table for details of which amino acid prefers which configuration:

Source


text:
Is there a standard formula/calculation for sexual dimorphism?
Is there a standard, or most accepted, way to present a value for sexual dimorphism? For example, one could use
$$\frac{\text{Female value}}{\text{Male value}} -1$$
This would give negative values when the female value is smaller than the males, and positive when male is smaller. My issue with this though is that when a female is twice the size of a male its value is -0.5, while when a male is twice the size of a female its value is 1.0, so they do not spread symmetrically around 0.
Edit:
Just playing around with some dummy data in R I came up with a possible solution
$$0.5 - \frac{\text{Female}}{\text{Female + Male}}$$
This gives a zero centred value with equal distribution around the mean. For example, when Females are twice the size of males the value is -0.166, and when males are twice the size of females the value is 0.166, when they are the same size it is 0.

I think you should consider something parametric, that takes the entire trait distribution into account, since there can probably be quite large intrasex variation (at least in some species). For instance, looking at distribution overlap between sexes.

Oh, and have you seen the Wikipedia page Sexual dimorphism measures? It should give you a couple of ideas.


text:
How do cats survive falling from great heights?
Among mammals, cats are able to land safely when falling from great heights. For example, when compared to dogs or humans they can survive drops from relative large heights. How do they manage?
A 1987 study from the Journal of the American Veterinary Medical Association. Two vets examined 132 cases of cats that had fallen out of high-rise windows and were brought to the Animal Medical Center, a New York veterinary hospital, for treatment. On average the cats fell 5.5 stories, yet 90 percent survived.
See wiki on cats.
How can cats do this?

insanely good reflexes; too high = broken cat.

I edited your question quite extensively. If it doesn't reflect your intentions anymore feel free to roll back.

I edited the question and vote for re-opening. The reason for question closure (unclear what you are asking) is not applicable any longer as it is edited. The question subject has been hardly researched and pretty interesting.

@ChrisStronks - in a study of 132 cats falling from an average height of 5.5 stories (most: 32 stories), about 2/3 required some sort of medical treatment as a result of their fall, and about half of those that required treatment (1/3 of the total cats brought in) would have died without medical aid.

@anongoodnurse, that makes sense. I wasn't thinking straight...

@ChrisStronks can you add the link to that article?

@WYSIWYG: the Nature paper is linked in the answer. The other one (5-stories falling kitties in Am Vet Med Assoc) was brought up by anongoodnurse and she should hopefully be able to link it in the question edits.

Keep in mind that there's a selection bias issue here: If a cat falls out the window and dies, it's unlikely the owner takes it to the vet. Also, if a cat falls out the window and doesn't look hurt, the owner doesn't take it to the vet. This was explored on the podcast/radio show Radio Lab: http://www.radiolab.org/story/102525-vertigo/

The reason why cats are superb jumpers has not received much attention, but one article in Nature was entirely devoted to just this (Diamond, 1988). Here follows a partly quoted and partly adapted text from this article:
First , because mass increases as the cube, but surface area as the square of linear dimensions, falling large animals are in general more injury-prone than small ones, as they suffer greater impact stress, their bones experience greater stress, and they reach higher terminal velocities in free-fall because of a less favorable area/mass ratio. While a small drop breaks an elephant's leg, a falling mouse reaches terminal velocity in the atmosphere much sooner and at a much lower value than do falling elephants.
Second, falling cats have a superb vestibular system and make gyroscopic turns
such that all four feet are soon pointing downwards, regardless of the cat's
orientation at the start of the fall. Hence cats dissipate the impact force over all four limbs. Falling human adults  tend to tumble uncontrollably but land most often
on two feet, next most often on their heads. These facts contribute to the low mortality of falling cats and to their low chance of breaking limbs after the fall.
Third, a cat falling in the atmosphere reaches a terminal  velocity  of  about  60 m.p.h. (compared with 120 m.p.h. for adult humans) after only  about  100 feet. As long as it experiences acceleration, the cat probably extends its limbs reflexively , but on reaching terminal velocity it may relax and extend the limbs more horizontally in flying-squirrel fashion, thus not only reducing the velocity of fall but also absorbing the  impact  over  a greater  area of its body. This may explain the paradoxical decrease of mortality and injury in cats that fall more than 100 feet.
Finally, cats that land with their limbs flexed dissipate much of the impact force through soft tissue. Parachutists are trained to dissipate impact forces by landing with knees and hips flexed, then rolling.
Reference
Diamond. Nature 1988; 332:586-7
Further reading
BBC news


text:
What senses are active while sleeping?
During sleep, our body activity decreases. I am wondering on the extent of the lowering of this activity regarding our five senses. Clearly, the sense of touch is still very efficient since shaking a body is the most common way to awake someone, and hearing is also quite unaffacted (most, if not all, alarm clock, rely on this sense). Most deaths due to fire are due to intoxication rather than the burnt of the fire, so it suggests that smell and taste are pretty dimmed during sleep.
My main question: To which extent each sense is dimmed during sleep?
For example,

Can we smell during sleep? I don't remember having been awoken by the smell of something during my life...
Similarly, can we taste? If someone gives me delicious food during my sleep, would I be able to feel its taste and remember this experience?
Can we see? REM are well known but it is a mechanical feature of the sleep. Some people sleep with the eyes opened: what do they see?

Note: This related question tries to explain how senses are dimmed during sleep but not how much they are.
Note 2: I am aware this is person-dependant: any sound would awake my mother (a skill during my nightly escapades) whereas I would not notice a party around me when I am in deep sleep. But there should be some kind of average... It also depends on the phase of sleep; I am mostly interested in deep sleep and REM sleep, but an answer detailing every phase would be awesome.
Note 3: This question is certainly naive in its current form. Please help me to improve it.

Hmm, technically all senses are active, but their imput has "access denied"  to your "standard output" until certain variable intensity is reached, I think.

Certainly sight is active, at least to the extent of being aware of and woken by bright light, such as sunrise.

@Taladris - I think you'll be interested in this question I just asked, which is similar to yours but doesn't quite duplicate it.

The answer is of interest not only in sleep but also the perceptions of patients under anesthesia, comatose states, etc.
Our senses aren't 'dimmed' in sleep. There is no effective way to turn off our senses. The best way to explain what happens in sleep is that at some point (the last point, actually), our cognitive processing of sensations changes. That is, our higher brain functions allow us to ignore certain sensory input. This effect has been most studied in sound perception.
In a sleep study involving sound and EEG/fMRI during all phases of (drug-free) sleep,

The first significant result of this study is that the pattern of brain activation associated with auditory stimulation was strikingly similar in wakefulness and sleep, suggesting that sensory processing occurred in both conditions. However, we found qualitative differences in brain activation associated with auditory processing during sleep compared to wakefulness. The reduced regional activity during sleep, compared to wakefulness, in the left parietal and, bilaterally, in the prefrontal cortex, thalamus, and cingulate gyrus (part of the limbic system) suggests that these areas may be involved in the further processing and perceptual integration of sensory inputs likely to occur during wakefulness only.[1]

Supporting this is evidence that some sounds awaken someone no matter at what stage they are in sleep, for example, young mothers are woken up by their infants' lightest movements[2], and the fact that we respond to our own names in a similar fashion in sleep and in wakefulness, but such responses are not shown for presentation of other first names.[3]

These results suggest that the sleeping brain, during SII and PS, elicits a differential cognitive response to the presentation of the subject's own name, comparable to that occurring during wakefulness, and therefore that the sleeping brain is able to detect and categorize some particular aspects of stimulus significance.[3]
Thus, the results suggest that when subjects were listening to their own name during sleep some brain regions were selectively more responsive than in any other condition. ...we have demonstrated that the sleeping brain is able to process auditory stimuli. In addition, we postulate the existence of a functional network capable of detecting and facilitating processing of emotionally relevant inputs during sleep.[1]
Our results support the view that PS is not a state of "sensory isolation"; failure to respond to external stimuli during this stage may depend upon mechanisms occurring only after the sensory input has undergone cognitive analysis.[4]

However, as you noted, odors are not good at waking people up.

Some suggest that the human olfactory system during sleep is sufficiently well tuned to ensure arousal to such threatening stimuli as odors associated with smoke from fire. Our results strongly suggest otherwise. The intensity, strength, and noxiousness of the pyridine stimulus elicited behavioral arousal or EEG activation on fewer than half of stage 2 trials, less than one third of REM-sleep trials, and virtually no stage-4- sleep trials. This is a nontrivial lack of response, since pyridine is a component of coal tar and is also used as a herbicide for firewood, and thus is a likely by-product of many real fires. In practical terms, therefore, olfactory awareness in humans is low to absent during sleep, and human olfaction appears insufficiently sensitive and reliable to act as a sentinel system. We further note that auditory arousal threshold is highest in young and sleep-deprived individuals, increasing the likelihood that olfactory processing is even worse for children and sleep-deprived adults.[5]

The methodology in the olfactory study varies quite significantly from the auditory study. Better studies may shed more evidence on why olfactory stimuli are processed differently from other stimuli.
As to what percent? That probably differs from person to person, and I did not search the literature for that.
[1] Auditory Processing across the Sleep-Wake Cycle: Simultaneous EEG and fMRI Monitoring in Humans
[2] Changes in sleep patterns of young women from late pregnancy to postpartum: relationships to their infants' movements
[3] A differential brain response to the subject's own name persist during sleep
[4] Brain Processing of Stimulus Deviance During Slow-Wave and Paradoxical Sleep: A Study of Human Auditory Evoked Responses Using the Oddball Paradigm.
[5] Minimal Olfactory Perception During Sleep: Why Odor Alarms Will Not Work for Humans


text:
What do "e" "-" "C" and "E" mean in this output?
I have given an input of this protein sequence:
MEPVDPRLEPWKHPGSQPKTACTTCYCKKCCFHCQVCFTTKALGISYGRKKRRQRRRPPQGSQTHQVSLSKQPTSQPRGDPTGPKE

from this website  along with the option of COBEpro. Now the output sent by this site to my email is as follows:
Name: temp_prot

Amino Acids:
MEPVDPRLEPWKHPGSQPKTACTTCYCKKCCFHCQVCFTTKALGISYGRKKRRQRRRPPQGSQTHQVSLSKQPTSQPRGDPTGPKE

Predicted Continuous B-cell Epitopes:
MOST LIKELY EPITOPES:
0.82848577 39 TKALGIS CCCCCEE eee-e-e
0.82036375 39 TKALGI CCCCCE eee-e-
0.76503265 38 TTKALGI ECCCCCE eeee-e-
0.73178638 73 TSQPRGDP CCCCCCCC -eeeeeee
…

and a few more. Now can you tell me, if I consider the very first result, I was able to find TKALGIS in the parent sequence but could not find CCCCCEE. What is this CCCCCEE?
And what does this eee-e-e mean?

have you tried other software to verify?

CCCEEE etc. are the secondary structural elements. In this case, the C refers to non-strand and non-helix regions i.e loop regions rather than a coiled region. The C or E usually refers to whether the residue is coiled (C) or part of a strand (E). H would be used to denote a helix, however, in the question, it appears that there are no helices. These letters are often different in different software: it's merely a point of semantics between different software.
e or - refers to if the amino acid at that position is exposed or not (- = buried).
For the method, here is the COBEpro paper, although it does seem very technical. The help page has more easily accessible information on the output.

And how is the predicted antigenic propensity score plotted?

I'm not sure what you mean. Perhaps open a new question.


text:
How do biologists infer correct ORF of a DNA sequence?
Each DNA (RNA) sequence has 6 possible Open Reading Frames(ORF). My question is: What are the theoretical bases of in vitro or in silico tries to find correct reading frame of a sequence?
Is it just distance between Start and Stop codons, or are there some other factors with more important impacts in this subject?

I have edited your question a bit. Please feel free to roll back if this does not suit you

Homology, ESTs, codon usage, length of ORF

The start and stop codons depend on the ORF selected. If one of the six ORFs has nicely paired start and stop codons and the other five do not, then that is a pretty good hint. There are other ways to tell (shine-dalgarno sequences in prokaryotes, Kozak consensus sequences in eukaryotes, etc).

canadianer please explain more

TransDecoder is a commonly used program for extracting likely coding regions from transcriptome assemblies, which does the following to make a call:

TransDecoder identifies likely coding sequences based on the following
  criteria:

a minimum length open reading frame (ORF) is found in a transcript
  sequence
a log-likelihood score similar to what is computed by the GeneID
  software is > 0.
the above coding score is greatest when the ORF is scored in the 1st
  reading frame as compared to scores in the other 5 reading frames.
if a candidate ORF is found fully encapsulated by the coordinates of
  another candidate ORF, the longer one is reported. However, a single
  transcript can report multiple ORFs (allowing for operons, chimeras,
  etc).
optional the putative peptide has a match to a Pfam domain above the
  noise cutoff score.

So in essence, look for the longest ORF, and then use some secondary metric (hidden Markov model, position weight array, database query, etc) to refine your prediction.


text:
Why are the fertility rates of large predators kept low?
Predators at the top of a food chain, like lions, seem to have a relatively low fertility rate, which fits well to the ecosystem and avoids overpredation. But what is the mechanism that keeps the fertility rate at this level? A mutation that increases fertility among the predators should quickly spread in such a population, eventually leading to an increase of the predator fertility rate followed by overpredation. But it seems that this is usually not the case. What does keep the fertility rate of predators at the level they are?
P.S: Many explanations on population dynamics cite Lotka Volterra, including the existing question on Bio.SE "What prevents predator overpopulation?". Population dynamics predict orbits for the population sizes of predator and prey. Still this does not explain why the fertility rate of predators shouldn't go up.

@Remi.b - I don't think so, as that post deals with fertility rates in specific, not the population characteristics

This question is clearly not a duplicate of the linked question, and they have completely different perspectives. This question is dealing with the evolution of life histories, while the other one deals with dynamic predator-prey models and population regulation. The original poster has also already addressed the proposed duplicate in the question.

I think fertility rate (or rate of offspring production) is correlated to the size of the animal more than anything else.

Relevant:  http://science.sciencemag.org/content/349/6252/aac6284.full.
Also, see the NY Times article:  https://www.nytimes.com/2015/09/08/science/study-reveals-consistent-predator-prey-pattern.html

This question can be tackled in several ways, and also seems to contain a couple of misconceptions about ecological processes (e.g. problematic group-selection ideas and how species 'fit' into the ecosystem).
However, I think it is most usefully answered from the perspective of life history theory and the evolution of life histories (see e.g. Roff, 2002 and Fabian & Flatt, 2012 for background), and at its core this question is dealing with tradeoffs between e.g. fecundity and mortality.
All organisms act under a limited energy budget, and when they spend energy on some activities that will limit what they can spend on other activities.
This lies at the core of life history tradeoffs.
If organisms use resources to produce or raise offspring, this can therefore have consequences on growth, maintenance (e.g. disease resistance), predator avoidance and many other traits and behaviours, which all affect fitness.
With regard to your question, there is a well-known tradeoff between survival and fecundity (an intraindividual effect), which has been shown both between individuals within species and across species.
As with almost all species traits, there is also variability between individuals within populations, so that some have higher fecundity than others, but may then also suffer lower adult survival rates (maybe under certain environmental conditions).
Therefore, there are certainly already "mutation(s) that increases fertility among the predators" within populations.
The reason that fertility is not continuously increasing over time, is that this would have negative fitness consequences overall.
So the reason that the (average) life history traits within a particular species are what they are, is that they are the result of the evolutionary pressures that the species have been experiencing over evolutionary timeframes, acting on the entire life history.
To be sure, hypothetical mutations/changes in life history traits that would increase fecundity with no negative tradeoffs whatsoever for either parents or offspring (i.e. no negative fitness consequences) would definitely increase in frequency.
From the perspective of life history theory, everything else equal, selection will maximize the survival function, $l(x)$ (survival to age x) and the reproductive function, $m(x)$ (number of offspring at age x), while minimizing maturation age.
However, tradeoffs between these functions (directly or indirectly) and between generations will prevent these from being optimized one by one.
Population growth in long-lived predator species is usually also very sensitive to changes in adult survival rate (Caswell, 2001).
This result comes from analysing stage or age structured population models, and is the result of a life history strategy with high adult survival rates, fairly high age of maturation and relatively low fecundity.
To increase fecundity in this situation with negative effects on adult survival will risk adult death and therefore loss of many future years of reproduction.
These kinds of results and models are often used to identify which life history traits and stages to target in conservation actions, but can also be used to understand evolutionary processes, since population growth rate can be used as an overall measure of fitness.
It should also be added that many other ecological processes must be considered.
For instance, large predators often care for their young for quite a long time, since their hunting/foraging behaviours are complex, and it takes a long time for young to learn how to hunt successfully by themselves.
This means that adults need to bear not only the direct cost of producing offspring, but also to support them until they are self-sufficient.
For an extreme case, look at the Orangutan (not a predator, but still) where the young stay with their mother and nurse for up to 5-6 years (sometimes more).
To increase fecundity in such a situation will put a large strain on adult mothers.
You also need to consider trade-offs between offspring number and offspring "quality", which have been demonstrated in many species (an intergenerational effect).
This means that an increase in fertility can result in lower offspring survival over longer timeframes, with overall negative effects on fitness.
Finally, life history evolution is a large and complex field, and these are just a couple of examples and suggestions for why the situation isn't as simple as your question makes it out to be.
Environmental variability and the predictability of the environment are other factors that I haven't considered at all, but are both important processes when you try to understand life history evolution.
This question can also be approached from a more theoretical perspective, but without a background in life-history evolution I think it is more useful to start reading about different processes and tradeoffs, and then later if you are interested to go into the theory for a deeper understanding.

In a given area there can be only a limited number of top predators due to resource limitations. Furthermore, as top predators are not hunted upon, a relatively high percentage of offspring will survive until adulthood. Hence, producing many offspring doesn't make sense as survival rates are high, while resources are limited. Producing many offspring is a huge investment of resources (must be raised and fed) and if in the end many offspring die of a lack of resources, then the invested effort and energy was for nothing. Hence, producing many offspring decreases fitness in top predators and this trait will have been selected against during evolution.

But it seems that this is exactly what lions do, that is produce a lot of offspring(about 6 cubs per lioness so 12 to 240 cubs for prides with 2 to 40 lionesses). This is all because the more offspring that are produced the more likely at least 1 will survive and because they live in large groups. If this isn't good for lions as a species since prey is getting more scarce than why didn't lions naturally go to extinction?

@Caters - "A lot of" is subjective. Rats have 10-12 per litter. That is what I would call a lot. Like rabbits they can also have multiple litters/annum.  Not what you would expect with lions.

The way you pose the question, as in what mechanisms limit the fertility of predators, together with your comment about the distinction to the population dynamic aspect, strongly that what you are thinking about an adaptional mechanism here and asking about its characteristics, right?
In that case, this is very similar to the kind of scenarios you find in the group selection arguments: It is better for the species to limit it's fertility rate, thus a limit on the fertility rate will evolve.
This simplified view on group selection is heavily criticized as it's not a ESS: As you pointed our yourself, a mutation that would increase the fertility rate would quickly spread.
But this is assuming that an increased fertility rate actually would be beneficial. And what we forget here is that we have an inherent balance of quality of offspring versus number of offspring: r/K selection. The view that evolution constantly strives to produce increasingly ferocious eating and breeding machines is obviously too simplified if we were to just take a look at the how the biosphere actually looks like and compare it to our imagination how it could be like.
So basically, we could assume that the local "mechanism" here is simply r/K selection, with the population dynamics providing a major influence of the overall dynamics behind the scenes.

However, group selection do have an influence in the general evolutionary dynamics, as even the otherwise avid opponent Richard Dawkins agrees upon, but this is under the condition that group selection really is active natural selection of distinctive groups, and not some omniscient mechanism that somehow makes groups inherently develop traits that is beneficial to the group.
And the other conditions like ESS still have to be valid here as well: If a trait could be positively selected for by group selection, it has to 1. Be developed before any selection can act on it and 2. Stay a ESS for it to persist (unless the group selection pressure is very high, and I think it's generally assumed that it's many orders of magnitude less influential than selection within groups)
I could imagine the possibility that group selection somehow has had an influence in limiting the genetic pool of top predators to the kind that uses a this r/K strategy that we see today but here I digress, it's not needed to explain the fertility rate of the top predators we see today.

Downvoter, comment please?

The premise,

A mutation that increases fertility among the predators should quickly spread in such a population

probably isn't true if there are tradeoffs involved. It also wouldn't be true if the increased death rates due to overpopulation, were concentrated more heavily on the over-breeders and their descendants than on the rest of the population. (This could happen due to spatial structure; for example, if each predator hunted and raised their offspring in their own patch of territory.)

Tradeoffs are the bread and butter of Life History Evolution. ("Life History Traits" are the traits which are most directly related to fitness: age-specific mortality rates, age-specific fecundity rates, age of maturity, etc. Size is an honorary life history trait, as is offspring size, since these often have strong effects on mortality and fecundity.)
One of the most famous examples from the early days of Life History Theory is the Lack Clutch. The ornithologist David Lack noticed that birds never laid as many eggs as they were capable of producing, and wondered why. He proposed that there was a tradeoff between the number of offspring, and the survival of each of the offspring. He suggested that clutch size was designed to maximize the number of offspring who would survive to the age of fledging, and that this would be an intermediate optimum.$^1$

Lack was right that the most fit clutch size would be intermediate. In detail, clutches are usually a little smaller than he predicted, because there are additional tradeoffs he didn't consider.
Here's a partial list of tradeoffs that are often thought to be important.

The more offspring there are in this clutch, the less fit each of them will be. For example, maybe the parent has a certain amount of resources to invest in creating offspring; the more of them there are, the smaller each of them has to be (larger animals are often more fecund).$^2$ If the offspring fitness cost is in terms of survival, then this is Lack's hypothesis.
The more offspring there are in this clutch, the less likely the parent is to survive to future breeding seasons. (This is often called the Cost of Reproduction.) For example, maybe the parent has some resources which it has to allocate between reproduction, and its own maintenance. The optimum will not favor perfect maintenance (this is the basis of the Disposable Soma theory of aging);$^3$ but it also favors intermediate clutches (which are a little smaller the Lack Clutch).$^4$
The more offspring there are in this clutch, the less offspring there will be in future clutches. For example, maybe the parent has some resources which it has to allocate between reproduction now and its own continued growth (which will make it more fecund in the future). This tradeoff also has to do with the age at maturity: at what ages should an organism not reproduce at all (devoting all its resources to growth), and at what age should it start?$^5$

(Tradeoffs are often modeled as limiting-resource allocation problems, but this isn't the only sort of tradeoff. A tradeoff occurs whenever getting more of one good thing requires getting less of a different good thing [or more of a bad thing], for whatever reason.)
So much for life history tradeoffs in general. But, in the face of these tradeoffs (and whatever other constraints), which can have different strengths and different shapes etc., different species hit on different strategies. Why? What leads to the large predator life history being optimal for large predators? I don't know. I don't even know if it is known! Life History Evolution is complicated, with many different traits coevolving together. It's hard to model more than a few of these (holding the others constant) at a time. I don't know if anyone's actually explained the conditions that would lead to an entire suite of life history traits, from scratch. (Once upon a time, attempts would have been made to try and explain the large predator life history as one end of the r-selection vs. K-selection spectrum. But that paradigm has fallen out of favour among researchers.$^6$)
Here's another factor, elaborating on the first tradeoff, which I think is probably relevant.
If there are too many predators, then there won't be enough prey, and the average death rate will soon catch up. If this food-shortage cost were applied to every member of the predator population equally, then a mutation for increased fecundity would indeed be favoured: although all members shared the cost (increased mortality), only the mutant would get the benefit (increased fertility); on average the mutant would be fitter and the mutation would spread. (This is ignoring the other costs, such as slower parental growth and faster parental aging.)
But now suppose that you are a predator, and you own a patch of territory; and whether you over- or under-hunt mostly affects your territory. Suppose also that you care for your offspring, or at least let them share the hunting in your territory, rather than sending them elsewhere. Then over-breeding will lead to over-hunting in your territory (or, to hunting the same amount but having lower-quality offspring). But the other territories'll be fine! The brunt of the mortality cost of over-breeding and over-hunting, as well as the fertility benefit, will fall on you and your offspring.
tl;dr: if conditions (eg. due to the population's being spatially structured) are such that the mortality cost of higher fertility applies more strongly to the over-breeders than to the rest of the population, then there will be selection against over-breeding. In addition to costs of overpopulation, higher fertility can also negatively affect the parent's fitness in other ways; for example, by using up resources that they would have used for self-maintenance, or resources that they would have used for growth.

Lack, "The Significance of Clutch Size". Ibis (1947).
Smith and Fretwell, "The Optimal Balance Between Offspring Size and Number". American Naturalist (1974).
Kirkwood and Rose, "Evolution of Senescence: Late Surival Sacrificed
for Reproduction". Philosophical Transactions B (1991).
Charnov and Krebs, "On Clutch Size and Fitness". Ibis (1974).
Kozlowski, "Optimal Allocation of Resources to Growth and
Reproduction: Implications for Age and Size at Maturity". Trends in
Ecology and Evolution (1992).
Reznick, "r- and K-Selection Revisited: The Role of Population Regulation in Life-History Evolution". Ecology (2002).

The classic textbook for Life History Evolution is Stearns' The Evolution of Life Histories (1992). A more recent one (I haven't read it) is Roff's Life History Evolution (2002).


text:
All UniprotIDs of a cancer pathway
I need to download all uniprotIDs of a cancer pathway, say the AKT Signaling. It may be super easy, but I don't know which resource to look at since it is a new field.

How/where do I find these?

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I would do this through the Reactome database. Searching for "AKT Signalling" returns, among other things, an entry for PI3K/AKT Signaling in Cancer (Homo sapiens) (REACT_147723). Clicking on that link will take you to the pathway's page, and if you click on "Disease" (under "Locations in the PathwayBrowser"), you will be shown a link to the pathway browser page of that particular pathway.
Once there, click on the "Molecules" tab, select "Proteins" and you will get a list of the proteins involved in the pathway and their UniProt accessions. There, you can click on the "Download" link and retrieve this list:
MoleculeType    Identifier  MoleculeName
Proteins    P31751  UniProt:P31751 AKT2
Proteins    P31749  UniProt:P31749 AKT1
Proteins    Q9Y243  UniProt:Q9Y243 AKT3
Proteins    P16220  UniProt:P16220 CREB1
Proteins    Q12778  UniProt:Q12778 FOXO1
Proteins    P98177  UniProt:P98177-2 FOXO4
Proteins    O43524  UniProt:O43524 FOXO3
Proteins    P98177  UniProt:P98177-1 FOXO4
Proteins    O15530  UniProt:O15530 PDPK1
Proteins    Q92934  UniProt:Q92934 BAD
Proteins    P46527  UniProt:P46527 CDKN1B
Proteins    P38936  UniProt:P38936 CDKN1A
Proteins    Q00987  UniProt:Q00987 MDM2
Proteins    P60484  UniProt:P60484 PTEN
Proteins    Q8WWG1  UniProt:Q8WWG1 NRG4
Proteins    P10721  UniProt:P10721 KIT
Proteins    Q9HCT0  UniProt:Q9HCT0 FGF22
Proteins    P15498  UniProt:P15498 VAV1
Proteins    P05230  UniProt:P05230 FGF1
Proteins    Q15303  UniProt:Q15303-1 ERBB4
Proteins    P08620  UniProt:P08620 FGF4
Proteins    P42338  UniProt:P42338 PIK3CB
Proteins    O14944  UniProt:O14944 EREG
Proteins    O15520  UniProt:O15520 FGF10
Proteins    P21802  UniProt:P21802-3 FGFR2
Proteins    Q13480  UniProt:Q13480 GAB1
Proteins    P55075  UniProt:P55075-1 FGF8
Proteins    O00459  UniProt:O00459 PIK3R2
Proteins    Q9UEF7  UniProt:Q9UEF7-1 KL
Proteins    P09619  UniProt:P09619 PDGFRB
Proteins    Q8WU20  UniProt:Q8WU20 FRS2
Proteins    Q86Z14  UniProt:Q86Z14 KLB
Proteins    O00329  UniProt:O00329 PIK3CD
Proteins    P11487  UniProt:P11487 FGF3
Proteins    Q9GZV9  UniProt:Q9GZV9 FGF23
Proteins    P42336  UniProt:P42336 PIK3CA
Proteins    P42081  UniProt:P42081 CD86
Proteins    P35568  UniProt:P35568 IRS1
Proteins    P04626  UniProt:P04626 ERBB2
Proteins    Q02297  UniProt:Q02297 NRG1
Proteins    P12034  UniProt:P12034-1 FGF5
Proteins    P56975  UniProt:P56975 NRG3
Proteins    Q9NP95  UniProt:Q9NP95 FGF20
Proteins    Q02297  UniProt:Q02297-10 NRG1
Proteins    P22607  UniProt:P22607-2 FGFR3
Proteins    P21802  UniProt:P21802-1 FGFR2
Proteins    Q15303  UniProt:Q15303-2 ERBB4
Proteins    P62993  UniProt:P62993-1 GRB2
Proteins    O60258  UniProt:O60258-1 FGF17
Proteins    P11362  UniProt:P11362-1 FGFR1
Proteins    P15391  UniProt:P15391 CD19
Proteins    Q9Y4H2  UniProt:Q9Y4H2 IRS2
Proteins    Q99075  UniProt:Q99075 HBEGF
Proteins    P21583  UniProt:P21583-1 KITLG
Proteins    P31371  UniProt:P31371 FGF9
Proteins    P27986  UniProt:P27986 PIK3R1
Proteins    P22455  UniProt:P22455 FGFR4
Proteins    P04085  UniProt:P04085-2 PDGFA
Proteins    P06241  UniProt:P06241 FYN
Proteins    P01127  UniProt:P01127 PDGFB
Proteins    P21802  UniProt:P21802-5 FGFR2
Proteins    Q06124  UniProt:Q06124 PTPN11
Proteins    P21781  UniProt:P21781 FGF7
Proteins    O95750  UniProt:O95750 FGF19
Proteins    P21860  UniProt:P21860-1 ERBB3
Proteins    O14511  UniProt:O14511 NRG2
Proteins    P01133  UniProt:P01133 EGF
Proteins    O76093  UniProt:O76093 FGF18
Proteins    P21802  UniProt:P21802-18 FGFR2
Proteins    O43320  UniProt:O43320 FGF16
Proteins    P04085  UniProt:P04085-1 PDGFA
Proteins    P10767  UniProt:P10767 FGF6
Proteins    P06239  UniProt:P06239 LCK
Proteins    Q92569  UniProt:Q92569 PIK3R3
Proteins    Q6PIZ9  UniProt:Q6PIZ9 TRAT1
Proteins    Q9UEF7  UniProt:Q9UEF7-2 KL
Proteins    P35070  UniProt:P35070 BTC
Proteins    P16234  UniProt:P16234 PDGFRA
Proteins    P33681  UniProt:P33681 CD80
Proteins    P22607  UniProt:P22607-1 FGFR3
Proteins    P09038  UniProt:P09038 FGF2
Proteins    P10747  UniProt:P10747 CD28
Proteins    P00533  UniProt:P00533 EGFR
Proteins    P55211  UniProt:P55211 CASP9
Proteins    P22736  UniProt:P22736 NR4A1
Proteins    Q6ZVD8  UniProt:Q6ZVD8 PHLPP2
Proteins    O60346  UniProt:O60346 PHLPP1
Proteins    Q9UKV8  UniProt:Q9UKV8 AGO2
Proteins    Q9HCE1  UniProt:Q9HCE1 MOV10
Proteins    Q9UPQ9  UniProt:Q9UPQ9 TNRC6B
Proteins    Q9HCJ0  UniProt:Q9HCJ0 TNRC6C
Proteins    Q9UL18  UniProt:Q9UL18 AGO1
Proteins    Q8NDV7  UniProt:Q8NDV7 TNRC6A
Proteins    Q9H9G7  UniProt:Q9H9G7 AGO3
Proteins    Q9HCK5  UniProt:Q9HCK5 AGO4
Proteins    Q96RU7  UniProt:Q96RU7 TRIB3
Proteins    Q5T1C6  UniProt:Q5T1C6 THEM4
Proteins    Q96B36  UniProt:Q96B36 AKT1S1
Proteins    P49841  UniProt:P49841 GSK3B
Proteins    P49840  UniProt:P49840 GSK3A
Proteins    O15111  UniProt:O15111 CHUK
Proteins    Q9BPZ7  UniProt:Q9BPZ7 MAPKAP1
Proteins    Q6R327  UniProt:Q6R327 RICTOR
Proteins    Q9BVC4  UniProt:Q9BVC4 MLST8
Proteins    P42345  UniProt:P42345 MTOR
Proteins    Q9UBS0  UniProt:Q9UBS0 RPS6KB2
Proteins    P49815  UniProt:P49815 TSC2

Thanks, that's great! Next thing would be to download the full network -> who interacts with whom. That would be great!

Ok, it's the SBML format. Found it.

The European Bioinformatics Institute (EBI) has a tool called "Quick GO", which allows you to search the Gene Ontology (GO) database using specific pathways or terms.
In the "Annotation Download" section (http://www.ebi.ac.uk/QuickGO/GAnnotation) enter your search term (e.g. "AKT signalling") and "search". QuickGO will present you with the search results, which for this search include;

protein kinase B signaling
regulation of protein kinase B signaling
positive regulation of protein kinase B signaling
negative regulation of protein kinase B signaling
...

Select a pathway by clicking the GO ID (e.g. "GO:0043491" for "protein kinase B signaling"). This takes you to the information pages for this pathway.
To download the UniProt information (amongst other things) navigate to the "Protein Annotation" table using the tabs. In the top right you are presented with a "Download" option for the whole table (for this pathway containing 1,337 proteins)!
Hope that helps.

This will not give you the proteins in the pathway, you say yourself there are more than a thousand results! What you are seeing are the many, many proteins that are somehow involved in that biological process, including the various regulatory proteins. This is not the pathway itself which only has a bit over 200 proteins. Remember that GO terms are inherited so if a protein is annotated to a child term of GO:0043491 (e.g.  GO:0051896, regulation of protein kinase B signaling) it will also be annotated to GO:0043491.

@terdon good point about child terms being included as well in GO terms - I have voted up your answer as it seems more appropriate in this context!


text:
What evolutionary advantages are provided by ovoviviparity?
I read that some sharks are ovoviviparous.  What advantages and disadvantages are provided by this type of reproduction as opposed to egg laying and live birth?

Reading this website (www.sharks-world.com/shark_reproduction) it seems that for most sharks the eggs develop inside the mother (ovoviviparity), and the young sharks ("pups") are born fully functional, but this is not true for all sharks (as you mention in your question).
This persons blog (morgana249/modern reptiles give birth to live young) discusses evolution of ovoviviparity in some reptiles, but not others. In some species this seems to have gone back and forth in their evolutionary history, which suggests that changing conditions favour one then the other at different times, possibly influenced by temperature, among other things.

The researchers stated, "These results suggest that parity mode is a labile trait that shifts frequently in response to ecological conditions."

This could be similar for sharks, although I could not find an article postulating this.
Alternatively, this could be because the mother does no "parenting"; the pups are immediately independent. Because sharks do not have many eggs at a time (according to the sharks-world website) each individual egg/pup has a higher "value" than each individual offspring in other fish species, which often lay many hundreds of eggs at once outside their body (oviparity). Therefore sharks that evolved this trait may have been selected because the offspring are more likely to survive if they are protected until fully functional within the parent.
No doubt there are other possible explanations, but as with all these questions along the lines of "What are the evolutionary reasons..." we cannot ever actually know, only suggest.