text:
Why people have less hair than other primates?
Well as you can figure out, most primates such as monkeys, gorillas and chimpanzees, have all their body covered with fur. As we know they are evolutional "relatives" to us humans, but we dont have much hair(only on the head,on the armpits, on the groin, etc.). I would like to know why this "evolution" happened in a such brief era and why.

Why are "relatives" and "evolution" in quotes?

Because their DNA (and more specificly the monkeys DNA) isnt much similar with the human one. If u want you can edit my question.

You obviously haven't been to many beaches, especially Greek ones. There are many people out there that are quite hairy, with uninterrupted hair from the top of the head to the top of the feet. All mammals are covered with hair (the thickness varies, of course), even whales and dolphins. You also have another misconception, about DNA differences - the sequences of humans and monkeys are very similar, which is why we use them in medical studies for efficacy and toxicity. Finally, the last common ancestor between humans and great apes was ~7.5 million years ago, not a "brief era" at all.

@Orphee From the phrasing of your question and especially from your comment, it feels like you could make good use of a short and very introductory source of information about evolutionary biology such as Understanding Evolution by UC Berkeley for example.

@Remi.b I had read a small article about human and its evolution at dw.com, so these are only my knowledge.

Hence my recommendation. It is not a necessary a priori for asking question, not at all. But it would quickly increase your knowledge and your ability to ask further questions about evolution incl. human evolution.


text:
What is the circulation that allows for nutrient absorption and excrete of metabolic wastes in humans?
Pulmonary veins carry oxygenated blood from lungs to heart, while pulmonary arteries carry deoxygenated/CO2 rich blood from heart to lungs. On the other hand, systemic arteries carry oxygen-rich blood from the heart to other parts of the body and likewise systemic veins carry CO2-rich blood from all the parts of body back to the heart and lungs. This makes sense to me, since oxygen and CO2 are used and generated in metabolic processes, respectively, and need to be transported to and from the lungs/systemic tissues continuously.
However, what I do not quite understand is what blood vessel carry absorbed nutrients from the intestine to other parts of body? Also, what blood vessels carry other metabolic wastes from the peripheral cells to the kidney for excretion?
Any reference/link to basic working of blood circulation would be helpful.

If you do a bit of research into "mesenteric circulation" (choose one with the stomach) and "renal circulation" on Google images, it should give you all the information you need.

Your first sentence is incorrect. Please [edit] your post and clarify.

This question always intrigued me, but i didn't think about it much. Time to study, and learn :D

source: Stack Exchange

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

sort: votes


text:
Forgot to vortex antibody before staining
Ugh. Did an immunofluorescence experiment last weekend, forgot to vortex both my primary and my secondary antibody solutions.
And my final result looks dimmer than it should be. Is it possible that not vortexing contributed to this?
I guess the question is, is vortexing really necessary? It would come down to the fluid dynamics. How long does it take for a drop of antibody to reach equilibrium in a 1000µL Eppendorf tube? Is it really more than just a few seconds? Is vortexing really necessary?

It depends on how much time elapsed between adding the concentrated antibodies to the diluting solution and adding the diluted antibodies to the slide. If it was just a couple of seconds, then I can abolutely see there being a difference. Even if it was longer - say 30-90 seconds, even - there potentially could be antibody gradients in the solution without vortexing. There are a few reasons why. First, many unconjugated primary antibodies that are not intended just for immunostaining are provided in a glycerol solution, with concentrations ranging from 10% or so up to 50% or more, sometimes in addition to a carrier protein like BSA (I used to work for a well-known antibody company, and theirs are in 50% glycerol with 10 µg - 2 mg BSA per ml, depending on the antibody type). The glycerol prevents the solution from freezing solid at -20°C, eliminating ice crystal formation, protecting the antibody protein from degradation and allowing for longer storage times without loss of activity. As a result, however, the solution takes longer to solubilize in PBS or whatever diluent you're using on its own, with no additional mechanical activity.
On the other hand, even if the primary (or secondary) antibody is simply formulated in PBS, the equal diffusion of the proteins to all parts of the tube can take some time. As an experiment, put 1 ml of PBS in an Eppendorf tube, then add perhaps 10-50 µl of a dark dye, such as methylene blue, bromphenol blue, or Trypan blue. Watch it dissociate into the solution over time against a solid white background like a piece of paper. While none of these have the exact same solubility profile as antibodies, it's good enough to show you what happens over the first 30 seconds or so until you can't distinguish the dye anymore.
So, always vortex, even if it's at a relatively slow speed, for a couple of seconds to ensure everything is evenly distributed.

I assume that a small molecule dye will probably diffuse faster than a large antibody. So if a dye takes time to fill the entire volume, an antibody likely needs more time.

@user137 that's exactly my point.

i was taught never to vortex proteins that i wanted to do something useful, but the even mixing (by pipetting or inversion or extended nutation or whatever) of a solution is pretty much required for us to say anything meaningful about any biochemical reaction. In conclusion, the @MattDMO answer is right allowing for local variation in methodological customs.

@MaximilianPress you were taught incorrectly. The only protein I don't vortex is DNase I, used for digesting DNA on an RNA prep spin column - and only because the directions say to not vortex it. Proteins are in general very structurally stable, and a weak force such as vortexing won't damage them one bit, I promise. I have been working with proteins for nearly 20 years, and I've never met a biochemist who said that proteins in general, or antibodies specifically, shouldn't be vortexed. Now, if you're doing native conformation co-IPs, for example, you can of course be a little more (...)

(...) delicate than when working with an antibody for Western blotting or immunofluorescence, but even there the danger is more heat than physical force. Antibodies are incredibly tough and resilient, can often work in a wide range of chemical environments, and in general only need to be treated specially when they're conjugated to light-sensitive fluorochromes. Yes, you don't want bubbles to necessarily form in your solution, but again that's only when you're working in a conformationally-sensitive assay.

Thanks for your answer. I imagine that they don't contain glycerol, since they're kept at -4 degrees. Still, a good thing to consider. I will definitely try the dye experiment.
On that note, how long does it take, if at all, for antibodies to "go bad" at -4 degrees? Could that have contributed?

@amd1972 just a friendly reminder - if this answer addressed your problem, please consider accepting it by clicking on the check mark/tick to the left of the answer, turning it green. This marks the question as resolved to your satisfaction, and awards reputation both to you and the person who answered. If you have >= 15 reputation points, you may also upvote the answer if you wish. There is no obligation to do either.

@amd1972 in response to your question - it depends. If there is sodium azide in the antibody, it shouldn't get contaminated, especially if you're using filtered pipette tips (I never use regular tips anymore). You could check with the vendor to see if they've done any stability studies, or if the lot you have has an expiration date. As long as you're careful with it, it should last at least a couple of years - some can last much longer, others not so much. If you wish, you can add 50% glycerol to it and store it at -20, remembering to label it and alter the dilution factor.

Awesome, thanks. One last question. I made another thread about this: what about the ice cooling step after antigen retrieval that's in most immunofluorescence protocols? I forgot that step too. I've been in school and it's been a long time since I've done these experiments, so, as you can tell, I'm rusty.

@amd1972 not sure about that one - I usually do staining on cells, not tissues, and I'm a little rusty on my IHC.

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text:
RNA interference and the former Petunias experiment >
I'm having problems trying to understand how RNA interference works.
From what I understood, in simple terms there is this  dsRNA which is fragmented into siRNA by the enzyme called Dicer, and those siRNA make the RISC complex active, which leads to the degradation of mRNA which are complementary to one of the strands of the original dsRNA.
Said this (which I don't even know if it is correct), how this relates to the petunias experiment? From what I understood the researchers put into the petunias an enzyme that coded for the pigment and not strands of dsRNA which then would have created the inhibition...
What am I missing?
PS. I don't have technical knowledge about Technologies so excuse me in case I said wrong things.
Thanks in advance everyone.

Can you please provide a citation for the "petunias experiment"?

By Andrew Fire and Craig C. Mello - For the petunias pigments.

They introduced a foreign gene responsible for petunia leaf colour, with the intentions of up-regulating gene expression for this colour, which was purple. What was observed however was intriguing. Rather than an up-regulation of the purple colour, the leaves were all white instead. This finding showed that the RNAi system in plants recognised the foreign gene and degraded it. Not only that, but the RNAi system also identified the endogenous equivalent of the foreign gene and down-regulated this also thinking it was foreign. This is how they discovered this miraculous finding :)

Hi Chris - on this site when you answer a question you need to include some background information and references to back up the claims you make in your answer. Without this important information your post will potentially be voted down and you will lose reputation points or deleted altogether. Looking forward to see your edits - thanks for your contribution.


text:
Deducing protein sequence length from gene DNA sequence length
Is there a standard way to deduce protein sequence length from gene DNA sequence length of the gene coding for it?
Naively I had assumed that amino_acid_seq_length / 3 -1 (deleting one for the stop codon)ought to work but apparently not always. Is there a better way?
Let's assume the gene is eukaryotic, specifically a plant gene.
e.g.

Or

(AA Seq. / 3 ) - 1 should be a good approximate in bacteria and archea. Since generally transcript RNA is mature. In eukaryotic orgsnism you have all sorts of processing complexity,  so unless you intron spliced sequence, you wont know for sure the protein sequence

Thanks @SciEnt. But if you express a eukaryotic gene in something like E Coli the resultant recombinant protein should still be (AA / 3) - 1 since they will lack the post-processing machinery?

curious_cat, if so that is what we would expect, you are correct.

If you look at the DNA sequence in the patent, you will see that it does not start with ATG and does not end with a stop codon. The disclosed sequence has some additional bases in it, therefore the discrepancy in protein and DNA length. Those additional bases almost always occur in cDNA, e.g. because of polyadenylation, Kozak sequences, etc.

Thanks! So, if you were to want to use the sequence for (say) heterologous expression would it be imperative to correct those aberrations? i.e. How does one infer what the right length of the Amino Acid will be or which bases exactly are the additional bases? In other words, how does one "clean up" a cDNA sequence?

You can use a tool like this one: http://web.expasy.org/translate/ Just enter the sequence and look for the longest open reading frame.

Thanks again Ashafix. That explains a lot to me. One small question: Your tool predicts the correct 569 AA protein in the case of my second snippet. That's great. But in the case of the first sequence the tool gives 569 whereas the patent snippet lists 570. http://web.expasy.org/cgi-bin/translate/dna_sequences?/work/expasy/tmp/http/seqdna.6001,2,2 Any idea why I'm off by one AA? Am I making a mistake? Or....?

Seems like patent data obfuscation to me, the actual sequence in the patent is 569 but if you look at the last 5 amino acids in the translated sequence, it is PLGEE, while in the patent amino acid sequence a aspartate appears out of nowhere:  PLDEE. Two recommendations: 1) Start organizing your sequences with some program, it is easier to visually compare them 2) treat patents with caution, they have to tell the truth otherwise they will be invalid, but they don't necessarily tell the whole truth and it might be hidden deep in the patent to confuse the reader.

Thanks for the tips! Any recommendations for a program to organize my sequences? What do you use?

I don't think it is appropriate here to recommend commercial software but on Researchgate you should find plenty of hints.


text:
Stopping the Gag Reflex: How and why does it work?
I was talking to some friends over the weekend, and one of them made a comment about gagging. He said that he read or watched that clenching your thumb with your other fingers (making a tight fist with your thumb in the middle) stops your gag reflex. So, naturally, as a bunch of stupid teenagers, all 7 of us proceed to do this while shoving our fingers down our throats as far as possible. None of us had a gag reflex.
Why does this work? it seems totally random and weird.

It might work because it distracts you. When you have a gastroscopy (stomach investigation) in hospital, the nurses try to make you focus on other parts of your body ("try to relax your legs"). It helps.

OK, that's what I thought at first too. Just tried it while looking at my leg, and that also worked. Can you add that as an answer with some some source so I can mark it answered?

is this relatable to jendrassiks?


text:
Is there evidence to suggest that sharks from prehistoric times live in the deep of the oceans?
I've had friends see the boat and giant teeth of a giant shark attack of a boat in Japan. (Teeth larger than a great white). [I can't find anything about this on the Internet].
In addition, this report from Pakistan seems to suggest that there are large sharks in the deep of the Oceans.

15-TON PREHISTORIC SHARK CAPTURED OFF COAST OF PAKISTAN

Karachi | A giant prehistoric shark previously thought to be extinct for more than 20 million years has been captured by local fishermen off the coast of Pakistan, reports the Islamabad Herald this morning.
The giant creature first thought to be a great white shark was rapidly declared by experts to be an unknown species of shark as it’s great weight and size were unheard of. Analysis of the teeth suggest the shark to be a parent of the Megalodon, an extinct species of shark that lived approximately 28 to 1.5 million years ago, during the Cenozoic Era.
The sea creature that measures an incredible 10.4 meters and weighs an astounding 15.6 tons is the largest living shark ever caught to date, great white sharks reaching an impressive 7 tons at full growth, a size that is no match for this giant prehistoric shark that can reach an imposing 20 meters in length and possibly weight up to 30 tons, depending on estimates.

My question is: Is there evidence to suggest that sharks from prehistoric times live in the deep of the oceans?

Not exactly an answer, but about 95% of Earth's oceans are unexplored, so I would say that it is pretty likely that there is something, or somethings, that are bigger than currently discovered sharks are alive somewhere in this world. Also, organisms like crocodiles have existed since before the dinosaurs. There's more shark friendly land than crocodile friendly land. If a croc can live 200 million years, then why couldn't a shark?

As an aside, even assuming arguendo that the shark is real, it cannot be the parent of Megalodon, only a descendant or a relative.

The "Cenozoic era" includes the present, so that isn't helpful. Also, technically, since "historic" times only go back a few thousand years, virtually every species, let alone every shark species, is "prehistoric".

No.
The article linked to is a hoax, and was debunked by Snopes.
The website is known for its hoaxes and satirical articles, and it states itself that its articles are faked.

WNDR assumes however all responsibility for the satirical nature of its articles and for the fictional nature of their content. All characters appearing in the articles in this website – even those based on real people –  are entirely fictional and any resemblance between them and any persons, living, dead, or undead is purely a miracle.

The image of the shark was taken from a 2009 photograph of a great white shark caught in South Africa. The shark was reportedly 4.3m long, a normal length for a great white shark.
The large apparent size of the shark as compared to the fisherman is due to a trick of perspective. This article shows the shark in perspective in a second image, which clearly shows that it is not as large as it apparently is in the first image.


text:
How to put a gene under the control of a regulable promoter?
Suppose I have a hetrologous (eukaryotic, plant) gene sequence that I want to express in E Coli under the control of a regulable promoter (say the lac promoter induced by IPTG) how exactly does one add the promoter sequence upstream of the gene?
Are there any tools to do this?
e.g. Say this is the gene itself, what sequence modification is needed to put it under the control of the lac promoter? The goal is to induce overexpression of the protein coded for by the gene on addition of IPTG to the medium (if I understand the strategy correctly)
atggctaccg ataatgacag ctctgaaaac cgtcgtatgg gtaattacaa gccgtccatc       60

tggaactacg acttcctgca gtccctggct acccgccaca atatcatgga agagcgccac      120

ttgaaactgg cggagaaact gaaaggccag gtgaagttta tgtttggtgc cccgatggag      180
.................................................................
gagccgttcg tgacgttcaa cctgaacagc gttcgtggtt cccatttctt ttacgagttt     1560

ggtgacggtt tcggtgtgac gaatagctgg accaaggttg acatgaagag cgtcctgatt     1620

gatccgattc cactggatga agaataatga                                      1650

If you're expressing the gene in E. coli, then you're almost certain to be using a plasmid or other ectopic gene vector. There are a wide variety of plasmids available, with many different promoters. With a commercial plasmid, you're not adding in the promoter sequence, but the gene sequence. You pick the promoter you want and then clone your gene sequence into the plasmid's multiple cloning site, which is designed to lie downstream the promoter.
There are a variety of tools to design and order plasmids. A common plasmid repository is addgene and my favorite tool for designing plasmids prior to ordering is APE.
Design the plasmid with APE or another tool, to be sure that everything looks good, then you can order the appropriate plasmid vector and enzyme cut site-flanked gene sequence and go to town cloning.

I have asked a follow up question here & it would be great if you can help with any comments / advice: http://biology.stackexchange.com/questions/48451/how-to-specify-a-promoter-in-de-novo-gene-synthesis-service

I believe that @March Ho's comment to your follow-up question provides the best answer. I've never seen a 'promoter menu' offered. Rather, promoter sequences are generally specified within a given cloning vector and can otherwise be found using tools such as GenBank. Hope that helps.


text:
How does plant life obey the constraint that the change in Gibbs free energy in a reaction must be negative?
My understanding is that if a reaction takes place, either entropy of the system must rise, or energy must be released from the system as heat, or both. (Citation: paraphrasing from The Vital Question, by Nick Lane). But plant life seems to both decrease entropy, and absorb (not release) energy from its surroundings, by way of photosynthesis. How is this adhering to the constraint that the change in Gibbs free energy in a reaction must be negative?

You are not looking at a closed system (energywise). Which would be necessary to be able to make such observations.

Your title was nonsense as it stood (as was your last sentence). It mentioned free energy, rather than free energy change, and did not indicate what it referred to. I have altered it in accordance with your actual question, but please take more care in future. Titles are used for indexing and are important.

Possible duplicate (or at least quite related) to question on entropy and evolution

"My understanding is that if a reaction takes place, either entropy of the system must rise, or energy must be released from the system as heat, or both."... No, that is if a reaction takes place spontaneously. You can  perform work on the system to move it against the energy gradient. That's what the second law of thermodynamics says. In photosythesis, the energy of the light is indirectly used to perform that work.


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Are all genetic instructions in DNA?
Wiki says

DNA is a molecule that carries most of the genetic instructions used
  in the growth, development, functioning and reproduction of all known
  living organisms and many viruses.

What bugs me is the "most" there, it implies some of the genetic instructions are elsewhere, but where?

Are all _____ instructions in DNA.. Genetic: yes. Inheritable: no.

Would you please expand on that, or give me a general direction on where to look for?

maybe you mean histone modification

Genetic information specifically means DNA or RNA in case of certain viruses. There are, however, other information that can be inherited which include cytoplasmic factors like mRNAs, proteins, vesicles etc. Check maternal inheritance.

Generally, in Biology it is better to use "most". Because we can't be sure that we have done a complete research about it. And about your question:
Yes. But note that the whole genetic instructions are NOT located in the Nucleus(of course, in eukaryotic cells like ours). Also note that some genes like Metabolic Enzymes's Genes are located in the Mitochondria(and the Chloroplast in Plant cells).

Food for thought: If you just have DNA, you can't set and forget a cell. The genes have all the information, but you have to borrow proteins that are already there from cells that already exist (and you get these during cell divisions, like DNA/RNA polymerases). This is a sort of cellular memory.

I don't know why it says "most". I think it is misleading and it should be written "all" (or "most" should be removed). Note though, that the genetic information of an individual is (in most species) is contained in more than a single DNA molecule, which makes the sentence even more confusing. Note also, that in eukaryotes (which includes plants, funghi, animals and some others but does not include bacteria and viruses), there are DNA in the nucleus and DNA in the mitochondrion (and other double-membrane organelles).

@Remi.b The statement is fair, especially if you are willing to consider RNA viruses as a form of life. Also, if you think about Maternal Effect in embryonic development, these are usually mRNA gradients that are established prior to fertilization and have a significant effect on embryonic patterning and axis formation. While the genes are expressed from DNA initially, they are not expressed by the organism that develops, so you can argue that these instructions are RNA-based, as they were expressed in the parent organism and not the resulting organism.

Genetic information is the heritable information used by organisms to guide their self-assembly. It's why traits can persist across generations. DNA is, by far, the primary material used (by life) to encode genetic information, but it's not the only one. RNA is a pretty common alternative to DNA.
If we're looking to Wikipedia, this is actually referred to (in passing) on many pages about genetics. They usually link to the page on the best known edge case, RNA viruses:

An RNA virus is a virus that has RNA (ribonucleic acid) as its genetic material. This nucleic acid is usually single-stranded RNA (ssRNA) but may be double-stranded RNA (dsRNA). Notable human diseases caused by RNA viruses include Ebola hemorrhoragic fever, SARS, influenza, hepatitis C, West Nile fever, polio, and measles.

While viruses fall into a weird middle ground between life and inanimacy, they still all need genes, and many of them use RNA for that. Side note: retroviruses get their name from the fact that they use reverse transcription to synthesize DNA from an RNA template.

I guess that's excluded where it says "many viruses" instead of "all viruses"

I'm not sure what you're referring to being excluded (too many pronouns), but 1) biology is full of exceptions, and 2) many viruses store their genes in DNA.

RNA is an alternative, not a complement, by using "many viruses" I think wiki rules out RNA viruses from that sentence. The use of "most" suggests that there is a complement. About mitochondrial DNA, it's still DNA. So it probably is just a wording mistake in wiki or a misinterpretation by me as so far I know of no such complement.

@erik Maternal effect genes during embryonic development are set up in the oocyte prior to fertilization on mRNA. Obviously these genes are found on maternal chromosomes (DNA), but they are not expressed by the oocyte or the embryo, so technically the instructions are stored on RNA and the RNA is heritable, They may also be referring to epigenetic modifications, though there is still a bit more controversy about whether or not those are heritable.


text:
What is meant by topographic barrier?
There are three types of barriers, physical , climatic and biological barriers that can prevent the dispersal of organisms.
Topographic barrier falls in the category of physical barrier but exactly what should be considered as topographic barriers is not clear to me.
The source from which I actually came across the term says that mountain range is a topographic barrier like the Himalayan range separating the North-asian fauna (partly Palearctic fauna) from the Oriental fauna. But what else falls under topographic barriers is my question?

Topograhpy refers to earth's physical features and a topographic barrier refers to physical features that prevent free movement from one position to another. As GForce pointed out, whether or not something is a barrier can depend heavily on the animal in question. A long, wide canyon can be a barrier for squirrels, but not for birds.
Think of topographic as referring to features on a map, which is a type of topological graph.

Whether something is considered a topographic barrier for an organism depends on the species being considered and its ability to traverse the terrain from one side of the barrier to the other. There's no blanket classification of what is considered a topographic barrier and what isn't.
For example, a certain mountain range may be a topographic gradient to a salamander (due to limited food, extreme weather conditions, etc.), but these same mountains might not be for a brown bear.


text:
Forgot to cool slides before washing
I just finished an immunofluorescence experiment and I'm wondering what went wrong. The tissues seem dimmer than they should be.
One mistake I made was: I completed the antigen retrieval step, in a 90 degree sodium citrate bath for an hour. The next step is to cool the tissue in ice for 8 minutes before washing. I forgot to cool the tissue, and just put it straight in the wash.
Could this rapid temperature change have affected my results? How important is this step?

Are you using secondary immunofluorescence?  If you are, the 8 minutes of cooling are probably intended for the signal amplification.  In other words, as you leave it for the time specified, the flourochromated secondary antibodies have more time to attach themselves in greater numbers to the primary antibody without your sample disintegrating.

I do use a primary and a secondary. But the cooling step is before any antibodies are added. Rather, it goes: deparaffinization, antigen retrieval (90 degrees citrate buffer), 8 MINUTES ICE, pbs wash, blocking, primary antibody.
Honestly, I'm not sure what the cooling step is for. I was thinking it was just to prevent rapid cooling of the glass slide, so it doesn't break. But I'm hoping to know if it has anything to do with the tissue.


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How to batch convert gene names to protein IDs in Uniprot?
I have a list of >1000 "ordered locus names" from the STRING database (also called gene numbers, ORF numbers, or CDS numbers by uniprot). They're in the form of 'b0014', 'b0015', etc. I'd like to convert them all to Uniprot protein IDs.
I know how to do it in a non-batch way, since searching Uniprot for 'b0014' returns what (I think) is a protein ID. However I'd like a batch solution since there are so many IDs that need converting.

http://www.uniprot.org/help/programmatic_access

also cross posted here

@MattDMo Thanks. I haven't tried it yet, but the solution that looks like it will work is the UniProt ID converter http://www.uniprot.org/uploadlists/.

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

list_to_convert = ["b0014", "b0015"]
url = 'http://www.uniprot.org/mapping/'

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

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

The output from this looks like:
From    To
b0014   P0A6Y8
b0015   P08622

Web GUI
b0014 and b0015 aren't actually STRING IDs. They are IDs referred to as gene names and are used across a variety of databases including Uniprot.
The mapper:

Note in section 2 of the ID mapping that I have set the left option to "gene name". "STRING" won't work.
The result is below:

The first answer is good!
Here I want to suggest another useful tool when you are thinking about ID Mapping.
That is bioDBnet: db2db, which is used for "Database to Database Conversions".
The introduction of this tool is:

db2db allows for conversions of identifiers from one database to other
  database identifiers or annotations. To use db2db select the input
  type of your data, changing the input type automatically changes the
  output options to the ones specific for the input selected. Then
  select one or more output types and add your identifiers in the ID
  list box. Set the remove duplicate values to 'No' if you do not want
  duplicates to be removed. Clicking on submit then returns a table of
  your inputs matched against all the outputs selected in the exact
  order as entered. Results can be limited to a particular taxon by
  entering it's Taxon ID. The performance will vary widely depending on
  the number of outputs and the options selected. Conversions to a
  single output with the default options should complete in a few
  seconds

The above is my favorite tool, and sometimes using from ensemble will help you solve the problem in a more efficient way if you are dealing with model organism, like mouse and human.


text:
How should "the human genome" be interpreted?
What does sequencing "the human genome" mean? Don't individuals have unique genomes?

Certainly individuals have unique genomes. The human genome sequencing project used DNA from a handful of volunteers, and the reference human genome that resulted from this project can be thought of as an "average" genome for those individuals. Where sequences differed between the individuals, a representative consensus sequence was chosen. Hence, the sequence of a gene from a given individual may not perfectly match the reference genome, although mostly the differences are small: genetic difference between humans is estimated to be around 0.1 --- 0.4%, which means a few million base pairs in total.
As DNA sequencing is nowadays orders of magnitude cheaper, genomes for larger number of individuals are being sequenced; see for example the 1000 genomes project.

A good start to an answer - might you want to talk about SNPs and gene variants (various blood groups, for instance) to get into a little more detail?

What percent of genome same for each individuals and What is the maximum number of genetically unique individuals that human genome allows?

@Abusayed  added a point about % differences. Theoretically I guess there are 4^(3*10^9) possible genomes with 3 billion base pairs, but of course it doesn't work like that  :)  But still there is enough variation that there is virtually no chance of encountering two completely identical genomes by chance.

@MattDMo, feel free to edit if you want.  It was a short, focused question though and I didn't want to respond with a population genetics lecture ;)

@Abu sayed: You might also be interested in these two facts: 1. The human reference genome's current release is version 20 (hg38). 2. Every newborn carries about 60-100 (which is not much at all) new private SNV due to mutations in the parents germline.

I think there are two concepts that you need to understand to understand what "sequence the human genome" mean; within vs between species variation and genome consensus
Within vs between species variation
There is indeed variation in the human population. We are not clones of each other. One can for example consider the average number of pairwise differences as a statistics of variation. Consider the two following sequences

ATCAATTCAGAA
AGCAATTAAGAA

Here, there are 2 pairwise differences. One can average the number of pairwise differences among any pair of individuals to get the average number of pairwise differences. The average number of pairwise differences within species is much lower than the average number of pairwise differences among species. It therefore makes sense to consider a standard genome of a species as variation within the species is negligible compared to variation among species.
Genome consensus
In order to obtain the "human genome", we samples DNA from a number of people, sequence them and then try to form a consensus among al these slightly different genomes. You can think of this consensus as some kind of average genome. Consider for example the following sequences:

AATGCA
AATGCA
AATGTA
AATGCA
AATGCG
AATGCA
AATGCA
ATTGCA
AATGCA

Sure, there is some variation but a priori AATGCA seems to be a good consensus.
Interestingly, it is very likely nobody on earth has the exact same genome as the consensus genome just. One simple reason is that there are sequencing errors occuring at a known rate but the other reason is that as sequences becomes long enough (the whole genome), every single individual carries at least one rare mutation that will not end up in the consensus.


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How are constitutive enzymes regulated?
I found that inducible enzymes can be regulated by many ways, but
I cannot find how constitutive enzymes are regulated...

A constitutive or "housekeeping" enzyme is usually defined as an enzyme whose expression level (amount of protein) is always constant, independent of any environmental factors. Hence, regulation of constitutive enzymes must be post-translational, for example allosteric regulation of the enzymatic activity by substrates or products.
Note that constitutive enzymes is mostly a theoretical concept. There are probably no enzymes whose expression is completely unaffected by any environmental factor.

why do you say constitutive enzymes is mostly a theoretical concept?

Because I have yet to see an enzyme whose expression is not regulated at the transcriptional/translational level in some experimental condition. An enzyme's protein level might be constant in some particular experiment, but who's to say what will happen in another setting. It's the same problem as with "housekeeping genes" in RT-PCR.


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Are different eye colors indicative of chimerism?
If an animal or person has different colored eyes, does that mean they are a chimera?

You will find this wiki entry [1] informative.
While chimerism is one possible explanation, it is certainly not the only one.
[1] https://en.wikipedia.org/wiki/Heterochromia_iridum

A possibly easier to understand explanation of eye color here. One thing to consider thats not mentioned in the wiki article in answer is incomplete penetrance


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Parameters of Variant calling analysis
What is the good or stringent parameter for variant calling?
At present using the DP > 10 and Q > 30 for Variant calling. Is it ok?

What tool are you using and what are you calling on, whole genome, exome?

@CMosychuk, its Whole genome sequencing

We will be needing some additional information to answer your question more completely:
What sequencing platform are you using? Illumina HiSeq/MySeq; Ion proton
What type of sequencing (as noted by @CMosychuk): Exome or Whole Genome?
What type of variant caller (as noted by @CMosychuk): Unified Genotyper; Haplotype Caller; TVC
The QUAL metric is heavily dictated my sequencing depth, so if you use 30 (phred-scaled), that would be an accuracy of 99.9%.
The typical QUAL metric used by most sequencing studies is 20 so using 30 may cause accumulation of false negatives. But again, depends on the type of sequencing and platform used.

this looks more like a comment than an answer - once you have earned some more reputation points you will be able to comment anywhere, but until then please refrain from commenting as an "answer" - thanks for your contribution!

@VanceLAlbaugh I won't classify this as a comment outright, the latter parts of the answer are in fact answers to the question.

@MarchHo I'll take your word for it - not obvious to me (an outsider in that specific field)

Its whole genome sequencing, Illumina HiSeq 1000 platform, Type of cariant caller is Unified genotyper. Tools using samtool, vcftool.

For variant filter using SNPeff

Try sticking with a QUAL of 20. Illumina usually produces well-mapped reads. If you think some of the lower quality variants are artifacts, try sanger sequencing them and see if they validate. A QUAL of 30 seems high for Illumina data.

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


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Name of dominant dinosaur
I seem to remember reading some time ago about a dinosaur appearing very prominently in the fossil record, with continent-wise distribution. The layer is known specifically for having so many fossils of this dinosaur and might be named as such. Terms "cow-sized", "vegetarian", and "near to extinction event" come to mind. Does this ring a bell?
My memory might be so faulty that it could be an early amphibian, reptile or even mammal!

The closest example I can think of is Lystrosaurus, which was one of the most common animals in the early Triassic period. It was distributed across many modern continents, and was roughly the size of a pig or cow, depending on the species. Lystrosaurus was not a dinosaur, despite its name.

Excerpt from the Wikipedia page (emphasis mine):

Lystrosaurus is notable for dominating southern Pangaea during the Early Triassic for millions of years. At least one unidentified species of this genus survived the end-Permian mass extinction and, in the absence of predators and of herbivorous competitors, went on to thrive and re-radiate into a number of species within the genus, becoming the most common group of terrestrial vertebrates during the Early Triassic; for a while 95% of land vertebrates were Lystrosaurus. This is the only time that a single species or genus of land animal dominated the Earth to such a degree

Note that Lystrosaurus was not a dinosaur; it was a dicynodont therapsid.  However, it may well be the answer to the question anyway.

Thank you, that's what I was looking for. For some reason, I can't mark this answer as correct, doesn't give me the option. Maybe a moderator can do it?


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Identification of a spider from my basement
It's a little over 1" long including legs, and I found it in my basement in Pennsylvania. My guess is a funnel weaver, which would be nice since then I can free it (right?) from the tin can it's currently sitting in.

Thanks!

It is not a Brown Recluse, but it doesn't look like any of the other spiders in that document either. This isn't an ID, but it might at least help you feel a little better about it.

I've changed the title so that it uses the verb "identify" instead of the noun abbreviation, "ID". There was also no need for a question mark as your title was not a question.

I think it's a common wolf spider, which closely resemble funnel weavers. It's almost a toss-up. I can't tell from the resolution of your photograph, but funnel weavers have spiny legs whereas the wolf spider has smooth legs and has a bit more of a difference in the comparative size of the abdomen to thorax.
Wolf spider (coloration varies) vs. funnel weaver (in this case, a barn dweller)

Another distinctive feature of the wolf spider are the two especially large eyes (The Tenegra domestica's eye arrangement is different) which gives the wolf spider such great eyesight. If the legs are smooth, and you shine a light on your spider and see two eyes shine back at you (called eyeshine), I think you have your answer.

Wolf spiders can be found in a wide range of habitats both coastal and inland. These include shrublands, woodland, wet coastal forest, alpine meadows, suburban gardens, and homes.

I let it out of the tin can after user137 ID'd it as not a Brown Recluse, but thanks for the details, especially the bit about eyeshine.

Based on abdominal coloration I'd go with funnel weaver, but it's not really my area.

@arboviral - It's not my area either. :) I agree that the abdominal coloration (and thoracic) is a dead ringer, but the wolf spider coloration is highly variable, and the abdomen shape/size is no help. Unfortunately the specimen is free now, so we'll never know for sure.

I agree with @arboviral . The abdomen pattern is classic barn funnel weaver, and the striped/banded legs are extra confirmation.

Yes, it's Tegenaria domestica, the common funnelweaver House Spider.  It's not a wolf spider; the color patterns on both abdomen and cephalothorax are completely consistent with Tegenaria, but not terribly like the wolf spiders common in our area.  I also find the Tegenaria cephalothorax shape to be more blocky in the front than the normal Wolf Spider shape, but that's a sort of subjective call.  You should be able to find more of them in your basement, especially if you have a furnace or laundry area with bare blocks for walls.  When you find another one, look for the two tailpipe spinnerets sticking out the back end - while not as long as on the outdoor Agelenids, the spinnerets on these indoor ones are still noticeable.  Wolf Spiders don't have that.
Source - any of the spider guides, but let's go with Bug Guide on this one: https://bugguide.net/node/view/31445

Thanks for the answer. Species ID answers need to be accompanied by a proper source, and preferably an image of the species you think it is.

Ah - well, for sources, try Kaston, BJ 1972 How to Know the Spiders (which I realize is more of a lab manual, and which is somewhat outdated, but which is useful also for field work) and perhaps also Cushing and Ubick 2009, Spiders of North America: An Identification Manual and the very attractive (the book, not the author, although I'm sure Mr. Bradley is also lovely) Bradley 2012, Common Spiders of North America.  Also, approximately 40 years of personal experience, although naturally that is a somewhat subjective qualification.

For images of Tegenaria domestica, I could hardly do better than the photo which appears in the original post, but let me add a few to it (from this link):  https://bugguide.net/node/view/31445    Edit:  I seem unable to post images, but when I figure out how to do it, I shall return and toss them in.


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Can a firefly control its glow?
I've just seen this animation:

I always thought the firefly glow is ongoing slow chemical reaction, like in glowsticks though through different chemicals. As such it seems impossible to control quickly, like on this image.
Is this image real or edited? Can firefly control it's glow? If it can, how much?

Yes, fireflies control their glow patterns. Different species have different patterns. You can read about the luciferase reaction and its regulation here.


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Fish and microplastic particles
How does exposure of fish to microplastic particles decrease egg-hatching and give young fish a craving for them?
From Garbage in, garbage out: marine plastic 2016-06-24 | Espresso

There is more than just ocean beautification at stake; many creatures
  ingest plastic, and a recent study showed that exposing fish to
  microplastic particles not only decreases egg-hatching but also gives
  young fish a craving for the stuff.


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What do the letters 'p' and 'c' mean in mutation descriptions?
Example:

NM_000525.3(KCNJ11):c. 67A>G ( p. Lys23Glu) AND Permanent neonatal diabetes mellitus

Does "p" stand for "polymorphism"?
What does the letter "c" stand for?

I think c refers to cDNA and p refers to protein. Similarly there is g which most likely refers to genomic DNA.

You could check the whole HGVS guideline http://varnomen.hgvs.org/ for explanations (also @WYSIWYG is right).

According to the HGVS guidelines, a letter prefix should be used to indicate the reference sequence used. Accepted prefixes are:

“g.” for a genomic reference sequence
“m.” for a mitochondrial reference sequence
“c.” for a coding DNA reference sequence
“n.” for a non-coding DNA reference sequence
“r.” for an RNA reference sequence (transcript)
“p.” for a protein reference sequence


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Comparative effectiveness of antibiotics against colonies and growing bacteria
Appropriate antibiotics usually eliminate bacteria. However are the same antibiotics as effective against bacteria that have grown to form a colony?

I'm not entirely sure what you're asking, but some bacteria can form structures called biofilms, which often allow them to resist concentrations of antibiotics that are normally fatal to individual bacteria.

Usually, if there is a need to take antibiotics, it means there are multiple colonies of bacteria already in the body and as such the express purpose of taking antibiotics is to destroy those colonies.

I have rewritten the title and question, based on the accepted  answer. I am not a bacteriologist so, if necessary, perhaps @WYSIWYG might need to make further modifications.

It depends on the kind of antibiotic. Some antibiotic are bacteriostatic  i.e. they primarily stop the growth while some are bactericidal i.e. they kill the living bacterial cells. Some antibiotics can have mixed effects. Bacteriostatic antibiotics would not be very efficient in eliminating a colony.
Apart from the mechanism of action, there can be other factors that would dictate the efficacy of the antibiotic; these can all be considered under pharmacokinetics/pharmacodynamics:

Degradation/clearance rate of antibiotic
Rate of diffusion of antibiotic inside the bacterial colony (this rate would be less when the cells are inside a big colony compared to when they are disperse).
Community organization and dynamics inside the colony (like user137 said in their comment, certain biofilms can be more resistant to antibiotics)

can bacteriostatic antibiotics kill individual organisms?

@OneFace Eventually because the organisms won't be able to grow, but not directly.


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How to specify a promoter in de novo gene synthesis service?
I am trying to use a de novo gene synthesis service (Genscript) and one part confuses me:
Where do I pick the choice of promoter? Or is the promoter choice automatic based on my plasmid choice?
e.g. Say I want a regulable promoter (say lac induced by IPTG) how do I specify it? https://www.genscript.com/account/gene_services_gene_synthesis.html
I was given to understand in a related question that with a commercial gene you essentially just "pick the promoter you want"? Or must I somehow manually edit the gene sequence I have to incorporate the promoter I want?
How to put a gene under the control of a regulable promoter?
I can definitely email Genscript in case it is not a part of their default interface but I just wanted to verify my understanding of the matter before I do so.
PS. I even checked out Fischer's GeneArt service & even that interface has nowhere for me to select a specific promoter. Makes me wonder if I am getting the workflow wrong?

Wouldn't their sales team be able to help out?

@James Sure. I will email them. I just wanted to confirm that my understanding of the workflow is right. i.e. That I ought to "pick a promoter" when ordering the plasmid rather than manually modify my gene sequence before I submit.

I'm not familiar with this service. I don't think it's a bad question to ask them if their site is unclear.

@James Thanks. I've emailed them. Are you familiar with any alternative gene synthesis services? Do you remember if they offer a option to select a promoter? In any case, thanks for confirming that my question isn't too silly or obvious to ask them!

If I am not mistaken, the promoter should be specified by the cloning plasmid.

Thanks @MarchHo. Do you mean that as soon as I indicate my choice of the pUC57 plasmid that automatically fixes my promoter? If so, what's the promoter for the pUC57 plasmid, any idea?

If you need to add a promoter in an unusual location, you can add it into the synthesized DNA sequence. But normally that's decided by the cloning plasmid. If you put in the right restriction sites you can put your synthesized DNA into any cloning plasmid you want.

@user137 Thanks. No, I don't think I need a promoter at an unusual location. All I need is a regulatable promoter. I was thinking of using the lac promoter & induction using IPTG but none of the gene synthesis sites I checked out seem to offer an option to let me indicate my promoter choice. That is what is confusing me.

@user137  Perhaps there is a default promoter for the pUC57 plasmid? But I am not sure which promoter that would be.

I would start with the pUC57 sequence. I would check with your manufacturer just in case their plasmid has a different sequence. If the promoter isn't one you like, plan to move your gene into a better plasmid.

@user137 Thanks that helped a lot. So the lacZ shows it is lac promoted & IPTG induction ought to work! http://www.genscript.com/gsfiles/techfiles/GenScript_pUC57-Simple_Plasmid_Map.pdf

Usually you should provide the entire sequence that you want to have (including promoter, polyA sites etc). They will clone this sequence in a plasmid and give it to you. They generally do not check for expression or any other function. That's your job. They just ensure that the sequence provided is correctly synthesized and cloned.

Just a comment about the PolyA sites, they are not the same as PolyA sequences. If you try to put 20 or more Adenosine in a row they will refuse to synthesize it. Our lab has made plasmids with "120", "240", or "360" adenosine PolyA tails built in, but these are our best estimates because producing these oligos is hard, and sequencing them is almost impossible.


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What's the highest temperature that algae can survive at?
I know there are a lot of different species of algae and that each one has different environmental tolerances. I've seen data on different species:

brown alga Sargassum echinocarpum J. Agardh - grows well at 35°
Dictyopteris australis - grows poorly above 28°
halophilic blue-green algae A. fertilissima - temperatures of 47° stimulates germination

What's the highest temperature that growing algae or its spores can survive at? In other words, what temperature would guarantee that no algae could grow afterwards unless reintroduced?

Based on the habitat of Algaes, a classification called "Thermophytes" can bear high temperature. The Thermophyte algaes use to grow around hot springs and can live around 70°C.
Please find below the reference for all classifications and more details.
http://www.yourarticlelibrary.com/biology/8-types-of-algae-classified-according-to-their-habitats/7098/
http://www.biologydiscussion.com/essay/essay-on-algae/20891


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Relation between biomass and radius of roots system
Is there a known relation between the mass of a plant to the size of its roots?
For example, can I take the root size to be proportional to the biomass of the plant like in this relation: $$R = R_0 (1+EB) $$, where $R_0$ is the minimal size of the root (i.e. the diameter of the seedling), $B$ is the biomass of the plant, $E$ is some parameter, and $R$ is the length of a typical root?

Your question specifically asks for an equation which gives root radius and your sample equation is for typical root length, neither of which I'm aware of. However, there is a known relation between the above-ground biomass and the below-ground biomass of a plant, which varies with species and environmental factors. This is the root:shoot ratio.

This is a linear model where the constants represent differences in starting conditions (the intercept) and biomass partitioning (slope).

Roots and shoots are functionally interdependent and these two systems
  maintain a dynamic balance in biomass which reflects relative
  abundance of above-ground resources (light and CO2) compared with
  root-zone resources (water and nutrients). Whole-plant growth rate and
  root : shoot ratio are thus an outcome of genotype × environment
  interaction, but source of control is ambiguous.

The actual size of the roots - as in their extent - will depend on the soil characteristics, water table, the plant species, etc.
Source: http://plantsinaction.science.uq.edu.au/edition1/?q=content/6-3-1-biomass-distribution


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How long would it take for a change to the DNA would take effect?
I am not a Biology Student (sorry guys!) but I have thought about this question for a while and hope that maybe one of you can answer it. Lets say that I had my DNA changed so that I wouldn't be vulnerable to certain diseases or perhaps to make my body change so that I'd lose weight easier (Just a hypothetical here not sure if sci-fi have skewed my view on DNA).
From the change occurs to the DNA until the changes take effect, how long would that hypothetically be?

See http://people.umass.edu/bioch623/623/Second.Section/7.%20CoT.Web.2.08.pdf . Assuming that you've inserted desired gene (I don't think weight loss can be stimuulated by genes) in bone marrow and protein synthesis starts immediately, it shouldn't  take more than 5 minutes for protein to show effect. Of course, practical value would vary.

OK, let's set up a specific hypothetical situation so we have some details: A virus (we'll call it Human Nasty Virus 1 (HNV-1)) can infect T cells (a type of white blood cell in the immune system) by binding to a certain receptor on its surface, which we'll call the Nasty Virus Receptor (NVR). Scientists have found that HNV-1 absolutely needs a certain protein sequence in NVR to bind, as people with a certain mutation lacking that sequence are completely immune to HNV-1 infection.
You sign up for a clinical trial using gene editing to specifically remove that DNA sequence from the NVR gene. Once that changed gene is transcribed and translated into protein, it is expressed on the surface of the cell, and HNV-1 can no longer bind.
T cells are derived from stem cells that live in the bone marrow. In order for the gene therapy to work, doctors will need to perform a bone marrow transplant - they will remove a sample of bone marrow, give it to the scientists for the gene editing process, then reinject the edited cells back into you. The editing process involves subjecting purified stem cells to a process called CRISPR, allowing them to grow in culture for a while, then screening the cells to select only those where the editing was successful. The successfully-edited cells are separated, cultured some more to expand their numbers, then given back to the doctors, who put them into your body, either into the bloodstream or directly back into the marrow.
So now you have your edited cells back inside you - how long will it take to become immune to HNV-1? Well, the honest answer is that, in the absence of ablative chemotherapy (see the bone marrow transplant link above for more info) prior to reinjection of the edited stem cells, you may never become completely immune. Here's why: Unless all of the bone marrow stem cells in your body are destroyed before reinjecting the edited ones, you will still have fairly high numbers of what are called "wild-type" or un-edited stem cells and mature T cells in your body, and those stem cells will continue making new wild-type T cells. Additionally, there are already wild-type T cells in circulation and in secondary lymphoid organs such as lymph nodes and the spleen, and some of these cells can be very long-lived (months to years). If for some reason you decide to undergo complete ablative chemotherapy to essentially destroy your immune system, the reinjected stem cells will eventually repopulate everything and you'll be immune to HNV-1, although you will have potentially lost your immunity to everything else you've ever been exposed to, unless the chemo is done in such a way as to preserve your immune memory cells.

This is actually a best-case scenario, as we were working with cells that can (relatively) easily be removed from the body, edited, screened, and reinjected. If you were trying to cure a genetic disease that affected solid tissue like the muscles (see Duchenne muscular dystrophy for an example), you obviously wouldn't be able to remove all the muscles and edit them ex vivo, you'd have to do the editing in the body, most likely using a viral delivery system for the editing machinery. The viruses wouldn't infect every single cell, and the editing wouldn't work in every cell that got infected, so the best you could hope for would be a partial cure. For some diseases, this may be enough, and many companies are working on this from various angles. There are also other options besides CRISPR-mediated gene editing that have higher success rates in vivo.
Finally, getting back to your original question of how long it takes from DNA alteration to expression of the gene product, the answer is that it depends on the gene and the context. In the case of our hypothetical situation earlier, as soon as the NVR gene's DNA is edited, the new sequence begins to be transcribed and translated into protein. There is still some wild-type protein left over initially, so it depends on the transcription rate of the gene and the turnover of the existing protein. Some proteins have an extremely long half-life, on the order of years or decades (or more!), while some degrade within minutes to hours of being synthesized.

Well thanks for that! That was a very thoroughly explained answer and I learned a few things too. Thanks again! :) If you don't mind me asking, what is your background in biology?

Glad to help. I have a Master's degree in Molecular Medicine and over 10 years of experience working in various facets of industry, doing biochemistry, cell biology, and molecular biology in a few different fields (cellular signaling, rare diseases, immunology, oncology, etc.). I'm an immunologist by training, which explains all the T cell business in my answer :)

Thanks for answering! I'm just a lowly Professions Bachelor Programmer xD


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why are malarial parasites specific for anopheles
why are malarial parasites specific for anopheles mosquito. why do they need only anopheles, they just need lower temperature to complete their life cycle. all mosquitoes are cold blooded, so they can get a suitable environment in any of them, why only anopheles?

Did you look this up - research it - in any way? Can you provide some of the information you found? People (myself included) are happy to answer if the poster shows the research they've done. Thanks.

I looked this up but didn't get any satisfactory answer. I just want to know why their is specific relationship for their sexual cycle to complete. All they need is lower temperature because when they are inside human body the temperature is not suitable for the syngamy to occur that's the reason they go into anopheles' body but every other mosquito is cold blooded and is capable of providing the atmosphere for the process to occur

One major factor to consider: not all mosquitoes feed on humans. The malaria-carrying mosquitoes must. That's only one factor. There are many more. Saying you researched it and showing your research are two different things.

@anongoodnurse The Plasmodium falsciparium carrying mosquitoes must feed on humans, but there are other forms of (rodent) malaria. They still are carried by anopheles.

This isn't actually a bad question, although I agree it needs to show some effort. Short answer, though: they aren't. Avian malaria (Plasmodium relictum) is transmitted by Culex mosquitoes (and possibly by Culicoides biting midges, although there are some issues with that study). The reverse question is also interesting; why do arboviruses seem to be almost-exclusively transmitted by everything else? The only arbovirus transmitted by Anopheles is O N'yong N'yong virus (ONNV). Alain Kohl's group published a nice paper on this recently (http://www.ncbi.nlm.nih.gov/pubmed/25548172).

The host/parasite relationship is normally very specific: because there are a lot of molecules that have to bind each other for the parasite to complete its cycle, a parasite is not capable of invading any given organism; the same way, a host is not invaded by any given parasite.
That being said, you have to keep in mind that mosquitoes are also hosts (despite of, in the case of malaria, having less symptoms when compared to the human host). In fact, regarding malaria, some parasitology books classify the mosquitoes as the "definitive hosts", while humans are "intermediate hosts" (because the sexual reproduction of Plasmodium happens in the mosquito, not in the human being). So, there are a lot of molecules that have to be present for the parasite finding its way through the mosquito's organism. A plasmodium cannot survive inside a Lutzomyia mosquito, the same way a Leishmania cannot survive inside a Anopheles mosquito. There is specificity.
Actually, not all Anopheles are the same (just as not all human beings are the same). They have differences regarding the susceptibility to the parasite:

Some Anopheles species are poor vectors of malaria, as the parasites do not develop well (or at all) within them. There is also variation within species. In the laboratory, it has been possible to select for strains of An. gambiae that are refractory to infection by malaria parasites. These refractory strains have an immune response that encapsulates and kills the parasites after they have invaded the mosquito's stomach wall.

(source: https://www.cdc.gov/malaria/about/biology/mosquitoes/)
Please note that other mosquito species are not resistant to the plasmodium, because we call "resistant" a host that's capable to fight the parasite. The other species are not even hosts!


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Do blurry images cause eye strain? At what point is an image so blurry the eye stops trying to focus it?
I'm a user experience designer concerned about a new trend of blurring screens when showing a lightbox/dialog box over top (see below).
From what I know, blurry images cause the brain to work hard unnecessarily as the eye tries to focus an image. If my team really wants to blur images, perhaps I can give them guidance on how blurry the image needs to be.
Here's an example of a page loading, using the blurry effect:

Other than the dialog box in the foreground, you can see that the rest of the words are blurry but are just clear enough to make out, which makes me fear the eye is trying to focus them.
Whereas something like Apple's iPhone blurs the app icons in the background of its Search feature so much that it looks like a pretty image when you search, and it seems the eye wouldn't focus on that background:

So my questions are,

Does trying to focus a blurry image cause eye strain, cognitive load or any sort of discomfort?
At what point does the eye stop trying to focus and just accept the blur as an abstract image, something that can't be focused, at which time it might relax?  Or is that point subjective and, hence, cannot be measured or put into words?


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Common Errors For Low R Value in Bradford Assay
I've recently started doing Bradford Assays for my samples and my standard curve has been non-linear and I have been getting low R values (.90-.95). I initially thought the error was in pipetting, most likely in adding BSA while establishing the standards but I have repeated in care and somehow still get low R values. Are there any other possible sources of error?

You could be measuring outside the dynamic range of the assay (you can only add so much / so little BSA to a certain amount of reagent).
You could be outside the linear range of your spectrophotometer, usually under 1 is fine, although some old/crappy ones might not even be reliable over 0.5.
If you're fast you're measuring your different concentrations also at different times. Bradford is a little bit time-dependent, so waiting the recommended time before measuring your standards is not a bad idea.

Probably it's still pipetting though, try pipetting at least 20 uL in every dilution step and see if you're still off.


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Human Demography - Where can I find this statistic?
In "An Introduction to Genetics" by David J. Merrell, copyright 1975 by W.W. Norton + Co., p. 742, in the Chapter "Genetic Counseling and Eugenics," the author states: "... 50% of the women produce 85% of all children born in the United States."
The author provides an Additional Reading list, but I'm not a geneticist, nor do I have access to much of the listed material.  With that in mind, 1) where can one find the statistic mentioned above? and  2) has this number changed over time?
OP EDIT: In response to comment (a few examples from Reading List of 30 items):
Davis, 1970, Prospects for Genetic Intervention in Man, Science, 170 279-1283
Dubos,1965,  Man Adapting, Yale Univ. Press
Dunn, 1962, Cross Currents in the History of Human Genetics, Amer. J. Human Genet, 14: 1-13
Ehrlich, 1968, The Population Bomb, Ballantine NY
...
Lynch, 1969, Dynamic Genetic Counseling for Clinicians, C. C. Thomas, Springfield, Mass.
...
Petersen, 1969, Population, 2nd Ed. Macmillan
...
1969, WHO Expert Comm. on Human Genetics, "Genetic Counselling(sic), Tech Rept 416, pp. 1-23
I know I can find stats like average ages, etc from the Statistical Abstract of the United States, but where do geneticists find items like the one cited in the Merrell book?

Welcome to Biology.SE! Could please copy paste the reading list or any source that Merrell has indicated?

Note that it is more a question of human demography than genetics. It is still on-topic though.

Isn't this just an interpretation of the rate of childlessness? Say 41.2% of women don't have children. This means that the remaining 58.8% of women produce 100% of children and therefore that 50% of the women produce 85% of children.

If a reading list is given, but it isn't clear from which book the statement is derived, it often works to google the unique aspects of the statement. If general search, which includes books, doesn't work: google scholar, with temporal filter for years prior citing work, often manage to retrieve original source

The CDC has some good stuff. http://www.cdc.gov/nchs/data/nhsr/nhsr051.pdf
But keep in mind that number from your book is likely based on yearly findings in which more than half the women would not be able to have children due to age, voluntary contraception, or other conditions. So it is not reflecting how many children they have over their lifetime. Even in the CDC study more than half the women had no children but few had no plans to have children, couples are moving their first pregnancy to later and later in life, which is going to make it look like few are having children at all on first glance.
 And it's probably not accounting for death rates, the poorest people tend to have the most children but they also have the fewest number live to maturity, which is why they tend to have more (not necessarily consciously mind you) .

You can try to use some standart data sources, for example:

NASA's Gridded Population of the World - LINK
Geonames - LINK

That information seems to be censored very often. In certain countries there are even laws preventing asking certain quesitons about demography, i.e. France, and In America you should have transparency for the government censors on household numbers, but apparently the official numbers discreetly use 4+, to not publish families of 8,9 and 10.
Your question doesn't say if that figure holds for 1-2-3 generations.
Big family traditions extend for more than one generation. so 5*5 becomes 25, and 2*2=4
If you square the figures, the add up very fast... Unfortunately the statistics don't measure higher than 2 children... What you need is a graph like this:
It illustrates that "4+" children actually averages about 5.5-6.5 children (vaguely)...
If your square that sum, his statistic may be true.
If you multiply the household percentage and the number of children you get a bell curve that is different:

The 50 percent of the women represented by the black and white graph, it seems to 3.5 children at that village, and the number of children is in the top graph, so it indeed appears that in only one generation, women with more than 3 children, for that graph, indeed produce 75 percent of the population.
Sorry that's my lame attempt to answer the question. Having checked it may help a teeny bit. it's not a sci reference though. sorry.
family size is a factor of education, professional ambition, culture, religion and ethnicity.
https://www.mtholyoke.edu/courses/rschwart/encounters/family_size.htm
http://www.pewsocialtrends.org/2015/05/07/family-size-among-mothers/


text:
Why haven't modern grass based crops overrun wild grasses?
Modern grass based crops are significantly superior to wild grasses, they grow faster, are stronger stemmed, have larger leaves and higher seed yields in terms of individual seed size, giving germinating seeds a significant head start vs other wild breeds.
I've heard time and again that GM crops will escape into the wild with potentially devastating consequences, out-competing wild plants for space and destroying biodiversity.
So why hasn't this happened already? Our crops are already GM (albeit through different methods and over a much longer time)
Edit:
I have seen the odd crop plant growing in the wild, amongst other grasses, but rarely more than one or two clumps of wheat or barely grass amongst a sea of wild grasses.

Which plants do you have in mind specifically?

@James my question is specific to grasses, though the rhetoric regarding GM plants depends on the particular GM technology being attacked.

There are something like 10,000+ species of grass. There are many GM crops and they have a huge range of modifications. If you're unsure about what your question is about, then please cite the article stating that GM crops will escape into the wild. Perhaps that will provide some insight. Currently the question is not clear enough to answer.

Ignore the GM part of my question if you must. My question is exactly as stated. Why are wild grasses still dominant in the wild when crop grasses are so morphologically superior.

The selection process employed in agriculture selects for high yield, disease and weather resistant crops. Not necessarily their invasiveness, which would probably be selected for in nature. Perhaps there are some examples where they have overrun wild plants.

Many of the popular grass varieties that are used in lawns are originally from Europe (namely the UK). They have quite a different and particular moisture requirement compared to the many different types of wild grasses that have evolved all across the world. Also cultivated species having had to compete less with other species for territory and resources can sometimes be less "aggressive". I think it's important to acknowledge there is a large difference between GM varieties cross-breeding with the non-GM varieties of the same domesticated species vs. competing with wild species.

Also, "morphologically superior" seems subjective when viewed from the standpoint of agriculture, but from a natural perspective, is not so subjective. Any favorable trait might also have an unfavorable consequence, faster growth could mean more water dependency, stronger stems could mean weaker defense against harsh winds and weather.

Crops are not superior in a whole range of ways, especially in things that deal with direct competition (like nutrient efficiency).  more importantly they are often worse at reproduction (wheat cannot even spread its seeds without human help), which is the ultimate negative selective pressure.

Modern grass crops (cereals) haven't run out in the wild is because that was the whole purpose of their development. What differs them from their wild counterparts are the domestication traits, like, seed shattering, uniform maturity, day length sensitivity etc.

Modern grass based crops are significantly superior to wild grasses, they grow faster, are stronger stemmed, have larger leaves and higher seed yields in terms of individual seed size, giving germinating seeds a significant head start vs other wild breeds.

This is only true under well resourced conditions, such as, irrigation, fertilizer, planned planting density etc. They grow faster and stronger because that is how they are bred. They are bred to utilize these resources better and produce better.

I've heard time and again that GM crops will escape into the wild with potentially devastating consequences, out-competing wild plants for space and destroying biodiversity.

What people generally talk about here is the genetic transfer due to pollen contamination. But this is generally hard because of species differentiation. Even if that happens it will be with very low frequency compared to wild population. As far as I know modern crops do not and probably will not out compete wild plants under natural conditions.

So why hasn't this happened already? Our crops are already GM (albeit through different methods and over a much longer time)

Explanation above applies here too.

Edit: I have seen the odd crop plant growing in the wild, amongst other grasses, but rarely more than one or two clumps of wheat or barely grass amongst a sea of wild grasses.

That is generally due to seed contamination due to somebody threw a seed there. Or it is due to remnant seed from previous year's crop, these plants we call volunteer plants.

I believe the OP is referring to the fact all our crops have been genetically modified through artificial selection and selective breeding, often just through domestication alone. The vast majority of our crops are genetically modified in this sense.

In that case, true, they have been genetically modified.

It is a common issue in any scientific sense the colloquial usage of GM is completely unsound, there is no definition of GM that does not cover the either the vast majority of crops or such a small insignificant percentage that it you will likely never eat them anyway.

Exactly. I find it funny when people talk about GM (the colloquial use) to say they have been genome edited but fail to realize that what we have today is all GM via artificial selection, selective breeding, mutagenesis, domestication etc.

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


text:
Looking for dataset of proteotypic and non-proteotypic peptide
I doing experimentation for peptide prediction using machine learning. I need some data for testing. My background is Computer Science.
Any advice how to find proteotypic and non-proteotypic peptides. I already got one dataset "Y.pestis". However, I'm looking for another dataset (for verification). For example, S.typhimurium or S.oneidensis, but any other peptides will be OK.
I tried PRIDE archive, but I couldn't figure out how to get two datasets; one for proteotypic and another for non-proteotypic
Any advice is appreciated!
Thanks!

I suppose anyone answering this question would already know what a proteotypic peptide was. I don't find the definition totally clear from brief literature searching. From your question it would seem to mean a peptide that is unique for the proteome of one organism. Is that so? Do you know how the Y.Pestis dataset was prepared? I should imagine it was done computationally, in which case it would presumably be easy to apply to any other characterized bacterial genome.

Yes, peptide that is unique for the proteome of one organism e.x E.coli


text:
The drawing of genetic crosses
I'm preparing myself for the GRE. The quantitative stuff has all been going well. I'm aiming for a geology grad scheme. In the event of having to take subject specific tests, I'm teaching myself a few "out there" things in science.
I'm going through biology and looking at genetics for the first time since high school(!)
I just had a question here really to do with genetic crosses. I've been looking at Mendel and the experiments he carried out. One specifically looking at short pea plants. I'm looking at an example where all F1 plants are tall (F1 being the generation of plants). In the example the F2 generation are created in selfing the F1 plants.
Now, I've got my head around the science involved, but I just basically wondered if any biologists here could show me how to make a genetic cross of F2 in order that I could show the genotypes and phenotypes of the offspring.
This isn't necessary but I feel as though it would help my understanding.
At the moment I'm drawing a two by two grid. I suppose I need to fill it with the appropriate alleles?
Thanks.

One of my most valuable sources has been this:
http://www.indiana.edu/~p1013447/dictionary/mendel.htm

The diagram that you are looking for is called a punnet square.

What's a GRE? (I have Googled it now, but I wanted to make you aware that's not a widely known term outside the US - you might want to explain it).

(I also added the 'homework' tag. Please don't consider this as a negative - in my opinion this is an example of a 'good' homework tag!)

The cross you're studying is Mendel's monohybrid cross. Which looks something like this.

Now here, the genotype of F1 gen plants is Tt.
To draw this cross, proceed exactly like you decided. Draw the 2/2 grid and cross the alleles Tt x Tt
Your cross should look like this (ignore the plant drawings):

(Source: classes.midlandstech.com)


text:
Why didn't Mendel ever see the recombination?
I saw a video on youtube of a professor saying it's because of the quantity of peas. So Mendel would never have published his work if by any chance he had found a pea with recombination.
Someone can explain to me in a dummie way the reason?

Mendel did not do sufficient number of experiments. :P

Both are real biologists. Mendel pioneered genetics and his findings provided leads for others. In the process of science there is continuous validation and re-examination of facts. Some may be proven false; that doesn't mean that the initial scientists did not contribute anything.

But the reason is because he did not do sufficient number of experiments. Do you have some biological way to explain this to me?

Before Mendel, humans has been trying to figure out heredity for over 2000 years without being able to reach any conclusions more specific then that offspring tend to inherit the traits of their parents. This is because the full process of inheritance is staggeringly complex. Mendel's contribution was to demonstrate that there were least a few traits that were inherited in specific and quantifiable patterns. He had to look very hard to find those traits. As @swbarnes2 suggests, his search may have led him to traits on separate chromosomes, eliminating the complication of recombination.

Of course, it's also possible that he looked at more than 7 traits, but didn't publish on traits which violated his laws.  The probability of randomly picking 7 traits on 7 chromosomes is quite low.

@swbarnes2, indeed, a lot of historians and biologists think that Mendel did exactly that: he narrowed down the results to the ones that he could explain.

I'm not sure what you mean by "recombination".  Peas have 7 chromosomes.  Mendel's seven published traits are each on a different chromosome.  Mendel's second law states that all genes assort independently.  This is wrong, but it is correct for genes located on different chromosomes, which Mendel's were.

Actually, two of them are in the same chromosome.


text:
Does A/T, G/C pairing exist in haploid?
I'm trying to understanding base pairing. So every linear chromosome is a double stranded double helix. Is this double stranded property the same as saying an organism is diploid? Or do the chromosomes of a haploid eukaryotic organism, like a member of Fungi, each have 2 strands (with the purines always pairing w/ pyrimidines), which would imply that diploids organisms actually have 4 strands?
EDIT: Part of my confusion comes from the fact that in diploid organisms, each parent gives 1 chromosome to the child. If the double stranded property is the same as saying an organism is diploid, does this mean that say if a nucleotide on one chromosome is A, then the nucleotide on the other chromosome in the same loci must be T? Doesn't chromosome mean a paired up strand, not a single strand?

All chromosomes are double-stranded (they wouldn't be stable otherwise). Diploid organisms have two double-strands, for a total of 4 strands. Haploid organisms one have one double-strand, for a total of 2 strands.

Is this double stranded property the same as saying an organism is
  diploid?

No.  You are a diploid organism because you have two copies of every chromosome.*  You got one from your mother, and one from your father.  All your cells are also diploid, except for your gametes, each of which contains only one copy of every chromosome (due to crossing over, each chromosome is partially from your mother, partially from your father).
Bacteria just have one copy of their genome.  They duplicate it prior to cell division, and each resulting cell has one copy of each chromosome.
*Unless your sex chromosomes are XY, or are anuploidic.


text:
Are thunder and lightning necessary for any organisms?
Comparatively irregular events such as forest fires are necessary for some plants to grow (see here).
But do any plant or animal species have similar dependence on thunder and/or lightning?

Lightning is more or less the only non-human cause of forest fires

@C_Z_ Ah, yes. That was not an intended connection, even though it is obvious now that you point it out. I was more thinking of direct effects of the immense light and sound…

do you mean for reproductive purposes? Or just in general?

@C_Z_ +1 for trees

@C_Z_ What about dry fires in summer/dry season? They happen very frequently. Are they always started by people (genuinely curious)?

@James The only way for those fires to start in the dry season is with a spark. As far as I know, lightning is the only non-human source of a spark

@C_Z I disagree, volcanic action is also known to cause natural fires. Other sources of literature even suggest rubbing of some reactive rock materia can cause these sparks

I think it is higly unlikely that there are species that directly depend upon lighting. Lighting strikes occur to infrequently and random to be of any use to an organism from energetic point of view.

@VanceLAlbaugh Generally, was my thought. I realise this easily becomes open ended. But every necessary aspect of an organism's life cycle is reproductive in some way, maybe?

Lightning results in nitrogen fixation (Draphco et al., 1967; Hill et al., 1980). It is one of the main abiotic nitrogen fixation mechanisms. As you would know very well, nitrogen fixation is important for all organisms.

This is very good, but if there are other sources of nitrogen fixation, organisms are not really dependent on this source of it?

@trmdttr there are some organisms (mostly micro-organisms) that can fix nitrogen on their own.

So basically, all other organisms that cannot fix nitrogen themselves are dependent on lightning? Or do they use the fixed nitrogen from those microorganisms?

@trmdttr they can depend on the other organisms that fix nitrogen as well as use the nitrogen fixed by the lightning. I believe initial lifeforms consumed the abiotically fixed nitrogen; subsequently some evolved to fix nitrogen themselves.

So, this answer doesn't really catch a necessary reliance on thunder or lightning for any specific organism? More a need for fixated nitrogen of which the majority comes from that source (but also from others)?

@trmdttr the necessity will depend on many bio-geographical factors.


text:
What is the rate of mRNA decay in saccharomyces cerevisiae?
I am just looking for a number whether that is a mean or an estimate. I am having trouble finding this value on papers because the papers mention only the methods for calculating such a value. Is there a reason why a reasonable mean is hard to obtain?

It is highly variable. Do you want the range? Did you check BioNumbers?

Here is my best attempt at answering this question:
The median mRNA degradation lifetime is roughly 20 minutes in the case of yeast. Also, the total transcription for RNA pol II in a yeast cell growing in standard conditions is about 60200 mRNAs/h. I am going to go ahead and suppose that the transcription rate is constant throughout time. Thus we have that total transcription rate is equal to 1003 mRNAs/min. Furthermore, I am going to make the rough approximation that all mRNAs live exactly 20 minutes. Therefore, mRNAs will start degrading after 20 minutes. In one hour, 1003 mRNAs will degrade every minute for 40 minutes. It follows that the rate of mRNA decay in yeast is roughly 40120 mRNAs/h.

Now I understand why it is so hard to find a specific number...

in practice nearly everything about the mRNA sequence may cause the rate to vary from mean values.  That includes the sequence itself, the rate of translation, motifs within and outside the coding region that bind to some proteins etc etc.


text:
R/Bioconductor query for a gene?
I'm fairly new to bioinformatics, so please be gentle ;0
Is there a way to query a particular gene using a script in R/Bioconductor? I'm particularly interested in Gene Ontology terms. There are many websites that, given the gene name, will return relevant GO terms. My question is, can it be automated?

Please ask questions about Bioconductor on the Bioconductor support site.
Bioconductor also distributes 'annotation' packages with curated information. These don't rely on a web service, so are always available, and are fixed at each (6 month) Bioconductor release, but are less comprehensive. Choose your organism
BiocInstaller::biocLite(c("org.Hs.eg.db", "GO.db"))  # first time only
library("org.Hs.eg.db"); library("GO.db")

Query for GO ids
symbols = c("BRCA1", "BRCA2")
df = select(org.Hs.eg.db, symbols, columns="GO", keytype="SYMBOL")

Symbol - GO mappings are 1:many, so
> dim(df)
[1] 149   4
> head(df)
  SYMBOL         GO EVIDENCE ONTOLOGY
1  BRCA1 GO:0000151      NAS       CC
2  BRCA1 GO:0000724      IDA       BP
3  BRCA1 GO:0000724      TAS       BP
4  BRCA1 GO:0000794      IEA       CC
5  BRCA1 GO:0003677      TAS       MF
6  BRCA1 GO:0003682      IEA       MF

Use the GO.db package to gain more insight into the GO ids
> head(select(GO.db, df$GO, "TERM"))
'select()' returned many:1 mapping between keys and columns
        GOID                                                    TERM
1 GO:0000151                                ubiquitin ligase complex
2 GO:0000724 double-strand break repair via homologous recombination
3 GO:0000724 double-strand break repair via homologous recombination
4 GO:0000794                            condensed nuclear chromosome
5 GO:0003677                                             DNA binding
6 GO:0003682                                       chromatin binding

See the vignettes on the AnnotationDbi landing page, the annotation-related work flows, and the training material on the Bioconductor web site.

Take a look at the biomaRt package. This package allows you to access some databases in R directly. Quote from the user's guide:

The package enables retrieval of large amounts of data
  in a uniform way without the need to know the underlying database schemas
  or write complex SQL queries. Examples of BioMart databases are Ensembl,
  Uniprot  and  HapMap.   These  major  databases  give  biomaRt  users  direct
  access to a diverse set of data and enable a wide range of powerful online
  queries from R.

In the user's guide you will find anything you need, i.e. description and example tasks, for doing queries on HGNC symbols, GO terms, and more.


text:
"CO2 is plant food" - What is the actual effect of increased CO2 on plant growth?
A frequent talking point by global warming deniers is that CO2 in the atmosphere is actually beneficial because "CO2 is plant food". I'm a non biologist trying to figure out under what circumstances this is actually true.
Here are my thoughts so far:

Plant growth is more or less governed by Liebig's law of the minimum - the plant needs sunlight, CO2, water, nutrients in a certain composition, whatever is lacking limits growth
In addition to it's role in photosynthesis, water is needed to transport nutrients from the soil, so dry conditions can limit effective nutrient availability
The energy needed to assimilate CO2-carbon is independent of the CO2 concentration
The rate of photosynthesis is (within the limits given by energy etc.) governed by CO2 concentration and active plant matter
photosynthesis only works in a more or less narrow temperature band

From this, it follows that a higher CO2 concentration in air will boost plant growth only if everything else (light, water, nutrients) is abundant.
So I have two interconnecteed questions:

How wrong is my simplistic view, does my conclusion hold?
What do we actually observe in the wild or in experiments?

Possible duplicate of http://biology.stackexchange.com/q/681/3340

Definitly helpful. Need some time to read linked papers in the answers over there.

@mart In brief: High CO2: Toxic effect. Photosynth rate drop.  Stomata closes.
Medium CO2: Optimum photosynth.
Low CO2: photosynth rate drastic fall in C3. in C4 plant, fall not so drastic.
Very Low CO2: C3 stop photosynth, enter "photorespiration". C4 very low rate photosynth.


text:
Identify this plant from the Netherlands with big white flower
The picture was taken today in the Netherlands. Can you identify this plant species?

From the leaves and flower it could be a clematis.

Like @skymningen thought, this is a Clematis. However, the only wild Clematis in the Netherlands is Clematis vitalba, that has much smaller flowers (about 2 cm diameter) see "Heukels' Flora van Nederland" (the official Dutch flora) and here.
So you have photographed a plant that "escaped" from a garden. Most garden Clematis are hybrids from Chinese or Japanese origen. As there are about 300 species and new hybrids constantly being produced, the likelyhood of finding it's name is low. https://en.wikipedia.org/wiki/Clematis


text:
what does 'invoking the ghost of competition past" mean? Why is it important for present research on interspecific competition?
Ecological and evolutionairy effects are sometimes difficult to distinguish.

This sounds more like a question about english language, as 'invoking the ghost of competition past' sounds more lyric than scientific. Otherwise, without context there is no real way to answer.

First, the setting for this question is almost always related to explaining some aspect of broadly defined trait differences in extant (currently-living) species. The specific problem at hand is one in which someone is trying to explain what may drive the observed differences among competitors. It is unclear whether such differences are relatively recent (ecological time) or old (evolutionary time).
Consequently, the phrase "invoking the ghost of competition past" implies that someone thinks the observed pattern of differences may have been caused by a process that took place a long time ago, and may not be presently observable/measurable. Anyone performing research on this topic would then have a comparably hard time ascribing causes of differences to ongoing competition, as opposed to past competition.


text:
Is there a place or tool from which I can find or generate genome data for epistasis detection?
I am busy researching a school project for my honors in Electrical Engineering. The project is to create a deep neural network to detect epistasis. I have very little knowledge in the bioinformatics field and while I have managed to pick up most of the theory on epistasis and all of the new terminology, I still lack knowledge of the resources that are available to someone in my position.
I will be needing a large amount of data to train my neural network. I do not mind what form the data is in I just need many examples of epistasis. Where can I find high quality, easily accessible data for this kind? Or alternatively, what tools can I use to generate this kind of data?

What specific kind of data are you looking for? What research have you done so far?

@MattDMo What I'd like is data that takes the form of a vectors of As, Ts, Cs and Gs, one for each chromosome perhaps. I'm not 100% sure though. I have looked at a tool called GAMETES which generates SNP based models for simulation studies and can also be used to generate data, however the data isn't quite in the form I just described. I have also had a look at PLINK, however, the data it generates is in linkage equilibrium which as I understand it means that it won't be of use for epistasis detection because epistasis occurs when there is linkage disequilibrium.