text:
How to seek for available genetic data relevant to ecology and evolution?
I had a quick look online. There seems to exist many different website of database archiving. Some data might be free of charge while some others might not be. I found things such as Dryad, TreeBase, DataOne or GeneBank. I think that several journals (American Naturalist, Molecular Ecology, Science and Nature for examples) force their authors to make their data available
General Question
Can you make a short review of what different database exist, what are their properties (what kind of data, what license and fees) and how to seek for data (are datasets associated to keywords or do we have to look for a paper and then look for their data).
Case study
Imagine for example, you are looking for SNP data of a spatially explicit population that recently underwent a range expansion (might be too accurate, you may want to drop down some specifications). How would you go about to look for this kind of data? (No need to pull out data but only to describe a procedure).

Please leave a comment when downvoting

I am working a lot with databases, and I have to say your question is too broad. There are heaps of different databases and thousands of ways to use them. Even describing GenBank in detail would make half a book. In you case, if you can describe the biological question so well, try looking for relevant publications, take the database identifiers they give for the data they used and look at what you get.

@skymningen Thanks for your comment. So, for the case study I am asking you would not try to look with keyword in a specific database but you would rather look for articles that may have potentially uploaded their datasets? Seems like it would take a long time to find relevant data. Would it be too broad to ask for a list of the different databases that exist along with their very basic feature such as broadly speaking, the nature of the data (genetic/phenotypic for example) or the field that have produced those data (ecology/biochemistry/evolutionary biology/...)?

That is still too many databases and I by far do not know all of them. I am specialised in -omics data, so I could mainly guide you there. The NCBI-databases are your best guess to get datasets, but the descriptions given there are often hard to understand if you did not read the publication. It is much easier to skim over a publication and decide if the data they used or produced is something that could help you. To help you with your case study I am already failing at the meaning of "spatially explicit", sorry.

@skymningen Ok. Well I guess you actually made the answer one could give through your two comments. Could make an answer out of your comments? Maybe something along the lines of: 1; One cannot summarize all data bases, there are too many of them 2; Because the datasets usually don't have enough metainformation (and eventually because tagging is not super efficient), your best bet is to look at the literature directly.

As a bioinformatician, one of my tasks is quite often to get information from databases or find the correct database to compare to. There are several big databases around, but even those are way too many for any single person to know.
There are databases specialising on genetic data, some specialising on taxonomic information, some on ecological information and then there are species specific databases which collect all kinds of data from a given species, genus or clade.
For me the biggest source of generalised information would be the NCBI databases, including GenBank for nucleotide sequence, their Protein database and maybe dbSNP for, well, SNPs. Then there are multiple 16S databases I have used, there is UCSC for the basic data about the human genome, flyBase for Drosophila,... I think the point should be clear. And those are only the ones that just sprang to my mind.
If you don't have a very exact question to answer like "Is there a gene similar to gene x from Drosophila present in any Bacteria?" it can be very hard to both choose the correct database and also find the important information in it efficiently.
Then there is the problem of metadata. I might be able to find sequencing data from the gut microbiome of a human treated with antibiotics quite easily. If I am looking for a specific antibiotic given over a minimal time of seven days to a different healthy humans, preferably including at least one breastfed child and it's mother (which was the one taking the antibiotics, not the child), then it's getting complicated. Here it is generally way easier to scan PubMed for some relevant publications on the matter and find out if they used published datasets or published their own.


text:
18S rRNA sequence
I have this phenomenon that the human 18S rRNA reverse transcribed with polydT oligos serve as faithful RTPCR normalizers, tested with better known house keepers. I want to know what I'm amplifying exactly, so where can I find the reference sequence for mammalian rRNAs?

If you're looking for reference sequences, RefSeq is a good bet.
http://www.ncbi.nlm.nih.gov/nuccore/?term=18S+ribosomal+RNA+AND+srcdb_refseq%5BPROP%5D

source: Stack Exchange

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

sort: votes


text:
Is the human biological clock genetically programmed or learnt?
Argument favouring learning:
A newborn sleeps for 20-22 hours. But overtime (s)he learns to focus sleeping time to night time, according to his or her needs and family needs. Some sleep from 1 am to 7 am, some from 11pm to 5 am. So it is learnt.
Argument favouring a genetic origin:
Somewhere I read (I don't exactly remember the article) where it was told that the biological clock is not of 24, but of 25 hours. This means that the synchronisation is not maintained with the earth. If it would be learnt, then why is it not in synchrony with the world?

The circadian clock is hardwired at ~25h and reset according to various cues, mainly day/night, but also time of food supply, parents who put you to bed at a certain time, among other things. And kids definitely sleep longer than 6 hours :)

The sleeping time was just an example... Also AliceD, can you give me more details of circadian clock you are speaking of? May be some article. Also, it is not clear what is the answer to the question.

related question: How do humans perceive time?

Short answer
The biological master clock is neurologically and genetically hardwired. The biological clock is not affected by learning. Instead, it is constantly entrained mainly by daylight.
Background
The biological clock is hardwired in the human body and can be traced back to the master clock in the suprachiasmatic nuclei (SCN) of the hypothalamus (Fig. 1).

Fig. 1. The SCN is entrained by environmental light captured by the retina in the eyes. Source: Neuroscience News.
The SCN is an intrinsic oscillator that governs sleep and wake timing, rhythms of temperature, hormones, mood and cognitive acuity etc. etc. These rhythms are entrained to 24 hours by the environmental light-dark cycle primarily via a subset of photosensitive retinal ganglion cells that project directly to the SCN (Fig. 1). Using hormones and neuronal signals, the SCN entrains peripheral clocks of similar molecular mechanism present in many tissues (Pagani et al., 2010).
In humans and other organisms, the timing of 24-hour behavior is governed by the period length of the circadian oscillator. This period is approximately, but not exactly, 24 hours long (circa diem), and ranges from 23.47–24.64 across people (23 hours 28 min to 24 hours 38 minutes) in laboratory conditions (Pagani et al., 2010).
Why is it circa diem and not exactly 24 hours? Note that the absolute length of a day depends on the definition used. For example, one complete rotation of the earth around its axis (the sidereal day) actually takes 23 hours, 56 minutes and 4.1 seconds. The solar day is 24 hours and is defined by the time it takes the sun to make an apparent circuit across the skies. More importantly, there is apparent solar time, sometimes called true solar time, which is determined by the daily apparent motion of the observed sun. It is based on the interval between two successive returns of the sun to the local meridian. The length of a solar day varies throughout the year, and the accumulated effect of these variations (equation of time) produces seasonal deviations of up to 16 minutes.
The length of a day can also be defined in the number or hours from sunrise to sunset, which varies where you are on earth. At the equator every day of the year is exactly 12 hours long. At 50° latitude (e.g., England & Canada) the longest day is 16.5 hours and the shortest day 7.5 hours. At 35° latitude (e.g. many US states and Greece) the longest day is 14.5 hours and the shortest day 9.5 hours. Given that light is the most effective way to entrain the circadian rhythm, it is obvious why the absolute length of the intrinsic circadian rhythm is not important. As long as it is circa diem, it will do.
Reference
- Pagani et al., PloSONE (2010); 5(10): e13376

Good answer. Note however that the complete rotation of Earth on itself is not the definition of a solar day: you want the duration between two occurrences of the sun being at the zenith, and this is 24h. (23h56'4.1'' is the duration before two occurrences of a given star being at zenith)

@Joce - thanks for your suggestion - I will look into this later. Are you saying my information is incorrect then? If so, I will make some edits. Thanks again!

It's not incorrect, but I'd say that the duration of earth revolution upon itself is not relevant : 23h56min is the time until stars are back at the same position, for circadian rhythm it is the time until the sun is back at the same position which is relevant. (Then on top of that you have the "true solar time" correction)

@Joce - I adapted the answer

Is the human biological clock genetically programmed or learnt?

It is genetically programmed.

A newborn sleeps for 20-22 hours. But overtime (s)he learns to focus
  sleeping time to night time, according to his or her needs and family
  needs. Some sleep from 1 am to 7 am, some from 11pm to 5 am. So it is
  learnt.

Sleep clears the brain of toxic metabolic byproducts. A newborn have different sleep requirement than an adult (it would be an interesting question why). The connection with the age is something like this:

- Figure 1. - Sleep requirements by age - ref
So it is not learnt, if they wouldn't sleep enough, they could have health problems or they could even die because of brain damage.

Somewhere I read (I don't exactly remember the article) where it was
  told that the biological clock is not of 24, but of 25 hours. This
  means that the synchronisation is not maintained with the earth. If it
  would be learnt, then why is it not in synchrony with the world?

It is in sync with the world, every morning the blue light resets the clock, that's why we tend to use red light at night.
There is a clock in the hypothalamus (brain), which is entrained directly by the daily light/dark cycle. There are peripheral clocks in the liver, heart and in other tissues (probably in every single cell), which are weakly affected by the light/dark cycle, and strongly affected by the food intake (probably by other factors as well). The sleep/awake rhythm depends on all of these clocks. So it depends on the actual light/dark pattern and the metabolic (feeding) pattern of the individual.

When food is plentiful, circadian rhythms of animals are powerfully
  entrained by the light-dark cycle. However, if animals have access to
  food only during their normal sleep cycle, they will shift most of
  their circadian rhythms to match the food availability.

2008 - Differential Rescue of Light- and Food-Entrainable Circadian Rhythms
2008 - How to Beat Jet Lag: Don't Eat
2006 - Nuclear Receptor Expression Links the Circadian Clock to Metabolism
2008 - Effects of light cues on re-entrainment of the food-dominated peripheral clocks in mammals
2011 - The circadian clock and metabolism
2009 - Food-anticipatory circadian rhythms: concepts and methods
2009 - Rev-erb-α: an integrator of circadian rhythms and metabolism

If they [newborns] won't sleep they would die because of brain damage? Do you have any reference to that? The linked NIH website doesn't mention that. +1 for the reference to food-based resetting

@AliceD I just applied logic, people die because of too much sleep deprivation, but you are right, it is exaggeration, because less, but chronic sleep deprivation can cause just health issues, but not instant death. I'll edit that part, thanks! :-)

@AliceD Edited. Not the best references, but I think it is enough in this case.

Better for sure, great. Can't +1 you again unfortunately :)

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


text:
Why cannot there be multiple sources for same species origins?
We often associate Africa as the geographical location of the origin of humans. Why cannot there exist multiple geographic locations of origin (given same environmental conditions)?
The same argument exists for other species as well. So what is the basis of the common ancestor (from single geographical location) theory?
Please give me references so that I can read more on this subject.

Partly depends on the resolution at which you look (both spatially and temporally) but the further you zoom in the harder it becomes to define where one species becomes two because its a gradual process which takes place over time and space. It's relatively easy to show that humans originate from Africa, harder to show that humans originate from east Africa ~400,000 years ago, and harder to show that humans originated 378,058 years ago in northern Kenya. One part of the problem is pinpointing when homo erectus (?) became homo sapiens which depends on the definition of a species...

@rg255 Why cannot there be multiple sources of origin say for at Australia and Africa?

There is no reason why it cannot be. Just that the likelihood (of two exactly similar events happening at the same time) is less.

To me, it is unclear what you are asking. Are you asking if two different taxa can give rise to the same species at two different locations (i.e. A -> C and B -> C, if they all would all co-occur you would have A, B & C)? If so, how do you view the relationship between A & B - can they be sister taxa?

@fileunderwater : I think question will make it clear. Why cannot homosapiens independently originate at may be europe and africa?

Why is this question voted for closure because it is unclear? It sounds OK. Also because of the hypothesis that Neanderthal and hominids may have successfully interbred. Both were deemed unrelated. Although it's not my expertise and although i cannot answer this question, i feel it is a good question. Vote to leave open here.

@dexterdev So evolving from H. erectus to H. sapiens independently at two different locations?

@fileunderwater : Yes. That's what I mean.

@dexterdev: But why (and how!) would two separate populations of H. erectus both evolve to the same H. sapiens?  Closest you could get would be two subspecies, which later interbreed to form a single species again.  (Which might indeed have happened with Neandertals...)

This is a very fundamental, and in my opinion, interesting question. You might not find many sources that directly cover this question because it is hard to test. If speciation did happen in two separate locations and the resulting species were so similar that they could breed with one another and not the original species, how would we be able to tell if the species originated in separate locations and that the new species didn't just travel to the new location? Below I'll try and explain why it's safe to assume they probably didn't have different locations for speciation.
Thought Experiment
Here is what happened in hypothetical land. Species X exists in happy land. Individuals of X then move to water land. Some more individuals from X move from happy land to H2O land (very similar to water land). Species X undergoes speciation in water land to species Y and speciation of X also occur in the H2O land to species Z.
Can Z and Y be the same species with different origins where the niche conditions are the same?
As you can imagine, the longer after geographical isolation the more mutations occur and the less likely it is that the new species will be able to breed successfully with similar species.
Although the two environments may seem identical, ecology is notoriously complex and chaotic, and so in reality as far as ecology is concerned, they are very different environments. Even the slightest difference between niches will naturally select different traits that could make Z and Y sexually incompatible.
Furthermore, when dealing with the geographical origin, you must assume that there was geographical isolation between the two speciation event locations. Since there is typically no contact between Z and Y species, there is no selective pressure to remain genetically compatible and given enough time, they will become unable to breed.

Humans
There is a contentious claim that ancient humans bred with chimpanzees after both speciation events from our common ancestor to humans and chimpanzees. Broadly I think this has now been dismissed. However, it is reasonably well accepted that in a more recent "Tolkien-esque" world humans bred with Neanderthals.
But ultimately I don't think there is a single example (I am thoroughly open to being proven wrong!) in the natural world of two similar geographical isolation events driving exactly the same species to evolve and both versions of the new species are more genetically similar to one another than they are to the origin species. The odds are just too slim even if to us the conditions seem identical.

References - Wiki article about the theory of multiregional origin for humans. The wiki article clearly states up front that this is "an alternative explanation to the more widely accepted Out of Africa model". One issue brought up in this article, is although there doesn't seem to be any unique localized single feature, there has been unique combinations of localized features found in early fossils in locations like Australia. The wiki article includes further references.
http://en.wikipedia.org/wiki/Multiregional_origin_of_modern_humans
The more accepted theory is "Out of Africa". Wiki articles:
http://en.wikipedia.org/wiki/Out_of_Africa_I
http://en.wikipedia.org/wiki/Recent_African_origin_of_modern_humans
http://en.wikipedia.org/wiki/Early_human_migrations
Another article that explains why "Out of Africa" is the more accepted theory:
http://www.actionbioscience.org/evolution/johanson.html
Note that all of this is with respect to modern humans. I don't know if there are any animals or plants where multiple source for the same species is the more accepted theory.
Hybrids (the offspring of two compatible, but different species parents) could occur if the parents where multi-regional. You can do a web search for polyploid hybrids and tree frog for examples of this, but these are hybrids, not mutations.

Citing wikipedia alone is risky, as its contents are dynamic and often based on questionable sources

@AliceD - The OP asked for references. The wiki article clearly states up front that this is "an alternative explanation to the more widely accepted Out of Africa model", and the wiki article contains links to references (again, what the OP was asking for). I updated my answer to make this more clear.

Those references may be disputed or deleted altogether over time. Cite the primary references if they are good.

@AliceD - the wiki article was originally created July 2014, and has been continually updated since by multiple people. The references have been there during much of this time, and should have been deleted by now if that was an issue. I would assume that less accepted already means it's disputed, and the wiki article covers this. The talk page should include discussions about the article or disputed references.  I'm not a proponent of this theory, and only posted the link since the OP asked for references.

All good. I'm just explaining my downvote. I'm not saying wiki is per definition not OK, I'm saying I am not a fan of wiki-only answers. That's all. You might get a bunch of upvotes from others. Because of your research into the wiki page I'll remove the -1 :)


text:
Factors on which one compound transforming to another compound depend
Considering the Metabolic Pathway:
http://www.genome.jp/kegg-bin/show_module?M00166
Consider the reaction R01523(the very first reaction). How is it possible to know that the compound  C00199(D-Ribulose 5-phosphate) will get transformed to C01182(D-Ribulose 1,5-bisphosphate)? What are the factors on which this transformation depends?One factor I know is structure but how does structure effect this transformation? Does two similar structured compound means that one of the compound can get transformed to the other one?

Cross posted http://chemistry.stackexchange.com/questions/32012/factors-on-which-one-compound-transforming-to-another-compound-depend

From my answer on chemistry:
After looking at the website I found the reaction is based off of an enzyme called: phosphoribulokinase. In biological systems many reactions occur under the auspice of enzymes or proteins. These are incredibly large molecules made of an extremely long chain of amino acids which are a set of 26 or so small molecules that can 'hook' into the chain structure of a protein. Each amino acid has different properties and thus experiences different forces pulling it towards and away from other amino acids on the chain. What this means is the whole chain folds up into an extremely complex structure. For a protein to allow a reaction to occur it has a small region that the reacting molecule can hook into. There are then sets of atoms and molecules that act as scaffolds that allow atoms in the reacting molecule to be moved without the need for nearly as much energy as would be required without the scaffold. Now this is how it changes structure. Now whilst the protein can just as easily allow the molecule produced to be converted back to the original, this may be less energetically favourable which brings us to equilibrium chemistry involving dynamic forward and backward reactions. What makes this more complicated is that proteins often have separate 'hooks' for molecules to disable them. That is if a lot of substance A is around then the protein will be disabled and no longer convert B into A until more A is consumed and thus stops inhibiting the protein.


text:
Why does an electrical shock freeze up muscles?
Why is it when someone comes into contact with an electrical supply that their body freezes up and is unable to move away from the electrical source?
Can someone explain this through a physiological perspective?

Your question is bit incorrect. Person undergoing electrical shock does not get frozen in place. He/she actively grips the wire and holds it with great force. Of course, this only happens if contact occurs with inside of the palm, so the closing fist can actually grab the wire.

Interesting question!
An important factor here is the let-go phenomenon, which is defined as the current level in the arm that will cause the hand to involuntarily grip the current source. When the fingers are wrapped around a large cable, most adults will be able to let go with a current of less than 6 mA. At 22 mA, however, more than 99% of adults will not be able to let go.
Nearly all cases of inability to let go involve alternating current. Alternating current repetitively stimulates nerves and muscles, resulting in a tetanic (sustained) contraction that lasts as long as the contact is continued. If this leads to the subject tightening his or her grip on a conductor, the result is continued electric current flow through the person and lowered contact resistance.
Given that the current flow in the forearm stimulates both the muscles of flexion and extension, it seems surprising that one cannot let go. However, the muscles of flexion are stronger, making the person unable to voluntarily let go (similar to the fact that a crocodile's jaws can be kept shut with your bare hands, but one should better not attempt to keep them open like that...).
Direct currents below 300 mA have no let-go phenomenon, because the hand is not involuntarily clamped.
Several different outcomes may occur when a person grasps a conductor giving 10 kV AC hand-to-hand voltage. Within 10 to 100 milliseconds, muscles in the current path will strongly contract. The person may grasp the conductor more tightly. However, mostly subjects are propelled away from the contact, likely due to generalized muscle contractions.
Reference
- Fish & Geddes, J Plastic Surg (2009); 9: 407-21

When the body comes in contact with an electrical power supply, two things can happen. If the current flow is high enough, the body heats up just like a heating resistor, and opposed to the resistor, the body can't handle the heat, thus severe burns occur after electric shock.
But if the current is low enough not to burn "the conductor" other effects are visible. The nervous system tissue has the best conductor properties from the body. More than that, it works with action potentials, which are small chemical generated currents. When an external current gets to a nervous fiber, the fiber will conduct electricity further to the efector tissue (muscle in this case).

If electric current of sufficient magnitude is conducted through a living creature (human or otherwise), its effect will be to override the tiny electrical impulses normally generated by the neurons, overloading the nervous system and preventing both reflex and volitional signals from being able to actuate muscles. Muscles triggered by an external (shock) current will involuntarily contract, and there's nothing the victim can do about it.

The result is a powerful contraction of the muscle. But the question is what muscular groups contract? Well, all that are under the influence of a nerve under electric shock. And from here comes the freeze effect, because antagonist muscular groups contract simultaneously (for example flexor and extensor, adductor and abductor muscles in the same time). The result of this forced contraction tends to move parts of the body as dictated by the muscles that are more powerful.

The forearm muscles responsible for bending fingers tend to be better developed than those muscles responsible for extending fingers, and so if both sets of muscles try to contract because of an electric current conducted through the person's arm, the "bending" muscles will win, clenching the fingers into a fist.

You can read more on All About Circuits.


text:
Recessiveness of allele for protection of organism
Heterozygous organisms profit from pairs of gene alleles. Harmful alleles when being recessive can be carried without any harm for the organism. Only when two harmful recessive alleles form a gene the negative effect is produced. As described in wiki article on allele:

A number of genetic disorders are caused when an individual inherits two recessive alleles for a single-gene trait. Recessive genetic disorders include Albinism, Cystic Fibrosis, Galactosemia, Phenylketonuria (PKU), and Tay-Sachs Disease. Other disorders are also due to recessive alleles, but because the gene locus is located on the X chromosome, so that males have only one copy (that is, they are hemizygous), they are more frequent in males than in females. Examples include red-green color blindness and Fragile X syndrome.

But some illnesses are carried by dominant alleles (from the same article):

Other disorders, such as Huntington disease, occur when an individual inherits only one dominant allele.

My questions are:

How does harm from alleles correlate with their recessiveness? Generally speaking, do harmful alleles tend to be more recessive?
How does benefits from alleles correlate with their dominance? Generally speaking, do "beneficial" alleles tend to be more dominant?

Very harmful dominant alleles tend to go extinct --> harmful alleles found in a population are usually recessive.

following up on fileunderwater's comment - dominant alleles (if complete) are exposed to selection every time they occur, recessive only when they are homozygous, which means recessive alleles with deleterious effects can persist at low frequencies easily (see Rice 1984 for a discussion related to X chromosome linkage and hemizygosity in males: http://www.jstor.org/stable/2408385?seq=1#page_scan_tab_contents) Novel deleterious mutations are not necessarily biased to being recessive as far as I know.

Instead of dividing mutations into two classes, dominant vs. recessive, consider categorizing them into classes based on how the mutation affects the gene--or the gene product.  This yields loss-of-function (lf) alleles, that reduce the activity of the gene, or its product, and gain-of-function (gf) alleles that act as if they somehow increase the activity of the gene, or its product.
The logic underlying this classification was described in this classic reference: Muller, H. J. 1932. Further studies on the nature and causes of gene mutations. Proceedings of the 6th International Congress of Genetics, pp. 213–255.  Since this was before DNA had been shown to be the genetic material his arguments are based solely on the phenotype of animals carrying various combinations of chromosomes.  In particular he relies on genetic duplications and deficiencies (or deletions).  In this nomenclature + indicates a chromosome carrying a wild-type (wt) allele of the gene, and m indicates a chromosome carrying a mutant allele of the gene.  So if an +/m animal appears Wild-Type then that allele is recessive.  Similarly, if an +/m animal has a Mutant phenotype then the allele is dominant.
There are two types of lf alleles:

a hypomorph is a partial reduction in function and retains some residual gene function (e.g., a weak missense mutation, or a temperature-sensitive (ts) mutation. A hypomorph is recessive to a wt allele.
an amorph is what we would call a true genetic and molecular null allele, a complete knockout of the gene, where there is no measurable function left (e.g., a nonsense mutation early in the protein coding region, or a small deletion that only removes a single gene).  Amorphs are normally recessive to a wt allele (but see below for an exception)

There are three types of gf alleles:

a hypermorph that elevates the level of the wt gene function (e.g., a promoter mutation that removes a negative regulatory site, leading to increased expression). Hypermorphs are dominant.
an antimorph, or so-called dominant-negative (dn) allele that produces a mutant gene product that somehow interferes with the wt gene product (think poison product as one model). Antimorphs are always dominant over wt.
a neomorph, an allele the results in a completely new gene function (e.g., if a glycolytic enzyme acquired sequence-specific DNA-binding activity, perhaps from a gene fusion event(?)). Neomorphic alleles are extremely rare and almost always dominant over wt.

So we have a straightforward mapping of lf alleles to recessive phenotypes, and gf alleles to dominant phenotypes.  However there is an important exception to this simple scheme for genes that are dose-sensitive, or haploinsufficient. These are dominant lf alleles. For example, when halving the level of the gene product causes a mutant phenotype: +/null. Some well-known examples from the developmental genetics of model organisms are the Ubx gene, and the Notch gene from D. melanogaster.
Further discussion of these terms can also be found in Wikipedia

Can you add references to some of your claims (e.g. "Neomorphic alleles are [...] almost always dominant over wt")?

@fileunderwater Done. As I recall, Muller did not discuss the fabled recessive neomorph as a category in his paper, and it is not clear to me if there are known examples of recessive neomorphic alleles, however my understanding is that this class remains a formal possibility. In general the literature treats all neomorphic alleles as dominant.

Honestly, I think the whole concept of recessive and dominant is unhelpful when trying to understand genetics and we'd be better off teaching the concepts in this answer from the very start.

Harmful alleles can be both recessive or dominant. They do not tend to be more recessive or more dominant. But, you must look at it from a population genetics point of view. When a allele is dominant, it tends to be a highly selected for trait, an analogy of this would be black eyes are a dominant trait compared to blue eyes or green eyes, which is why you see so many people with black eyes in the world than blue.
So therefore dominant alleles are highly selected than recessive ones and when a dominant trait is harmful, the subject tends to get killed off or the line is destroyed in the process by the natural course of reproduction. What remains are recessive alleles which do not get a chance to attain recessiveness and are therefore carried forward by evolution as passenger, never expressing themselves until they get the chance to attain homozygous recessive state.

Welcome to Biology! Could you add a reference or two please?


text:
What are multicell spheroids?
I'm from a maths background and I'm doing some research on mathematical models of cancer. I've come across a lot of literature mentioning "multicell spheroids" in the context of avascular tumours. I know that avascular means a lack of blood vessels, but I am having trouble finding an explanation for multicell spheroids. Are these some kind of model/approximation of a certain types of tumours, or are they actually a real phenomenon in and of themselves?
It would be great if someone could fill me in on what multicell spheroids actually are!

Classical cell culture is a monolayer of cells on the surface of a cell culture dish. These cultures differ strongly from the microenvironment which cells have in tumors, as the cells only interact with their direct neighbours, but have otherwise a relatively optimal supply of nutrients and oxygen.
In a real-life tumor, a cell mass is growing uncontrolledly in all three dimensions of the space, producing these typical "knots" of tumors. As long as these are not getting supplied by own blood vessels (meaning they are vascularized) supply of oxygen, nutrients and growth factors and hormones differ very much between the cells in the outer layers of the tumor and cells in the inside. This causes different levels of stress and also physiological reactions of the cells. This looks like in the figure below (from here):

To resemble these micro-environments for research (and 2D and 3D cell culture differ quite a bit in the results), people are trying to simulate these. Technically this is achieved by embedding small amounts of cells (typically a few hundred) into a gel matrix (for example matrigel or collagen) which is getting hard, and let the cells grow in small drops. If the conditions are right, the cells will develop into these multicellular spheroids.
You can even mix different cell types (for example tumor cells and cells which are usually present in the tissue where the tumor grows) to get an even better simulation. See the references for some more details.
References:

Three-dimensional cell cultures: from molecular mechanisms to
clinical applications.
Recent advances in three-dimensional multicellular spheroid culture
for biomedical research.
Spherical cancer models in tumor biology.
Development of 3D in vitro technology for medical applications.

Very nice answer, cheers!

They are three-dimensional cell cultures according to H Ma et al. 2012.

Multicellular tumor spheroids are one of the classic 3D culture models that can be applied to the development of anticancer drugs and treatments. By mimicking the 3D network of the cellular–matrix and cell–cell interactions, tumor spheroids resemble many aspects of the pathophysiologic environment within human tumor tissue.

Classical cell cultures are usually monolayer. Many of the differences between these cultures and real-life tissues has been overcome by 3D cultures according to Carver et al. 2014.

The multicellular tumor spheroid (MCTS), a three-dimensional model that closely resembles small avascular tumors and micrometastases, has been utilized as an intermediate between monolayer culture and in vivo studies for the screening of small-molecule drugs.

So is it a 'real life' entity or is it something that is computer generated? It is real life. Let's think of an organ. It's made up of a specific tissue(s) and a stroma that contains vascular, nervous and other components that supply nutrients and limit the organ's specific tissue. This structure develops in vivo in 3D. The blood vessels will follow tissue development in a tree-like 3D structure in order to reach to all cells. But what do you do with lab cell cultures? There are no blood vessels there. How do you supply nutrients to all cells? That is why most in vitro cell cultures are developed in monolayer structure. Yet cells are 3D structures. They are joined together in a tissue by intercellular junctions. Monolayer limits this joining to a single plane. Moreover, when it comes to cancer cells which have specific properties (they lose junctions and start to move) the monolayer model becomes limited. This is how spheroids have become a better model for studying in vivo processes using in vitro cell cultures.

So is it a 'real life' entity or is it something that is computer generated? Sorry if the question is dumb but I have no experience in biology so that is all complete jargon to me unfortunately. If you could explain like I'm 5 that would be great!

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


text:
Skin color explanation?
I do not understand how skin color in humans work, even after taking a basic genetics course and reading some on wikipedia.
From what I understand, skin is color based on multiple genes that control melanin and other products that affect appearance of skin. So then their are multiple alleles for "skin color" and also some of these alleles can be varying in their expression/inheritance? based on the other alleles presence?(epistasis)
So then a black person and a white person could have various skin colors (phenotypes?) And the offspring of these children could then have varying offspring as well?
Diagrams would help me maybe in explaining the concept.

I'm still a little uncertain as to where your question lies.  Are you wondering how different melanin types and levels create different skin phenotypes (of any animal, no real reason to limit this to humans), or are you interested in how genetic inheritance effects melanocytes?

I have the same problem. Do you look more into melanin production and how this is regulated or more into the genetic reasons for different skin color?

@AtlLED           Ummm, I want to know the underlying genetic components(how the genes work) more than their product(cells, proteins, etc..)

This is relatively complicated.

@RoSiv So is your question "How do genes work?"

The genetics of pigmentation is relatively complicated, as the pathway for the pigmentation (regulation of the pigment production, ratio between the melanins, maturation, trafficking and distribution of the melanins from the melanocytes to other cells) is quite long and also subject to different regulations. All the mutations found to date (at least to my knowledge) affect single parts of this long process (so for example MC1R mutations are affecting whether eumelanin is made, while Rab7 and Rab27a is most likely involved in the distribution of the melanosomes). Not all gene functions in this network have been understood so far.
Population studies have shown that the three main ethnic subgroups (west-africans, asians and europeans) have developed independently from a common ancestor with different (and independent) mutations in each arm. See the figure from reference 1 as an illustration, it also shows the genes involved in each arm:

Pigmentation is a protection against UV light, so there is a strong selection against mutations in areas with high UV light (west africa for example). The general theory is that in areas with less UV light the skin got lighter to allow the production of vitamin D (for which you need UV light). If you want to go through the single genes and their influence on pigmentation, please have a look at this Wikipedia page, which gives a good explanation. Also have a look at the references.
References:

Unpacking Human Evolution to Find the Genetic Determinants of Human
Skin Pigmentation
The genetics of pigmentation: from fancy genes to complex traits.
Molecular genetics of human pigmentation diversity
Human pigmentation genetics: the difference is only skin deep
The etiology and molecular genetics of human pigmentation disorders

This HHMI Biointeractive Video gives one of the better explanations I have seen on the genetics of Human Skin color. The Biology of Skin Color It is actually the destruction of folate, which is known to lead to birth defects and sperm fitness that selects for Eumelanin in regions with high levels of UV.

Ok, several genes are involved, which increases the combinatory. But still, this should give a finite number of genotypes, and thus of phenotypes, right ? -> is the combinatory just large enough (estimation?) so that we have the false impression of continuous shade ? Or is there something else occurring, making the shades really continuous ?


text:
Do both Carbamazepinum and Lamotriginum increase glutamate threshold?
I have in my notes that:

Carbamazepinum increases threshold for glutamate
Lamotriginum delays release of glutamic acid

I would like to simplify these sentences into a single line. I would like to know if it would be correct to say the following:

both Carbamazepinum and Lamotriginum increase glutamate threshold?
"both affect glutamate function" should at least be correct

Do both Carbamazepinum and Lamotriginum increase glutamate threshold?

Characterizing those drugs.
A = group, B = mechanism of action and C = indications.

Carbamazepinum
A. Anticonvulsant, antiepileptic.
B. Block Na+ ion channels and inhibit glutamatergic neurotransmission. Inhibit sustained repetitive neuronal firing.
C. 1st line of Epilepsy grand mall seizures, bipolar disorder, trigeminal neuralgia.
Lamotriginum
A. Unique antiepileptic.
B. Block Na+ ion channels and inhibit glutamatergic neurotransmission. Inhibit sustained repetitive neuronal firing.
C. 1st line Epilepsy - generalized, partial and absence - all types. Bipolar disorder - depression stage. Neuropathy.

Short answer
Both carbamazepine and lamotrigine are listed as Na+ channel blockers. Carbamezipine's action is mainly associated with inhibition of postsynaptic neural activity, while lamotrigine is thought to inhibit glutamate release. Given that glutamate is the principal excitatory neurotransmitter in the brain, and if you insist of using a one-liner I would go for:

Both lamotrigin and carbamazepine can be said to inhibit glutatamatergic neurotransmission, albeit carbamezipine does so in a non-specific way.

Background
My two most beloved drugs in one question!
First off, this answer is formulated from the perspective of both drugs being used as anticonvulsants in generalized tonic-clonic epilepsies. As anti-epileptics, Both lamotrigine (Lamictal) and carbamezipine (Tegretol) are listed as Na+-channel blockers.
Carbamezipine does so quite specifically, and it inhibits sustained repetitive firing by blocking sodium channels. It does so in a very clever way, as it only binds to Na+-channels of rapidly firing neurons, which is exactly what makes it a good anti-convulsant (Courtney & Etter, 1983). It also is believed to have anticholinergic, central antidiuretic, antiarrhythmic, muscle relaxant, antidepressant (possibly through blockade of norepinephrine release), sedative, and neuromuscular-blocking properties (Drug bank). Hence, your note that it increases the threshold for glutamate is true in the sense that it is likely to increase the firing threshold of glutamate-activated neurons.
However, note that carbamezipine (nor lamotrigine) does not increase the threshold for glutamate - glutamate has no threshold and hence it cannot be raised. It is incorrect word use.
Lamotrigine is also listed as a Na+-channel blocker, but the exact mechanism(s) behind its anti-convulsive and mood-stabilizing effects are unknown. In vitro pharmacological studies suggest that lamotrigine's inhibiting effects on voltage-sensitive Na+ and/or Ca2+ channels stabilizes neuronal membranes and consequently modulates presynaptic transmitter release of excitatory amino acids (e.g., glutamate and aspartate). It has also been shown to enhance K+ currents and GABA-ergic inhibition (Coulter, 1997). Hence, your note that it decreases glutamate release is correct.
References
Coulter, J Child Neurol (1997); 12: S2-9
Courtney & Etter, Eur J Pharmac (1983); 88: 1-9.

What do you think about this? Block Na+ ion channels and inhibit glutamatergic neurotransmission stimulating GABA and balancing neuronal excitation and inhibition. I try to make a short one-linear about their common general functioning.

I don't think carbamezipine is generally associated with the GABA system, you have to be very explicit here.

It says it may involve GABA A/B in the mechanism of action here https://pubchem.ncbi.nlm.nih.gov/compound/2554#section=Mechanism-of-Action What do you think?

In lamotrigine, only in vitro studies about GABA here https://pubchem.ncbi.nlm.nih.gov/compound/3878#section=Mechanism-of-Action The exact mechanisms of both these systems are not known. How would summarize this?

I think the question now is: what disease are you looking at? In my answer, I assumed a focus on epilepsy, since the combination of CBZ and lamotrigine is a very successful one. The GABA effect listed is under neuralgia. Both drugs are 'dirty' drugs and will affect many many systems. The question becomes in which context you are comparing them. Again, in my answer, I reasoned mostly from the anti-convulsive perspective.

Again, I wouldn't focus on GABA when talking anti-convulsive therapy.

GABA drugs are contra-indicative for generalized tonic-clonic seizures.

@Masi - thanks for bringing this up - I have adapted my answer intro to specify the pitch of my answer.

I added my summary about those drugs in the body: group, mechanism of action and Indications. Do you agree? I do not know if I can write so many indications if then the mechanism of action is enough general. I am very uncertain about the groups. CYP-450 inductor does not sound good in the first drug.


text:
Does homeopathic or herbal treatment of cancer have any scientific recognition?
Even though we have a very high tech society, cancer is still a serious issue. We humans still are not entirely capable of fighting cancer.
Radiation and chemotherapy are still considered the best methods for treating it and frequently, even these don't work. And, as for this disease, it is a phenomenon of uncontrolled cell growth that has lead to the death of many people. Within these main two treatments, there is plenty of controversy surrounding applying radiation and chemo in a proper sequence.
However, there are also some different methods known and available on the market to treat cancer. Among them, homeopathic and herbal treatments are the most common. So, my question is, do they really work and is there any scientific evidence of that?  If yes then what is it?

Actually modern treatments do not fail most of the time. They most often fail in metastasized tumors - if you catch the primary tumor early enough it is usually removed and the patient can be completely healed. Additionally there is medicine (everything which has an effect) and there is pseudomedicine (everything which claims to have an effect but cannot proof it. Homeopathy and herbal medicine (unless you isolate some pharmacologically active agent from the plants) belong to the last category and don't have any scientific foundation.

While the question is not off-topic, you'd probably make a better fit (and get better answers) on skeptics.SE.

The methodology behind homeopathy is scientific nonsense.  If you dilute anything a billion times, it will have no chemical effect, not even if you shake it all the while.  So no, homeopathy does nothing for cancer, or any medical condition at all.
Of course plants can have active compounds in them, once scientists have identified those compounds, they can be tweaked to make them act better in the human body, and then manufactured under strict guidelines to ensure purity, and tested to determine the optimum dosage; then it's just medicine.  Taxol comes from yew trees, it doesn't mean that native herbalists were successfully treating cancer with it for hundreds of years.  Native herbalists were using willow bark, which contains salicylic acid, which has anti-inflammatory properties, but chemists improved on it, reducing some of its negative side effects, by modifying it to acetylsalicylic acid.
Millions of people get cancer.  Doctors get cancer.  Herbalists get cancer.  If curing cancer was as easy as mixing some leaves in a poultice, people would do that.

The worst thing is that a lot of these quack doctors explicitly tell people that the conventional (western) medicine is dangerous and only their medicine works. While a lot of western medicine is pushed to market by profit-driven drug companies, still a significant proportion are actually effective. In contrast, no homeopathic treatment can ever be effective, and herbal treatments are in general less effective than maintaining a healthy lifestyle!

The short answer: no.
The for-profit pharma companies that so many people love to slam for profiteering? On the other side are insurance companies who want to pay the absolute minimum they can. If there was a cheap plant or mixture of plants that scientifically showed significant success in stopping cancer, the insurance companies would demand its widespread use and stop paying for pharmaceuticals.
Homeopathy is (with few exceptions) ineffective at best and downright dangerous at worst. Most "homeopathic medications" are unregulated (at least in the USA) and unscreened - you have no idea what's going in them, and you have no guarantee that the content is what the bottle says.
A few years ago there was a study done on herbal alternative medicine and the findings were that plenty of these supplements didn't even contain what was advertised. The worst offenders actually substituted known toxic plants for the claimed product.
Even if the product is genuinely what's advertised, there can be processing and purity problems. Recently there was a news article about some people who were severely sickened after drinking improperly processed aconite (wolfsbane) herbal tea bought in a traditional Chinese herbal medicine shop.
The final (rhetorical) question to ask the quacks pushing their homeopathic crap: If ancient medicinal practices are so good, then why was life expectancy back then (and even now the areas where such practices remain in wide use) so low? And if Western medicine's so toxic with all of its side effects, why does the countries that practice Western medicine standards almost always have the best life expectancies?
You can't argue with results - and for all its shortcomings, Western medicine delivers far more than any other known medical practice on the planet.


text:
T7 Tagging in Synthetic Biology
What is a T7 tag and can if be used to purify synthesized proteins? Is it charge based like a His tag?

The T7 tag is the first 11 amino acids of the T7 gene 10 protein. Basically, if you engineer a protein with the T7 tag, you've engineered a small, known epitope to the protein of interest which may be detected immunologically. The small size of the epitope reduces the chance it will disrupt the protein's normal function (to which it's tagged). If we look at the affinity purification kit on the following product page we can see that specific vectors can be used to express T7-tagged proteins, and an immunoaffinity column can be used to purify the protein of interest. The T7 tag chemical structure is denoted here.

It also allows the discrimination of engineered protein from in vivo expressed proteins and you don't have to make specific antibodies for each protein but use antibodies against the t7 tag instead.

What makes it different from the FLAG-Tag? (Besides sequence of course)

I don't have any data on how each epitope may affect stability or what have you, but it generally follows that whether it be T7, FLAG, HA or Myc etc. they're just method of recognition through the use of an anti-tag antibody (anti-HA, anti-FLAG, etc.) in immunoassay.


text:
How does visual sexual arousal work between the eyes, brain, and genitals/gonads?
When many people look at sexual images, they often can become sexually aroused, including full genital arousal, and feel urges, known more often used as "horny" as slang/urban usage.
How does this process work in males and females? Is it different in males than in females, or is the network the same between the eyes and the brain, down to the genitals as a precursor to masturbation, sex, etc.? Also, what exactly happens in the brain before it tells the genitals to get horny or such? Examples would be in viewing porn, naughty images/pics, etc.
Men and women and girls and boys alike can get full arousal from this. How does the process work?

This is not opinion based. It is a little broad though. Please edit your question; if it can be worded properly then it is on topic.

Sexual arousal is a very complex response, that includes a whole range of physiological changes, firing of lots of neural pathways, increased muscle tension, elevated heart rate  with increased blood flow to the skin, primary and secondary sexual organs and a whole lot of hormonal spikes.

Sexual desire is defined as the behavioural drive that motivates individuals to fantasize about or seek out sexual activity. In contrast, sexual arousal is defined as the autonomic physiological processes that prepare the body for sexual activity (Toledano, Pfaus., 2006).

The brain is rightfully regarded as the largest sexual organ, with most of the pleasure arising from the limbic system of the brain (which interestingly enough, is common to all mammals  regulating emotion and encouraging the avoidance of painful of aversive stimuli and the repetition of pleasurable experiences).

From a physiological perspective sexual arousal is controlled by the parasympathetic portion of the autonomic nervous system and manifests itself as vasodilation in sexual organs along with several other physiological phenomena including an increase in heart rate. An orgasm and in particular male ejaculation is controlled by the sympathetic portion, this is also accompanied by deactivation of many areas in the brain relating to external stimuli in particular fear, allowing the mind to focus on the task at hand.

Now it is a bit long to go into the details of the sexual response cycle, and hence here is a brief summary:
Neural pathways:

Prior to the physical stimulation, comes sexual desire. Largely mediated by emotion through the limbic system, activation of the amygdala can trigger penile erection, sexual feelings,(Georgiadis and Holstege, 2005) sensations of extreme pleasure (Olds and Milner, 1954), memories of sexual intercourse (Gloor, 1986), as well as ovulation, uterine contractions, and orgasm.

The amygdala is sexually differentiated part of the brain that is known to produce sex specific responses. In short the amygdala has a pathway (amygdalofugal pathway) that connects with the major regions of the brain that regulates sexual feelings. An increased density of enkephalins and opiate receptors can be also found in amydala, which induces extreme feelings of pleasure.
interestingly...

Males more then females, were found to have greater amygdala activation when presented with a sexually pleasing, visual stimuli (Hamann et al., 2004).

Moving on, other areas of the brain implicated in sexual arousal are...

Input travels from the basolateral nuclei of the amygdala along the amygdalofugal pathway to the ventral striatum, made up of the nucleus accumbens, putamen and parts of the caudate nucleus. The nucleus accumbens plays a role in pleasure and reward due to a large large of dopaminergic neurons from the VTA (ventral tegmental area).
The Vagus nerve is known to lead to the Nucleus Tractus Solitarii (NTS) in the Medulla Oblongata.  Following this stimulation of the brain via the vagus nerve during orgasm there was a difference in activity between preorgasm and orgasm. Areas of activation during and after orgasm include the hypothalamic paraventricular nucleus (PVN), midbrain central gray, amygdala, hippocampus, anterior cingulate, frontal, parietal, temporal and insular cortices, anterior basal ganglia, and cerebellum (Whipple, 2008). Although this may be the explanation for female orgasms, there is no evidence to suggest that this is the case for males.

Hormonal changes:
I am not going to write too much about this as this information is readily accessible in the net. Sexual arousal causes the cerebral cortex to signal the hypothalamus to stimulate the production of testosterone, the production is regulated by a complex chain of events known as the hypothalamic-pituitary-gonadal axis, which ultimately causes the pitutary gland to release luteinizing hormone which signals the testes to produce testosterone and ovaries to produce oestrogen.
You can read more here: http://neurosciencefundamentals.unsw.wikispaces.net/Sex+and+the+Brain.+What+parts+are+involved%3F
For an in-depth analysis I recommend this book:
Greenberg, Jerrold S., Clint E. Bruess, and Sara B. Oswalt. Exploring the dimensions of human sexuality. Jones & Bartlett Publishers, 2014.
This is a good review for endocrinology in sexual arousal:
Bancroft, J. "The endocrinology of sexual arousal." Journal of Endocrinology 186.3 (2005): 411-427.
As usual, wikipedia also covers a few models of sexual arousal (Singer, Basson's etc..) that I have not mentioned here: http://en.wikipedia.org/wiki/Sexual_arousal


text:
T7 Tagging Next to Met
Will a T7 tag still work if it is placed next to a start codon? Meaning, will it still work with a Met attached to it in the amino acid sequence?
Thank you!

Homework questions are off-topic unless you show some effort solving them yourself. Not doing any research yourself is the same.

This isn't a homework question. We are an undergraduate research team (iGEM) asking a question as we need to know this to design our research project. I just worded my thoughts very clearly, no teacher nor professor wrote this.

Then you should probably explain this better in your question. Otherwise it might be closed.

@Kathryn if your team cannot find any local resources to answer your questions about designing your research project you may find the New England Biolabs Catalog a valuable resource with lots of plasmid maps and bacterial strain genotypes. If you have access to a research lab they very likely have some molecular cloning manuals and and lab recipe books that could also be valuable. Based on my brief experience here It seems like actual homework questions risk portraying the questioner as "too lazy to do it themselves". If you have a larger goal then disclosing that at the outset may help

By "still work" I assume you are asking if it will still be recognized by an antibody? It might. Internal T7 tag fusions are done, though they may require different antibodies than terminally tagged fusions.
That said, do you have a reason for inserting the the tag after methionine? The T7 tag already starts with methionine and naturally functions to initiate translation of T7 gene10. pET based vectors also contain it for this purpose.

[source]
In this vector, your gene of interest is typically inserted after the tag to create a fusion protein (using BamHI) or immediately after the start codon (using NheI). In either case, the T7 tag start codon is used.

Thank you very much. We didn't know that the T7 tag contained a methionine, and we were placing this tag after a stop codon, so we assumed we needed to place it after a start codon (Met).

You need a ribosomal binding site before the initial codon.

Or I am mistaken about what is asked...

This is more of a comment and you have enough rep to do so


text:
Plasmid: Empty Backbone?
When searching for a plasmid on Addgene what does it mean if it is said to be an "empty backbone"? Why would one want an empty backbone?

If you look on a very basic plasmid map, you usually see three different features: An origin of replication (often abbreviated ori or origin) which is necessary for the replication of the plasmid, a resistance gene (not necessary but useful to select for) and and multi cloning site (abbreviated MCS) which contains a number of unique restriction enzyme recognition sites, see the figure (from here):

In molecular biology plasmids are used to overexpress proteins in bacteria (or other cells) which are of any interest. To do this, you bring in the coding information for this gene into the plasmid using the MCS. Here you can cut the plasmid controlled (only open the ring on one site) and insert DNA of interest. An empty plasmid in this context means that it can readily used for cloning purposes as it does not contain any foreign DNA.

cause you want to put your own stuff in without worrying about other people's junk interfering with your stuff.
Something like why would you want an empty hard drive and not one which is almost full with stuff from somebody you don't know.


text:
Why Pan_troglodytes-2.1.3 Assembly renamed as a Pre in ENSEMBL?
I began working with panTro3 assembly of the UCSC. This assembly corresponds to CGSC Build 2.1.3. See here: https://genome.ucsc.edu/FAQ/FAQreleases.html
Now, I have to cross annotations with ENSEMBL (Indeed, I need to use Biomart tool: http://www.ensembl.org/biomart/martview/2e4aac505f5cf5e0ac255b4a215a056c). But It seems that between Release 64 and 65 they passed directly from Chimp 2.1 to Chimp 2.1.4. I researched some information and found that Chimp 2.1.3 renamed as a Pre! See here: http://pre.ensembl.org/Pan_troglodytes/Info/Index and here http://www.ensembl.info/blog/2011/06/10/new-pre-site-for-chimpanzee/
Is it a way to solve this problem? How may I use Chimp 2.1.3 assembly in Biomart with GrCh37 as reference genome (I was using an archived versions of the Ensembl: http://grch37.ensembl.org/biomart/martview/cbe191dccbe8e5a314cfebeaa8862ca0), but seems not possible to cross between different releases of the ENSEMBL.

Not that Bioinformatics is off-topic here, but you might get better answers over at Biostars, as they are dedicated to bioinformatics. There are not so many around here.

There may be other ways. Please [edit] your question and explain what you're actually trying to do. What do you mean by "cross annotations"? Do you want to find homologous genes? Syntenic regions? If you tell us what you need, we might be able to help without BioMart.

@Chris, is bioinformatics off-topic? Or do you mean programming/software related problems? I couldn't see anything about this in the help pages.

@ddiez That's what I am saying, bioinfiormatics is not off-topic. But still you might get better answer at biostars. Just for complementation.

@Chris sorry! I read "note that bioinformatics is off-topic here". My brain decided to complete "Not" to "Note"!


text:
Why do we do nested PCR?
Wikipedia:

Nested polymerase chain reaction (Nested PCR) is a modification of
  polymerase chain reaction intended to reduce non-specific binding in
  products due to the amplification of unexpected primer binding sites.

I understand that there are two steps and one of those steps involves a non-specific primer followed by a specific primer...
But this does not seem to have sense. What is the purpose of running a non-specific PCR just to hit it with a specific primer afterwards?
What do we gain when doing a nested PCR?
Practical example:
We are planning on sequencing human skin microbiome. Would the ratios of different bacterial species differ if we would use the nested PCR products for sequencing, as compared to standard PCR?

If your initial template results in multiple amplicons that cannot be removed by increasing annealing temperature, nested pcr can reduce these amplicons when coupled with a gel extraction.

To extend on @MarchHo comment, nested PCR is used for the amplification of a target when too many non-specific fragments are produced by direct PCR. Usually you would use a nested PCR when 1) the sample is complex (multiple DNA sequences) and your target is present in a very small amount as the target would not be amplified otherwise, or more precisely a direct PCR would produce way too many non-specific fragments. 2) When you have many non-specific fragments as a first PCR amplification enriches your "real target" sequence.

Thanks cagliari. If you could write it as an answer then I would gladly accept it, because it answers my question

In the paper by K. Lily Therese, U. Jayanthi & H.N. Madhavan traditional PCR wasn't sensitive enough to allow for an accurate reading on what they were trying to study. By using nPCR they were able to amplify around the gene they were interested in and then amplify just the gene they were interested in for a more accurate and sensitive study. The successive PCR allowed them to amplify their specific gene even if there was only one copy in the sample.
I recall using this procedure in Molecular Genetics Lab, it was used to make sure that our sample was purer.

It may depend on which protocol you looking at, but you can use a specific primer set for the first PCR and another specific primer set for the second PCR.
Even if you use a none specific primer set for the first PCR, it could be easier to amplify your target sequence because your target sequence would be more abundant than the original solution before the first PCR is performed.


text:
How does coconut water solidify into hardened coconut meat?
At first, the coconut is filled with liquid endosperm. Later when it ripens, the outer layers form brown fibrous covering, and the inner solid layer turns brown and hardens. Within that, a white layer forms (which is soft and thin at first and then gradually hardens and thickens). After ripening, there is a white layer with very little fluid. So, it's gotta be the liquid endosperm which has hardened over the course of time to form the white layer. So, how does it harden?

is it just an aqueous solution?  if so, evaporation?

@dbliss How does liquid evaporate in closed environment? And how does the white layer form due to evaporation?

The hollow nodes of bamboos also contain air-filled cavity.

There are three types of endosperms encountered in botany - nuclear, heliobial and cellular. The endosperm of Cocos nucifera is both special and interesting.
Initially, the cocunut is a nuclear liquid endosperm. Meaning, it is a coenocytic liquid tissue with lots of rapidly dividing nuclei. The reference I cite here (although pretty old), states that it is safe to assume the fluid to be the 'sol' phase of cytoplasm. At some point, gelification of the sol surrounding the nuclei occurs and cellular boundaries start to appear.
These cells and nuclei start to settle down on the endothelium (inner lining of the integuments) and the cells divide to produce a columnar sort of a covering over the it. This is what forms the characteristic coconut meat. Development of the cellular endosperm is by coalescence of these deposited cells and nuclei at the antipodal end (bottom end of the fruit) and continues towards the top end. You might have noticed that the meat is thicker at the bottom but thins out towards the top.
The cells right above the endothelium stay meristematic for a long time while the columnar cells on top of this meristematic layer grow radially inward.

If the terminology seems confusing, the bottom end is the antipodal end. End. in the diagram stands for endosperm - the coconut meat. The Sh. is for the shell, which is the thickened inner integument. The inner lining of this shell has been referred to in this answer as the endothelium. Mic. stands for micropyle where the stalk (pedicle)  of the fruit is. It is at the micropylar end that the embryo is placed. Remember! The coconut meat is not the growing embryo.
How does the meat harden?
As said, initially the deposited mass of cells and nuclei is jelly like and slowly hardens after proper cell wall synthesis etc. The hard white coconut meat that can be grated, is end stage of maturation and is formed when the above said tissue architecture has been established.
What happens to the coconut water?
After the cellular endosperm has reached its final state a little water is still left in the coconut. This water is opalescent compared to the clear water found in younger fruits. Interestingly this water is now totally devoid of nuclei.

Whether the decrease in liquid is the result of its incorporation into the endosperm cells or due to evaporation due to drying and cracking of the pericarp remains uncertain.

Sorry for the anticlimax. But this has been quoted from a 1955 paper. I was unable to find newer papers. Little work has been done in morphological botany in the recent past, but I'm pretty optimistic the answer would lie somewhere in literature.
References:

V.M. Cutter, Jr., K.S. Wilson and B Freeman. Nuclear Behavior and Cell Formation in the Developing Endosperm of Cocos nucifera. American Journal of Botany (1955), 42 (2), 109-15.
A. Abraham, P.M. Mathew. Cytology of Coconut Endosperm. Annals of Botany (1963), 27 (3): 505-512.
The Hindu (2002) : Mystery behind coconut water, R. Subramaniam.

Coenocytic is used when there are multiple nuclei where cytokinesis is not followed by karyokinesis. In a syncytium too, multiple nuclei are found but here, it is formed by fusion of cells leading to loss of their boundaries. This terminology is used quite loosely in literature.

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


text:
Is the amount of dNTPs rate limiting for very long PCR products?
I'm using the Q5 system and I'm PCRing a product that will have a final length of around 9500 bases. I have noticed that the product is there but very faint. The primer seems to be used up.
So my question is, can the dNTPs be rate limiting in a long reaction? That is, can all the dNTPs be used up in the first PCR cycles and maybe not be available for the later exponential rounds?
It seems you have about 1000 times the amount of dNTPs to the amount of primer (200 µM compared to 0.2 µM). So maybe...or is my basic chemistry off. Any precedence?

IIRC Q5 requires 0.5µM of each primer as mentioned in documentation. In any case, why not just add more dNTP if you suspect it to be the cause?

I am doing that now. But like anything in Biology, I'm sure there are consequences of adding too much.

Add controls in if in doubt

Yes it is possible. dNTPs can also get degraded at high temperatures. Therefore they are added in excess. You can add more and as long as you are not doing real-time PCR don't worry too much about smeary/multiple bands. You can always do a re-PCR.

Adding too much dNTPs can cause problems. They bind magnesium from the reaction buffer, so if you are going to increase the amount of dNTPs drastically, you will have to optimize the reaction again for magnesium.

200uM dNTPs in 50ul reaction mix could produce more than 10ug DNA if all dNTPs were consumed whatever the length of PCR products is. You could detect as low as 5ng DNA fragments by conventional electrophoresis using EtBr. You probably could see a clear band when you load more than 100ng of a DNA fragment. Therefore I am not worried much about the dNTP concentration.
The longer PCR products you amplify, the more difficult it is to amplify. Then you may not get enough efficiency to detect your PCR products. You might want to try lower annealing temp if you do not get any none-specific bands with/without some additives such as DMSO, betain, etc., or use more stronger enzymes. Also touch down PCR may be useful to get specific bands efficiently.
When you increase dNTP concentration, Mg++ effects may be muted because dNTP could chelate Mg++ as Chris mentioned in the comment column.

What do you mean by "stronger enzyme"? Q5 is one of (if not the) best commercially available DNA polymerases.

Oh, I am sorry, I missed that part... Of course, Q5 is one of the strongest. But, it does not mean that other enzymes are not useful. So still, you have a chance to get more PCR fragments by other enzymes such as primestar.


text:
What's the name of this flower?
I photographed this flower in Central Europe. I looked in online databases but can't really identify the actual flower, since there are so many that look quite similar. Can you help me? What's the name of this flower?

It looks like the common Geranium sylvaticum (also called wood cranesbill or Mayflower), and it is at least a close relative (member of the Geranium genus). This plant is commonly found across Europe and in parts of Asia (see map below), and it is sometimes planted in gardens. It is a perennial herb that grows in many types of habitats (woods, meadows, road sides, mountain areas), and the flowers are most commonly violet to blue, but can also be white. Geranium pratense is very similar, but usually has more narrow leaf lobes and bent flower stalks. However, it might not be possible to separate these two species based on your picture.
There are also similar relatives found in North America (e.g. Geranium maculatum) and Asia (e.g. Geranium himalayense) and many hybrids of plants from within this genus are cultivated.

(picture from Swedish Wikipedia)

(distribution map from the Swedish Museum of Natural History: Den virtuella floran)

Superb example of a good answer to an ID question!

@Oreotrephes Thanks. The same species is just about to start flowering in my garden.

My guess would be the meadow cranesbill (Geranium pratense), see this image (from here, more images are available there):

The flower is quite common on meadows in europe, see here.

This is certainly a possibility, and I have updated my answer to explain why I feel that G. sylvaticum is a better fit.

@fileunderwater I think we can be pretty sure that it is from the genus Geranium :-)


text:
What does the energy in an energy pyramid represent?
Suppose the energy at the second trophic level as given in an energy pyramid is 100 kcal per square metre. It could mean either of the two following things:

100 kcal is the energy this primary consumer has stored in its flesh - that is, the energy left over from the amount consumed, after assimilation and respiration. This would be the net productivity of that consumer, or the energy available to the secondary consumer which feeds on this.
100 kcal is the energy this primary consumer consumes. It will utilise a part of this in respiration, lose some amount in assimilation, so that a small amount is left over which is then stored in it as mass, or flesh - which would be its net productivity.

Similarly, the first trophic level, the autotrophs' energy could represent either the total amount of food they make (the GPP), that is, the energy akin to the second case above, or the energy stored in them and available to the next trophic level (the NPP), like in the case 1 above. So which of these is correct - what do we represent as the energy of a trophic level in an energy pyramid? I think it should be the first case, the stored energies, since after all these are what you will measure as the energy of any trophic level - the stored energy at that level.

Each layer in the energy pyramid represents the stored energy in biomass in that layer. This energy is obtained from the previous layer. Because every layer uses a certain amount of energy needed for survival (combustion of sugars and fats through respiratory processes) obtained from the previous layer, each subsequent level is smaller than the previous one. Also, the autotrophs in the photosynthetic layer use up (solar) energy for living. The higher up you get, the more energy is cumulatively taken away to sustain life and growth of the previous layers. Therefore, it's a pyramid shape.

Energy pyramid. Source: Biocab


text:
What ways are there to determine how big genera are?
I want to look at genera as a whole, across the animal kingdom to determine the range of sizes of genera. I have examined species richness and genetic diversity (pairwise distance from sequence data sets), but I am looking to find more ways to look at 'how big is a genus?' in terms of biodiversity. Any ideas or comments are greatly appreciated!

Or even species delineation techniques that could be used for genera?

If you are you aiming to compare genera widely across families and orders, you should consider that taxonomic levels (such as genus) are used very differently between orders. This means that taxonomists are using quite different criteria to delimitate genera, so the differences you might observe would probably be caused by these different definitions/criteria as much as "actual" differences.

Bearing in mind that the information is bound to be incomplete (as is the list of existing species), you could use the NCBI taxonomy database. For example, checking the page for the Drosophila genus will give you an idea of its size.
For more precise numbers, you can download the taxdump.tar.gz file from NCBI's FTP server (link), extract it and run the script below on the file nodes.dmp (a dump of the database info).
#!/usr/bin/perl
use strict;
use warnings;
use Getopt::Std;
my (%opts,%children,%ranks);
getopts('t:',\%opts) || do { print STDERR "Invalid option"; exit(1); };

my $taxid=$opts{t}||die "Need a taxid: -t\n";

sub getchildren{
    my $p=shift; ## The taxid of interest
        my $found=0; ## will be 0 unless we find a new kid
    ## For each child of this taxid
    foreach my $kid (keys%{$children{$p}}){
     ## Get the kid's kids
     foreach my $gkid (keys%{$children{$kid}}){
         ## If this one hasn't been seen before
         unless (defined($children{$p}{$gkid})) {
      ## Add it to the list of this taxid's children
      $children{$p}{$gkid}++;
      ## We found a new one, we need to test again.
      $found=1;
         }
     }
        }
        ## If we found a new one, run again
        getchildren($p) if $found==1;
    }
    while (<>) {
        ## Remove trailing newlines
        chomp;
        ## Parse the current line
        my ($name,$parent,$rank,$rest)=split(/\s*\|\s*/);
        ## Save the current taxid as a child of its parent
        $children{$parent}{$name}++;
        ## Save its rank (species, genus, order etc)
        $ranks{$name}=$rank;
}

## Recursively get all children of this taxid
getchildren($taxid);

# Count only species as children
my @kids=grep($ranks{$_} eq "species", keys(%{$children{$taxid}}));

# Print out the results
printf "Genus %s has %s members\n", $taxid, scalar(@kids);

Assuming you are on or have access to a *nix environment, save that file as genus.pl and run it on the nodes.dmp, giving the taxid of your genus of interest:
perl genus.pl -t 9257 nodes.dmp

The output of the above example (Ornithorhynchus) is:
$ perl genus.pl -t 9257 nodes.dmp
Genus 9257 has 1 members

If we try on Drosophila, we get:
$ perl genus.pl -t 7215 nodes.dmp
Genus 7215 has 738 members

This is realy not the most efficient way to do it (far better to do this in the script itself but I don't have the time to implement that now), but if you don't mind waiting, this will give you the numbers for all genera:
for i in $(grep -w genus nodes.dmp | awk '{print $1}'); do
        perl genus.pl -t $i nodes.dmp;
done

Genus sizes are usually measured in number of species, since a particular species under a single taxonomic authority shouldn't be found in more than one genus. Check out Strand and Panova, 2014 for some numbers on number of species found in each genus on average across several thousand genera from eight major taxonomic groups.


text:
What are these pathways called in Biology?
Considering the pentose phosphate pathway and the sulfate reduction pathway in bacteria;
What are these types of reactions called in biology? Bio degradation reactions or bio transformation reactions or something else? I wish to know whether there is a generalized names for these types of pathways.

They usually have specific names - your example is the pentose-phosphate way (or pathway).

is there no generalized names for such pathways?

If you want it short: Pathway. Otherwise you could think about metabolic pathways or the specific names.

so these types of chained reaction like pathways have no special names...

The special names of these chained reaction like pathways is metabolic pathways. This is it. For the first time in science, something actually has an intuitive name.

Metabolism is the term for all biochemical reactions. Degradative pathways (big to small molecules) are called catabolism and constructive pathways are called anabolism.

Short answer
Assuming you wish to have a common name for both of these (widely differing!) pathways I basically agree with @Chris, and I would go for general terminology, namely metabolic pathways.
Background
The pentose-phosphate pathway is neither anabolic nor catabolic so those terms won't do. The pentose-phosphate pathway is, however, closely linked to general metabolism to supply the body with C5 sugars. So metabolic pathway sounds right to me.
The other pathway is a sulfate reduction pathway, which is an anaerobic respiration pathway that uses sulfate as the terminal electron acceptor instead of oxygen. It is an entirely different pathway. However, it too is neither catabolic or anabolic, but still closely linked to metabolism. Hence, metabolic pathway is applicable here too.


text:
Species ID: Buckyball-like fungus
Previous research

A friend of mine shared a link of some beautiful fungi: https://i.stack.imgur.com/B81Pu.jpg. I was intrigued by the curious critter below -- it seems to have honed the power of buckyball geometry, presumably much before we Humans ever did (search: Buckminsterfullerene to learn about a feat of chemical engineering).
Google reverse-image search almost got me the answer I needed, but no species name.
I've asked friends on Facebook with no answers yet.

Question
What is the name of this species of fungus?

Related Questions on Stack Biology

Here's a related Species Identification question of a fungus: Puffball mushroom species ID? (by @rg255)

EDIT: I'm an idiot... the Imgur had species names, thus answering my question, post-mortem. Thanks @skymningen for pointing that out.

If you like the general idea of how wondrous mathematics in nature can be, read "What Shape is a Snowflake?" by Ian Stewart. It's a nice read, I loved it as a youth and I blame some of my fascination for biology to this book.

I understand the face palm, but it might be more useful to future readers if you change the title again.

@AtlLED, I'm not quite sure what you mean? As in to add the species name?

The question would appear as "answered", and @Ilan did technically answer it before I read the comments. I would suggest you voting to close my answer down, let the community decide.. I was about to delete it but then I read the deletion message

Sorry, I mean the top heading title not the question title.  The "Edit: I'm an idiot..." part is kind of jarring.  I don't think it needs to be deleted.  Maybe a more subtle note after the link?  Anyway, I guess this is more of a style point so feel free to ignore.

Almost same-looking: http://biology.stackexchange.com/questions/20553/is-this-a-plant-or-a-fungus

@skymningen so so wonderful

@skymningen, I am intrigued: why did you use the word "blame"?

@hello_there_andy I am not a native english speaker. Connotations of words might be different in my native language. It was supposed to be a cheeky comment.

I see @skymningen

Looks very similar to Clathrus ruber fungus.
Be careful, it is poisonous.

Actually... the link the OP gave has named pictures and it was also named as Clathus ruber there. So I guess you got it right.

@skymningen I didn't use the link in question. Hm, nice to know.

@skymningen thanks for pointing that out... I genuinely didn't notice those... *facepalm*... *re-edits the question*

@hello_there_andy Happens. Without that question I would have never known this interesting fungus!

Who knew fungi could be so... fun. Sorry that pun had to be done. @skymningen


text:
How is genetic speciation defined?
What determines speciation at a molecular level?
At what point does a scientist determine two lineages are different enough to be considered separate species?
Does it have a margin of error?

FYI, the term genetic speciation does not exist. It is just speciation. But one can use genetic tools to estimate divergence between lineages and eventually base its concept of species on those data.

As you probably know, there exists many different species concepts (or definitions of species). Often, you see a separation into at least six different categories of species concepts, which are then often subcategorized futher (and they can also overlap to some extent), namely:

Biological species concept
Phylogenetic/cladistic species concept
Evolutionary species concept
Ecological species concept
Cohesion species concept
Morphological/Phenetic species concept

Broadly, these groupings show up in different forms in e.g. Futuyma (1998), DeQueiroz (2007) and Mallet (2007). The Wikipedia page on species concepts also provides a useful overview.
The biological species concept is probably the most well-known, but is very difficult to apply for many organisms, due to for example lack of knowledge (we know very little about the reproductive biology for most species of earth), their breeding system or maybe because we are dealing with extinct organisms. Your question is most closely connected to the phylogenetic/cladistic group of species concepts, which aims to delimit species based on lineages/clades/monophyletic groups, often using molecular phylogenetics for inferences.
I don't know the literature of the phylogenetic/cladistic species concept well enought to answer your question fully, but I know that there exists multiple ways to delimit species within this group of species concepts. The most "extreme" forms/interpretations state that a species can be any monophyletic group with inhereted characteristics that you can diagnose, and this can lead to very narrow species definitions and "splitting" of one species into several. However, more conservative definitions look at e.g. monophyletic gene trees, where several geographic subspecies can be grouped withing the same species.
All-in-all, I don't think it is possible to give a definite answer to your question "At what point does a scientist determine two lineages are different enough to be considered separate species?". It depends on the species concept that is used, and how this is interpreted by the taxonomists conducting a specific study. Also note that phylogenetic/cladistic species concepts are related to the idea of Least-inclusive taxonomic units (LITUs, see Pleijel & Rouse, 2000), that aim to partially separate "species" from taxonomy and instead only consider taxonomic units, based on current knowledge.
References:

Futuyma. 1998. Evolutionary biology. Sinauer.
DeQueiroz. 2007. Species Concepts and Species Delimitation. Syst.Biol. 56
Mallet, J. (1998).  Species concepts.  In Calow, P. (ed.) Encyclopaedia of Ecology and Environmental Management. Blackwell Press
Pleijel & Rouse. 2000. Least-inclusive taxonomic unit: a new taxonomic concept for biology. Proc Biol Sci. 267

@AliceD I don't know about superior, but maybe a bit more comprehensive. Hopefully, somebody that is actually involved in taxonomic work using molecular methods can provide a more specific and detailed answer.

Speciation in sexually-reproducing organisms can be identified as the inability to produce viable offspring. In other words, when two suspected sub-species are not able to produce viable offspring, they can be considered to be two species. In this case it is not so much determined at the molecular level, but at the organismal level.
This mating procedure does not work in asexually reproducing species. In this case molecular techniques are needed. Navarro & Barton (2003) investigated what the molecular differences were induced by evolution by comparing the genomes of humans and chimpansees. These two species diverged relatively late in evolution and their DNA differs by about 2.1%. It turned out that the main differences between the two genomes were clustered around regions where chromosomes were rearranged. Although indicative of the cause of speciation, it can nonetheless also be the result of it. We can never be sure.
Reference
- Navarro & Barton, Science (2003); 300: 321-4

AFAIK, the test for speciation  is a genetic cross, or mating. If two individuals can mate to produce fertile offspring then by definition they are both members of the same species. The converse is also true (at the population level). Back in the 1970's experiments were done where fruit fly siblings were separated (reproductive isolation) for 10 generations, the resulting progeny (10th cousins), could no longer cross-breed.

I think this answer is taking a much too narrow view. Most taxonomic work is not using the biological species concept in operational terms (but it might be assumed implicitely), instead focusing on molecular phylogenies and the morphology of organisms. It is seldom that the biological species concept can actually be tested, even though it is important from an evolutionary perspective, and for most named/described species on earth the ability to interbreed has not been explicitely considered or tested.

The genus Rhododendron has been divided into some 900 plus species. Often these species hybridize in nature creating what are called hybrid swarms. Although most Rhododendron species are diploids there exists tetraploid, hexaploid, octaploid, and decaploid Rhododendron species. Contact zones between Rhododendron species containing diploid and tetraploids often result in triploids. Some of these triploids are semifertile and able to interact with both the diploid and tetraploid populations.
Man made hybrids between Rhododendron species can be very complex and multi-generational. Man made hybrids have created triploids and tetraploids using only diploid species. Hybrids can be created between the origin diploid species and the man made triploids and tetraploids.
Genetic studies of closely related Rhododendron species suggest that at least some evolution in Rhododendron is reticulated. In other words the barriers for sexual reproduction between species are often not complete. Moreover these lack of absolute sexual barriers actually allow gene flow between species even when species are of differing ploidy levels.
The concept of species implies separation. Yet often when one examines closely related species (populations) in genus such as Rhododendron, the separation sexually is not distinct and absolute. The terms species and hybrids blend when one introduces the concept of reticulated evolution in that the hybrid swarms become a potential source for new species.


text:
Do females retain oogonia after puberty?
Oogonia are the precursors of oocytes in females present during embryonic development. I was wondering whether these stem cells are still present in the ovaria at puberty?

I slightly modified your question for the sake of clarity. Please feel free to roll back if the question edits are not to your liking. Welcome to Biology and +1 for your question

From Developmental Biology, 6th edition I learned the following:
In humans, the oogonia divide to form a limited number of egg precursor cells. In the human embryo, the thousand or so oogonia divide rapidly from the second to the seventh month of gestation to form roughly 7 million germ cells. After the seventh month of embryonic development the number of germ cells drops and most oogonia die during this period, while the remaining oogonia enter the first meiotic division. These latter cells, called the primary oocytes, progress through the first meiotic prophase until the diplotene stage, at which point they are maintained until puberty.
Hence, at puberty the cells from the lineage of oogonia are called primary oocytes. So from a terminological perspective, you are correct that no oogonia are thought to be left at puberty.


text:
What is this Tree?
What is this plant?
Location: Bangalore, India

Breadfruit. Artocarpus incisus . With several other synonymous scientific names. Family moraceae. Close-relative of Jackfruit (Artocarpus heterophylla)

This is a famous species, available in  English dictionaries.

It looks very very suggestive for Artocarpus altilis or Breadfruit tree.
Another variants -  Artocarpus camansi.

How on earth do you manage to do this.... +1 :)

@AliceD Thanks, this tree has very special influence in design history, so the task was easily solvable. Learn more about it http://www.ctahr.hawaii.edu/oc/freepubs/pdf/breadfruit.pdf

Thanks Ilan for providing us with this info. What a beautiful tree. I like the cool leaves and fruits. Never tasted one though.


text:
Restriction sites
I would like to know: how many restriction sites does a restriction enzyme use on a DNA molecule? In other words: If a sequence on a plasmid contains the following bases:

ATTGCAGTCTG

and I want to have only the bases in bold as a new, separate molecule, will I need two restriction enzymes (One to cut the molecule between the T and G and another one to cut it between the T and C)? Or one restriction enzyme (that will cut them both)?
It wasn't clear enough in Wikipedia and in my biology book.

Welcome to Biology SE. Do I understand correctly that you wish to remove the bolded-out sequence, i.e., blunt-end cuts resulting in a oligo-nucleotide of 5 base pairs and the rest? The plasmid question - please google...

Yes. I have a question about a plasmide being cut by only one restriction digest, and I want to know if it will remain the same size...

This doesn't make sense... Your comment is a different question altogether. Please be specific in your question.

I have a plasmide (as much as I know - a round form of DNA sequence in prokaryotes). One restriction digest is cutting it - in one or two places. If it will be cut in just one place - the plasmide's size won't change, it will just open, beacuse it's round. If it will be cut in two places - there will be a cut plasmide and a new oligo-nucleotide.

please add the restriction enzyme to your question, that would help. It is all too abstract

Sorry, I confused the word "digest" with "restriction"... English is not my first language. I edited my question. I hope it will be clear now.

Let us continue this discussion in chat.

Which enzyme do you use for this experiment. Some (but rare) enzymes recognize a specific sequence and cut a DNA fragment out digesting both ends of the sequence.

Yes, bacterial plasmid DNA exists as covalently closed circles, both in vivo and after isolation and purification. IF: the plasmid contains one, or more, recognition sites for the restriction enzyme you are using, THEN: yes, if you follow the manufacturer's recommendations for the restriction enzyme digestion of the target sequence(s) on the plasmid, you should observe close to 100 % digestion (i.e., the introduction of a double-stranded cut in the DNA) at all the sites. So  1 site = 1 (linear full-length) fragment, 2 sites = 2 fragments, 3 sites = 3 fragments, etc.

Type II restriction enzymes always recognize palindrome sequences and the enzymes dimerize so both of the strands, Watson and Crick, get cleaved at almost the same time, each by one molecule in the dimer.

I use the enzymes ecoRI and BamHI. How many recognition sites do they have?

I might not fully understand what you want to do, but if you just need that short bold portion, why not have an oligo synthesized and save yourself the trouble of cutting and purifying? And if you're just cutting out that tiny portion, you'll never notice a size difference on the plasmid.

My question was theoretical. I don't need a new molecule syntesized, but a sequence to be cut. I just want to know if one restriction enzyme can cut a sequence from plasmide (and not just opening it to a chain). I put the sequence above just as example (its real size is much larger). There is a question about restriction enzymes in my course, and I would like to know this in order to answer it.

Most restriction enzymes have a 6bp restriction site (some have 8bp site also). So two restriction sites generally have to span 12bp. However some restriction sites can overlap. For example BamHI and SmaI:

BamHI
|______|
GGATCCCGGG
    |______|
     SmaI

In this case the total length has reduced to 10bp. However such combinations are not that common and at max you will achieve a 2-3bp overlap. A restriction endonuclease only makes a single cut. To make double cuts you need two restriction sites.
Even if the sites are non-overlapping there has to be a minimum length of separation otherwise the binding of one enzyme will hinder the binding of the other enzyme in a double digest. A 6 nucleotide gap between the restriction sites should be fine. If there is no gap then double digest may not be very efficient.
You can also have two restriction sites of the same enzyme so that you need not use two separate enzymes.
BTW the sequence in your question does not have any restriction site.
Hope this answers your question.

Just to bring another light to the question: a restriction enzyme cuts a double-stranded DNA two times, but it only cuts it once on each strand.
So yes, you would need two different restriction enzymes to excise the sequence in bold (assuming you want that sequence in double-stranded-form): one enzyme that would cut between the T and the G on the strand that you have represented, and one that would cut between the T and the C on this same strand.