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Evolutionarily speaking, why do humans have 46 chromosomes
In humans, each cell normally contains 23 pairs of chromosomes, for a total of 46. Monkeys, chimpanzees, and Apes have 24 pairs (twenty-four pairs), for a total of 48.
What caused humans to have 46?
EDIT:
@TomD is right, I was asking why we have one less chromosome pair than chimpanzees (for example) [23 pairs instead of 24].

I seriously doubt there was any selection on the number of chromosomes. It just happens that we have 23 pairs.

For info, all apes are known to have 48 (total), but monkeys vary (e.g. Rhesus monkeys have 42, but Capuchin monkeys have 54!). See the wiki list of chromosome counts here.

@nico Sure, but there was certainly (some) selection on conserving the number. Normally, large-scale mutations such as chromosome fusions are immediately fatal and even when they are not they potentially prevent procreation with individuals which don’t have that mutation. So at least superficially there should be quite strong selective pressure to preserve ploidy.

@Konrad Rudolph: but you are not selecting for the number of chromosomes, just for a configuration "that works".

@nico Sure. What I meant was: given that our close ancestors had a different number of chromosomes, when/why did it change? That’s an interesting question, and essentially what OP is asking.

@Konrad Rudolph: surely. It's just the question seemed to imply that a specific change in number had a particular significance, rather than being a side effect of something else that probably did have a particular significance. Semantics.

I think the OP is asking why we have one less chromosome pair than chimpanzees (for example) [23 pairs instead of 24].
The is an abundance of evidence, as alluded to above by shigeta, that human chromosome 2 is the result of a telomere-to-telomere fusion of two ancestral chromosomes (IJdo et al., 1991).  This event did not occur in our closest ancestors, hence we have one less chromosome pair.  In fact the sequence of human chromosome 2 contains the relic of an ancestral telomere-telomere fusion (IJdo et al., 1991).
The pdf of this key reference is freely available to all from PNAS
Reference
IJdo, J.W, Baldini, A, Ward, D.C, Reeders, S.T, Wells, R.A. (1991) Origin of human chromosome 2: an ancestral telomere-telomere fusion  Proc Natl Acad Sci U S A., 88 9051-9055.[pdf]
Actually it has now been shown that Neanderthals and Denisovans also exhibit the same chromosomal fusion as humans - http://m.motherjones.com/politics/2014/02/evolution-creationism-bonobos-neanderthals-denisovans-chromosome-two

This is a good Youtube video that discusses this, in the context of evidence for evolution. It's from a presentation given by Ken Miller about the Dover "intelligent design" trial. The whole presentation is here.

It seems to me this answers the 'how' question but not the 'why' question. I would guess the answer to 'why' is random chance but there could be a selective advantage? Is there any evidence either way?

@JackAidley It doesn't seem there is. Change in chromosome count cuts you off from sexual reproduction (unless you're self-fertilizing). It's an isolation from others of your (previous) species - in effect, if some population happens to undergo a change like this, they are guaranteed to form a new species. But that's not really a selection pressure - it's observaton bias; we see different chromosome counts in different species because they inevitably cause you to become a new species (dead or living). It's like a river forming between two populations of your species, a genetic rift.

@Luaan that cutoff only happen over many generation, the initial fusion has little impact, becasue both centromeres are still active. so it is more like a river gradually forming.

@nico is right.  the number of chromosomes is the result of an evolutionary timeline, puncutated by sometimes spontaneous events which shape the DNA.
These events occur in the course of evolution:
1) Chromosomal rearrangements.  Large sections of the genome can flip around or become integrated in other chromosomes.  By homologous recombination, regions of the genome can clip themselves out or duplicate themselves as well.  If you look at the alignment of human to say chimp, there are many segments that move relative to each other.
2) chromosomal breaking or combination.  Two smaller chromosomes may combine to form a larger one, or a larger one may break into two smaller chromosomes.  An example of this is human chromosome 2, which is found as two smaller chromosomes in the great apes (see figure in wikipedia).  We infer that this is a combination event exclusive to humans by comparing the other apes on the evolutionary tree.  Birds and reptiles tend to have lots of chromosomal breakage, even to the point  where the number of microchromosomes (less than 20 million bases).  Mammals tend to be more conservative and not allow viable chromosomal breaks - chickens have 78 chromosomes to our 23..
3) idiomatic chromosomal behavior.  Sex determining chromosomes are examples of chromosomes where a pair becomes distinctly different in size and composition.
Another example is in trypanosome which has many tiny DNA segments which code for variant surface coat proteins.
4) @rwst points, what I clean forgot, that occasionally (like maybe just a few times) there have been whole genome duplications.  This can be identified by chromosomal alignments within a single genome and has not happened very often since we became eukaryotic metazoans.  Not sure how many times, but perhaps just once or twice in our lineage.  If anyone knows about animals/humans that would be great. As you can see the link shows whole genome duplications in plants, which don't seem care how many chromosomes there are.  Plants have polyploidy, you see, so such duplication events are much better tolerated.  On the other hand plants can't play video games.
P. Dehal, J. L. Boore: Two rounds of whole genome duplication in the ancestral vertebrate. In: PLoS biology. 3, 10, Oct 2005, e314, doi:10.1371/journal.pbio.0030314. PMID 16128622. PMC 1197285.
You can see that these events happen at particular moments and help shape the species and the composition of the chromosomes.  It is not a priori possible to predict the number or type of chromosomes just by looking at an animal, but only by looking at the related animals.
Fungi and Plants have even more variations in chromosomal composition than animals.

Also, I think it is important to note that a certain mutation in chromosome number may, indeed, be selected, because it is associated to some other advantageous phenotype. The change in chromosome number will then also be selected, but only as a "side effect".

segmental rearrangements that might reflect a change in the chromosomal structure can change the phenotypes and organismal behavior quite a bit.  its a significant factor in the evolution of bacteria.

@shigeta: you missed whole genome duplication (WGD) --- okay the OP didn't ask that

@rwst - no that's a good point.  It should be in here. added with an attribution

added a reference. I would expect more information with more pre-vertebrate genomes sequenced

thanks - I remember reading about a complete genome duplication event known from the mouse genome paper, but was not exactly sure where I read it.

Here is a paper you might want to take a look at:
Phylogenetic Origin of Human Chromosomes 7, 16, and 19 and their Homologs in Placental Mammals
From the abstract:

From their origin, these chromosomes underwent the following rearrangements to give rise to current human chromosomes: centromeric fission of the two submetacentrics in ancestors of all primates (∼80 million years ago); fusion of the HSA19p and HSA19q sequences, originating the current HSA19, in ancestors of all simians (∼55 million years ago); fusions of the HSA16p and HSA16q sequences, originating the current HSA16 and the two components of HSA7 before the separation of Cercopithecoids and Hominoids (∼35 million years ago); and finally, pericentric and paracentric inversions of the homologs to HSA7 after the divergence of orangutan and gorilla, respectively. Thus, compared with HSA16 and HSA19, HSA7 is a fairly recent chromosome shared by man and chimpanzee only.

the citation doesn't account for vertebrate (and earlier) whole genome duplication (WGD) events --- okay the OP didn't ask that

Evolutionarily speaking, why do humans have 46 chromosomes

This is a question of why human have 10 fingers. There is nothing magical about 10 fingers and nothing magical about having 46 chromosomes. In fact there are people who have 44 chromosomes. The are normal people. They have normal fertility. However if the children with people of 46 chr, the fertility of their children (ie people with 45 chr) is reduce. Normal fertility can only be maintained by marrying other people with 44chr... who probably are their cousins.
http://genetics.thetech.org/original_news/news124
So the reason we have 46 chromosome is because we are descended from a homonid species which had 46. No reason really. Not everything produced by evolution has a purpose.

This is being discussed in more detail at https://biology.stackexchange.com/questions/1051/can-two-humans-with-44-chromosomes-produce-viable-offspring


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Transmission of epigenetic regulation through surrogate mother
I know the basics of epigenetics, but I do not know how epigenetic mechanisms are transmitted from parents to children (or if there is even enough literature to derive a consensus). My question is relates to surrogate motherhood, in which an egg is fertilized in vitro and then implanted in the womb of a woman other than the egg donor.
Are all the factors that affect epigenetic mechanisms encoded in the genome? Is it possible for the surrogate mother's epigenetics to influence the epigenetics of the child/children?

Epigenetic information is information that can be inherited through cell division that is not encoded in the DNA sequence. This includes, but is not limited to, DNA methylation and histone modifications (there is also non-chromatin based epigenetic information). A nice example is the centromere, the chromosomal region that binds the kinetochore and is important to attach chromosomes to the mitotic spindle during cell division. The location of the centromere on the chromosome is encoded by a specific nucleosome composition and does not seem to rely on the DNA that wraps around those nucleosomes: The DNA sequence at centromeres is not even conserved from chromosome to chromosome (with the exception of budding yeast), and there are several known examples of people and families where the centromere is in a different place. However, all the mechanisms for maintaining this epigenetic mark are encoded genetically.
As epigenetic information is transmitted through cell division, it is directly inherited from the biological mother (with the exception of e.g. the centromere, most epigenetic marks from the father's chromosomes are removed when sperm is created).
However, (some) epigenetic information can be modified. This is obviously important during development where gene expression patterns of a liver cell need to be stable but different from gene expression patterns of a neuron, even though both descend from the same cell.
There is evidence that the metabolism of the mother will influence the epigenetic program of the child; diet being one of the determinants. It has also been suggested that epigenetic changes may influence behavior. Thus, it is indeed possible for the surrogate mother's epigenetic state to influence the epigenetic information of the children.

The definition of an epigenetic mark I work with is the following:

impacts gene regulation without touching the DNA sequence,
is reversible,
is inheritable.

With this definition in mind, you could say that only DNA methylation is a true epigenetic mark, leaving histone modifications and the like to canonical transcription regulation machinery. Yet it really depends on what scale you place yourself. Epigenetics at the scale of the cell is not the same thing as at the scale of the organism.
So if a surrogate mother can alter the epigenetic state of the pup or child or foetus, it will not be due to transmission of information in the traditional sense, but rather be due to her physiological state in the case of the foetus (many hormones act through nuclear receptors that can recruit chromatin remodelers), or as mbq mentioned it, due to her behaviour in the case of the child or pup.

X inactivation is not due to DNA methylation but does impact gene regulation without touching the DNA sequence. Also, the inheritance of the location of the centromere would not fall under your definition, so what kind of mark would that be?

You are totally right, for some reason histone variants did not come to my mind when answering :)

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Sequencing the genomes of polyploid organisms
I've done some transcriptomics work in the past with a polyploid organism, and this presented some unique challenges in the data processing and analysis. Since then, I have been brainstorming about the technical challenges one may face when sequencing and assembling the genomes of a polyploid organism. As far as I am aware, there are no polyploids whose genomes have been sequenced.
If one wanted to sequence, for example, a tetraploid organism, one approach would be to prepare and sequence all of the DNA together and then rely on post-sequencing analysis to tease apart the two co-resident genomes. However, it would be difficult, if not impossible, with this approach to distinguish inter-genome variation from intra-genome variation.
An alternative approach would be to isolate DNA from both co-resident genomes separately, and then sequence and assemble the genomes separately, so that inter-genome variation and homology need not be considered. However, I'm thinking at a very high level and have little intuition as to the technical feasibility of this approach. When there are two or more co-resident genomes, is it be possible to isolate DNA from only one of those genomes? What would this rely on (for example, would thorough cytogenetic/cytogenomic characterization help)? If this task is not possible, what types of limitations must be overcome to enable it?

I'm interested in the issues related to transcriptomics on polyploid organisms (I'll be doing some comparative transcriptomics between related but different ploidy organisms). If I ask this as a separate question, could you elaborate on the issues involved and how you solved them?

I'm not sure, as the material is yet unpublished. I guess it would depend on the question.

@jmusser I reverted your title edit since it didn't really capture the question. The title "How are the genomes of polyploid organisms sequenced?" isn't really appropriate--it seems like you're asking how it is currently done (it's not). I'm asking how it should or could be done. If you have any more suggestions about improving the title, I'd be happy to consider these.

@DanielStandage, sorry, I just like to turn the title into a question. :)

@jmusser No worries, I have no problem with that assuming question adequately captures what is being asked.

Take a look at the strategies used to sequence the wheat genome. Wheat is hexaploid. The project is described at http://www.wheatgenome.org/.
For early work on the maize genome, we employed methyl filtration in order to reduce genome complexity and size - transposons are filtered out and genes + promoters and such remain. The gene sequences are different from the two genomes, so says the theory, and those can be distinguished. See http://www.ncbi.nlm.nih.gov/pubmed/10545948 for the reference.

As I know wheat (both 4n and 6n) is allpolyploid (it came into being by hybrydization of different species). Isn't it harder to sequence genome of autopolyploid species?

I'm not sure. Sequencing is not the real problem - it is accurate genome assembly.

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Why does RNA adopt an A-form helix?
RNA is known to form an A-form helix, while DNA generally forms a B-form helix under physiological conditions.

From left to right: A-form DNA, B-form DNA, Z-form DNA. Image created by Richard Wheeler
The preference of RNA for the different conformation is supposed to be caused by the 2'-OH, my question is now how exactly this favors the A-helix? Which interactions are important and cause RNA to adopt an A-form helix?

There are many factors that produce effect in that interaction. You could have a first look in detail at http://www.sciencedirect.com/science/article/pii/S0022283605014439

The beta-form of DNA and the alpha-form of DNA are based on the pucker on the sugar ribose. As DNA doesn't have a 2'-OH, it can obtain both conformations.

RNA does not have this luxury. The steric clash of the 2-OH with the 3'-OH makes the B-form to be very unfavorable thus constraining the RNA to adopt the A-form. Incidentally this steric limitation is also why RNA structures are more stable (see https://biology.stackexchange.com/a/769/389)


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Which factors besides the thermodynamic stability are important for the hairpin in intrinsic transcription termination?
Intrinsic termination (rho-independent) relies on a stable hairpin with a subsequent uridine repeat. The common explanation on how these sequences cause the termination of the transcription are based on the thermodynamic stability of the sequence. The GC-rich stable hairpin together with the destabilizing U-repeat supposedly destabilize the binding of the polymerase enough to cause it to disassociate from the template.
What I'm looking for are specific requirements on the termination sequences that are not based on thermodynamics.

Are there any specific requirements on the hairpin sequence beyond a certain thermodynamic stability.
Are there any loop variants that are known to reduce the termination efficiency?
Does the shape of the hairpin, e.g. any kinks or bulges in it, have an influence on termination efficiency?

The typical requirements I read are 5-14bp and GC-rich, and I'd like to know if there are any more specific requirements, especially ones related to the structure and not the stability of the hairpin.

I'm going to suggest this for now and write it up later: http://nar.oxfordjournals.org/content/37/14/4736.abstract

The RNA hairpin transcription terminator in prokaryotes is terminated by the GC rich hairpin followed by 4+ uracil bases as you describe it.
The original reference describing the hairpin, described the sequence requirements as being for the thermodynamic stability of the hairpin, but the protein nusA has also been found to stimulate termination.
You might think that there would be some protein that would precisely bind this motif and mediate the termination, but at least as far as I can find, it appears that the hairpin clogs up the polymerase itself, causing termination.  This review linked here has some nice pictures of the RNAP bindig pocket model.


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What are the limitations to current nucleotide sequencing technologies?
Using the Illumina platform, it is cheap and (relatively) easy to sequence huge amounts of DNA or RNA. There are various other platforms out there (Roche/454, SOLiD, PacBio, Ion Torrent) each with their own distinct advantages, but Illumina seems to be pretty popular for many applications, despite its limitations.
Ideally, we would like a sequencing technology that produces long, error-free reads with high throughput. However, at this point it seems we have to make a choice: throughput or length (and quality). PacBio seems promising, but the last I heard they have still been unable to deliver on their claims.
What are the molecular and biochemical limitations to our current sequencing technologies? Why don't we already have long, error-free reads with high throughput?

I suspect the project triangle is at work here. http://en.wikipedia.org/wiki/Project_triangle

@bobthejoe Ideally, we would like as long as possible, right? :) I consider the upper limit of Sanger read lengths (+/- 1000 bp) to be long, but it would also be nice to know why we can't get longer reads (with or without high throughput, low error rates, so on).

All or most of the limitations you describe can be simply overcome by brute force method. Almost any genome sequenced on any high throughput technology today will be of very high quality if you sequence it 100 times. It's just a matter of time and money. Remember the original human genome was sequenced by many Sanger machines and a lot of cloning.

@yotiao What you're saying is true, but only to a point. My experience is that assemblies and other analysis improve with coverage, but at a certain point adding more data provides only minimal improvements, even if there is a significant addition of new data. And to say that the human genome project was successful primarily because they dedicated a lot of Sanger sequencers to the project ignores the significant differences between the nature and quality of the data produced by the Sanger platform as opposed to today's high-throughput platforms.

@Daniel Yes, you're right in principle. But then if what you require is as-perfect and complete a sequence as possible, then I'd propose that the limitations are the same as they were before: DNA itself, with it's super high repetitive content, poliploidy. Sanger and positional cloning did not manage to solve this problem (hence gaps in finished human genome sequence) and they're regarded as the golden standard (am I that old already?).

It seems like you answered your own question,the signal from a few molecules running through an enzyme or a polymerase tend to fall out of synch after a few hundred bases.  If an enzyme for sequencing was more rigorously in time step that could help for instance.  The machines read traces in four channels with nice bumps for each base.  See this article for a nice example. You can see that if there are too many of the same base consecutively it gets hard to tell how many bases there are there.  Over time all four traces will start to smear out and you cant tell Adam from Thelma if you take my meaning.
But there are other bottlenecks.
The sequencers currently put out such a high volume of data that the analysis of the meaning of the output data can't be analyzed fast enough.  This follows the trend in biotech over the past 12 years or so - more sequence data, micro array data, more mutation data, more genomes than people who can actually use it to understand the biology.  There is a bit of an analysis bottleneck now.
So some of these sequencers have greater read lengths, which can make it easier to assemble a sequence.  These sequencers generally cost more.  For instance if you have a library to sequence a little fungal or algal genome - you will get the answer back in a day or less now.  In the form of 1 Tb of reads maybe 50 to 200 bp long.  It might take quite a bit of time to put that together into a novel genome sequence, still more to find the genes, build the gene networks from a template of pathways etc.  Just imagine a thousand sequencers pumping out day and night and you get the picture  I'm trying to paint here.
About cost.  Ion Torrent and the new oxford nanopore sequencers are really cheap - \$50k to perhaps \$900 for Oxford Nanopore's USB sequencer.  Most other systems cost hundreds of thousands of dollars.  Ion torrent and Nanopore have more disposables - you throw away a chip or even the entire sequencer - at a cost of hundreds of dollars a sample.

Over the summer I've been to a couple of conferences including a day seminar focused on assembly of 30x coverage genomes from MiSeq data and the biases in the sequencers were creating systematic errors that made some of the data difficult to interpret.  HTS data is not plug and play, even with open source software.  not yet.

Q1) What are the molecular and biochemical limitations to our current sequencing technologies?
A1) AFAIK:
Illumina has hard time producing long reads (although now miseq can generate reads that are 300bp and that can be paired, the so called paired end 2X300) because after a certain number of bases that are synthesized and recorded on camera (Illumina is sequencing by synthesis, basically you add bases and measure fluorescence at each cycle), i.e. after a certain number of "cycles" you can lose syncro, and the quality of bases decreases.
PacBio can generate very long molecules, but they still have big problems with reliability of the reading of the bases (I don't know what's the problem here)
Q2) Why don't we already have long, error-free reads with high throughput?
A2) Because it's hard to do! But we are moving towards this!


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Collective term for both exons and introns
Is there a term I can use to refer collectively to both exons and introns? By collectively, I don't mean ligated as with an unprocessed transcription product. I'm just writing about exons and introns and getting frustrated that I keep on having to write "exons and introns", wishing there was a more concise term I can use in the place of that phrase.
For example, the term I am looking for would fill in the following blank perfectly.

The gene has 5 exons and 4 introns, so it has 9 _____.

uh...a sequence!? a gene sequence? a sequence that get transcribed. I personnaly don't know any other word for that.

Could you clarify the context?  If on single RNA molecule you could say pre-mRNA or hnRNA, or in general "the transcript."

You should be aware that if you refer to "splicing fragments" with no explanation, I doubt you will be understood. With no context, I would assume you were talking about excised introns.

sorry for the late comment.. Instead of this you can say that the gene has 8 splice junctions- I guess it is more precise.

How about "splicing fragments"? It might be easier to refer to them according to the mechanism of production.

What of single exon genes with no introns and, therefore, no splicing?

Are they really exons with no introns? If there are no introns at all, it's just a transcript, or a coding sequence.

There are certainly single exon genes, yes. I am not 100% sure that they also have no introns but I would imagine so since splicing always joins two ends of a sequence excising what is in between.

There are definitely no-intron genes, that's usually one of the hallmarks of a former virus that was integrated into the genome.

This is a good answer - there is no explicit word to answer to this question I think.

I mean, there are lots of genes with no introns. Are they really exons if there aren't introns to compare against? Maybe that is semantic trickery.

Yes, they are exons because they are translated into amino acids. Given that the species in question has splicing, anything that is translated is an exon by definition. In species that lack splicing, all genes are single exon genes and you could call them exons but that might be semantic trickery indeed. In species with splicing however, things are quite clear cut, translated? therefore exon.

I think your best bet would be transcript. Gene is actually quite close but most of the current definitions include the promoter sequence in the gene so that is not restricted to introns and exons.
Transcripts, on the other hand, are all of a gene's sequence that is transcribed and consist exclusively of introns and exons (UTRs are also exons and are actually spliced in some cases). Note that I am using transcript and not mRNA since mature mRNAs do not of course contain introns. Immature ones do and transcript can apply.

This isn't the word I'm looking for. The word I'm looking for will fill in the following blank: "The gene has 5 exons and 4 introns, so it has 9 ____". Splicing fragments is the best answer so far, I was just hoping there was a more concise term for it.


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What is the eye muscle status when you stare at distant view through a glass wall?
The book said when you look at object close to you, the eye muscles contract and vice versa. I wonder what will be the status of the eye muscles when I stare at distance view (such as a mountain) inside an office through a glass wall. The mountain is far away but the glass wall is close to us. In this case, does the eye muscles relax?

In the situation you describe, the eye would be focused on the distant mountain.  This would mean that the lens would be stretched and thin in order to minimize the focussing power of the eye.  Therefore the ciliary muscles would be relaxed.
When you are looking out of the window, it is possible to make a conscious decision to focus on the window pane itself (thus adjusting the focus to be more powerful as the ciliary muscles contract), however then the distant object will be out of focus and uncomfortable to look at.
This is because the light rays reflecting from the mountain are barely affected by the pane of glass, hence its transparency.

I think this answer is correct that the transparency of the glass makes it irrelevant to how the eye focuses through it. However, the relationship between the ciliary muscles and near/far focus as stated here is reversed, or at least confused. The muscles contract when focusing on near objects.

To increase long range focus, the ciliary muscle is relaxed so that the zonular fibres flatten the lens. This flattening increases the focal distance and far away objects appear sharp.
The process is reversed when increasing short range focus.
In your example you are watching out of the window into distance. To see the mountains sharp you need to increase range focus and this means relaxing the ciliary muscle. This is also the reason why it is recreative for your eyes to watch into the distance after hours of computer work for example.
The window itself does not play any role because your focus is not on the window pane but somewhere in the distance.


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Protein construct design
I am trying to create some constructs of a certain protein deleting well defined domains (at either terminus) to determine interaction regions with other proteins etc., 3 constructs with varying start/end sites have ended up being aggregated in E coli (while the full length protein expresses reasonably well). My question is what considerations one should use to determine start/end sites to maximize chances of getting soluble, purifiable protein. The criterion I used were:

Preferably loop region in known x-ray structure
Use hydrophobicity plots to minimize hydrophobic residues at both termini
3-4 residue linker between protein and affinity tag (GST/6xHis)

From personal experience with an earlier construct, this can turn out to be an idiosyncratic exercise but I was wondering if I was missing any crucial parameters.
EDIT: I also played around with the PDB file of the non-truncated protein to check whether huge hydrophobic patches were exposed on deletion of the domain(s), and I didn't find any such patches that could potentially be exposed and lead to aggregation

Did you identify structural domains in the protein using Pfam or some other domain detecting peptide search?
It's pretty useful to cut your constructs at the boundaries of structurally independent domins in the protein if you know where they are.  Hydrophobicity plots might lead you to cut right in the middle of a protein fold, only exascerbating inclusion body formation/protein precipitation.

I used the x-ray structure to determine known loop regions that connect structured domain regions (pt #1)

I see - if this is a series of independent folding domains like SRC, what you have done makes sense.  In this case what you call 'loops' would be more like linker peptides.  In this case, sometimes things that look independent actually are not.  Its also possible to get precipitated protein for more conventional reason - problems with heterologous expression or codon choice when moving from human to e coli for instance.  its hard to be more specific without details.  does seem as if you made a reasonable effort.


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How does Iota-Carrageenan achieve an antiviral effect?
"Cold Defence" nasal sprays are recommended to be taken either preventatively or in the early stages of a cold.  The active ingredient in these sprays is Carrageenan.  After some research, the active compound is Iota-Carrageenan (ι-Carrageenan).
This study by Eccles et al[1] shows that this drug is clinically effective.  The study was only designed to test efficacy rather than to explain the mechanism, however. A fleeting mention is provided in the discussion section:

The above results suggest that the treatment with Iota-Carrageenan reduces the viral replication. Consequently fewer cells are infected, the immune reaction against the viruses is less pronounced and fewer symptoms occur.

How does ι-Carrageenan produce an anti-viral effect?

Eccles R, Meier C, Jawad M, Weinmüllner R, Grassauer A, Prieschl-Grassauer E. 2010. Efficacy and safety of an antiviral Iota-Carrageenan nasal spray: a randomized, double-blind, placebo-controlled exploratory study in volunteers with early symptoms of the common cold. Respiratory Research, 11:108, doi:10.1186/1465-9921-11-108.

Through two different pathways, one relying on a non-specific (innate) response, and another through a reactive oxygen species, the level of NF-kB(**) is amplified, as such a response would have happened as a result of the presence of the virus anyway.

In thousands of experiments, carrageenans have been used to
  induce inﬂammation, since inﬂammation is a predictable effect of
  exposure to carrageenan in animal and cell-based models. For the
  most part, these experiments were designed to test the effectiveness of anti-inﬂammatory agents or to study the mediators of inflammation
The innate immune pathway is mediated by toll-like
  receptor (TLR)-4 and B-cell leukemia lymphoma (BCL)10, leading
  to increased Interleukin (IL)-8 secretion by both canonical and noncanonical pathways of NF-kB activation. The ROS-mediated
  pathway of inﬂammation does not involve TLR4-BCL10, but
  requires Hsp27 and IkB-kinase (IKK)b, leading to increased phosphorylation of IkBa, and thereby enabling the nuclear translocation
  of NF-kB.

From the intro to:

Yang B, Bhattacharyya S, Linhardt R, Tobacman J. (2012) Exposure to common food additive carrageenan leads to reduced sulfatase activity and increase in sulfated glycosaminoglycans in human epithelial cells.  Biochemie, Mar 5,epub ahead of print, doi

(As an aside, the direct conclusions of this study are that these changes in GAGs may further influence transcription and play a role in determining cell fate, and perhaps may influence cell/cell interactions)

(**)NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) is a protein complex that controls the transcription of DNA. NF-κB is found in almost all animal cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, ultraviolet irradiation, oxidized LDL, and bacterial or viral antigens  wiki

In the publication by Leibbrandt et al.[1], it could be shown that the iota-carrageenan directly binds to viruses and thereby prevents the attachment to cells. This is a critical step in the viral life-cycle and therefore replication is reduced. Iota carrageenan rather acts unspecifically and besides influenza also other viruses such as human Rhinoviruses are inhibited[2]. Similarly, a direct binding to viruses has been shown for iota-carrageenan and papillomaviruses[3].
In contrast to lambda carrageenan that is widely used as proinflammatory compound in animal experiments, iota carrageenan lacks this activity and therefore a pharmacological / immunological mode of action can be excluded. In addition carrageenans have a high molecular weight which makes it very unlikely that it acts systemically.

Leibbrandt A, Meier C, König-Schuster M, Weinmüllner R, Kalthoff D, Pflugfelder B, Graf P, Frank-Gehrke B, Beer M, Fazekas T, Unger H, Prieschl-Grassauer E, Grassauer A. 2010. Iota-Carrageenan Is a Potent Inhibitor of Influenza A Virus Infection. PLoS ONE, 5(12): e14320 doi:10.1371/journal.pone.0014320.
Grassauer A, Weinmuellner R, Meier C, Pretsch A, Prieschl-Grassauer E, Unger H. 2008. Iota-Carrageenan is a potent inhibitor of rhinovirus infection. Virology Journal, 5:107, doi:10.1186/1743-422X-5-107.
Buck CB, Thompson CD, Roberts JN, Müller M, Lowy DR, Schiller JT. 2006. Carrageenan Is a Potent Inhibitor of Papillomavirus Infection. PLoS Pathogens, 2(7): e69, doi:10.1371/journal.ppat.0020069.


text:
How to build S16 rRNAs phylogenetic trees?
Here is what I know so far:

Multiple copies are present in prokaryotes, but according to a paper by Lukjancenko el al.[1] it is enough to select the most similar ones.
There are stem regions in the S16 which I suspect are much less variable than the loops.

And here are my questions:
About 1., it is this the usual procedure?
About 2., do people use the loops or the stems to construct a phylogenetic tree? It they use stems, do they consider the coupling between stem bases? And, if they do so, where can I get a "map" of this coupling (preferably in a parseable form, not an image)?
In the other hand, is it correct to use a simpler nucleotide substitution model? which one?
Thanks in advance for any hints.

Lukjancenko O, Wassenaar TM, Ussery DW. 2010. Comparison of 61 Sequenced Escherichia coli Genomes. Microbial Ecology, 60:708-720, doi:10.1007/s00248-010-9717-3.

OK, first of all do not use CLustalX to align the sequences. It is a very old algorithm and is outperformed by just about any modern aligner (including its descendent, clustal omega, and t-coffee, mafft, kalign etc etc).
As for 1) that depends on what you want to do, there is no perfect solution. What question are you trying to answer? If you want a tree with species-level resolution, use all sequences. If you don't need that high a resolution, choose a representative sequence from each order or genus or whatever. In all cases, remember to use a significantly different sequence as an outlier.
As a general rule, I would use the entire sequence to build a tree, both the stems and the loops. To include structural information in your alignment you may want to check out r-coffee from the t-coffee suite.
Finally, you don't really want to use a nucleotide substitution model. Most such models assume that the sequence codes for protein and are not suitable for non coding RNAs.


text:
Why do eukaryotic organisms have introns in their DNA?
We touched on introns and exons in my bio class, but unfortunately we didn't really talk about why Eukaryotes have introns. It would seem they would have to have some purpose since prokaryotes do not have them and they evolved first chronologically, but I could easily be wrong. Did the junk sections of DNA just evolve there by some sort of randomness or necessity as opposed to an actual evolutionary advantage? Why hasn't evolution stopped us from having introns since they seem to be a 'waste' of time and DNA? Why do prokaryotes not have introns?

Not everything needs a function to exist in biology.  One way to answer this question is to look to see what kind of selection pressure is acting on introns.  Do they evolve neutrally?

I guess a better response to your question is: Why not have introns?  Take a look at the neutral theory: https://en.wikipedia.org/wiki/Neutral_theory_of_molecular_evolution

There is still a lot to be learned about the roles introns play in biological processes, but there are a couple of things that have been pretty well established.

Introns enable alternative splicing, which enables a single gene to encode multiple proteins that perform different functions under different conditions. For example, a signal the cell receives could cause an exon that is normally included to be skipped, or an intron that is normally spliced out to be left in for translation (the Wikipedia article on the subject has a basic overview of the possibilities). This would not be possible, or at least would be much more difficult, without the presence of introns.
In recent years, we have discovered that RNA molecules (especially small RNAs such as siRNAs and miRNAs) are much more involved in regulating gene expression than previously thought. Often the small regulatory RNAs are derived from spliced introns.

There is probably more, but essentially introns enable a finer level of regulatory control. Biological complexity is often not the result of having a larger complement of genes, but of having additional layers of regulation to turn genes on and off at the right times. Prokaryotic genes are often organized into operons, and a single polycistronic mRNA will often encode multiple proteins from multiple adjacent genes. Since the biological processes required to sustain microbial life are much less complicated than those required to sustain eukaryotic life, they can get away with much less regulatory control.

I would add that there is a general assumption that this is a reason that eukaryotes might have the ability to adapt to roles higher on the food chain than prokaryotes, like form multicellular organisms (there are a few exceptions, but really very few and they are pretty simple like - cyanobacteria which form chains of cells).

While this is a good "how" answer that resumes what we know now, is not by any means a "why" answer. For example, what's the limitation of prokariotic regulation that introns solve? Why do nature needs to squeeze more proteins in a single gene and then have 93% of garbage in the rest of the genome? I think that  the answer by @apoz it is a better fit.

I was under the impression that a lot of our introns were just from retroviruses that got into our genome at some point in our evolutionary past. Since the competitive disadvantage incurred by carrying some non-expressed junk DNA is very low, there's not selection pressure to get them back out.

Prokaryotes can't have introns, because they have transcription coupled to translation. They don't have time/space for that, since intron splicing will stop the coupling. Eukaryotes evolved the nucleus, where splicing can be done. The ancestor of eukaryotes that developed the nucleus could afford more variability (because of introns) than species without it, so they had a greater fitness.
Bacteria can't afford high complexity compartmentalization, a process that requires a lot of available energy per gene, a eukaryotic cell can have tens, hundreds or even thousands of mitochondria that have similar energy output to a bacterial cell, while having a genome about 100-500 times smaller (16 kb of a human mitochondria compared to 4.000 kb for a E. coli cell).
I hope that clarifies your doubts, and you can see that this is a debatable answer.
Sorry for my bad English.
Sources:
Lane & Martin 2010.
Martin 2011

This is a good answer.  Comparing the lack of introns between prokaryotes with eukaryotes that do have introns does not mean that introns exist in eukaryotes because it infers an evolutionary advantage to have them.  A more likely reason is that introns are highly deleterious in prokaryotes due to genome size limits but not deleterious in eukaryotes.  See the C-value problem.

But prokaryotes do have introns - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC177115/ - although on nowhere near the scale that Eukaryotes do.

Many archaea (which are prokaryotes) also have introns.

Evolution - Douglas J. Futuyma, Chapter 19, p. 461

Michael Lynch and John Conery (2003) have pointed out that a variety
  of genomic features that appear to have little fitness advantage for
  organisms-introns, transposable elements, large tracts of noncoding
  DNA-may be more prevalent in species with small effective population
  sizes. They have suggested that viruses and bacteria have extremely
  large population sizes that facilitate the sweep of advantageous
  mutations that enable genomic streamlining. By contrast, eukaryotes
  have smaller population sizes that facilitate the fixation of
  nonadaptive traits. This is the best hypothesis advanced
  so far that would explain the diversity of genome sizes and
  structures.

I was explaining it to my girlfriend: imagine you have two rooms in your two-and-a-kitchen house full of cartridges of adhesive tape... you really don't need it, but have no way of getting rid of it. Now, the hose of the vacuum cleaner gets broken, and you take a small amount of adhesive tape (you have so much) and patch it...  nobody would seriously believe that you were storing all that much adhesive tape for that sake, and you rather should have ordered a new hose. But you did the best of your circumstances. That much is going on in eukariotic genetics: easy and dirty patches everywhere.

I think the Lynch and Conery paper is so far the most reasonable explanation on the origin of introns, and combined with the other answer (http://biology.stackexchange.com/a/1725/658), it gives a complete explanation about the origin and the current fitness advantage of having introns in certain organisms, but not in others.

Hi apoz - this answer is considered useful by the community but still needs to consist of more than direct quotes.

@149781-32509185: the Lynch & Conery paper does not explain introns by saying they have a fitness advantage.  A small population size that they refer to means that genetic drift is creating the fixation of the introns.

There are several good answers here already.  Daniel Standage points out the value of alternate splicing.  For a compelling example of the role in regulation of gene expression, read one of the reviews of sex determination in Drosophila melanogaster (sex-lethal, transformer, doublesex).
None mentions the idea of exons as "cassettes" of reusable function that can be introduced into an existing gene during evolution.
The bounding introns represent regions where inexact "grafting" can occur without destroying the already functioning reading frame of the newly introduced xeno-exon (I just made up that neologism) or of the recipient gene.
In other words, introns provide regions which allow for sloppy transposition of functional subunits while reducing the likelihood of wholesale chaos at the transcription/translation level.
Evolution shows over and over that it is capable of promoting mechanisms that promote evolution.  How else can you explain meiosis?

You need to read how to write a good answer for SE. You refer to the Drosophila sex determination system but do not provide any explanation or reference. How do you expect anyone to understand this? And if you talk about exons as "cassettes of reusable functions", you should provide an example. Do you know of any? And your language, even when you are not inventing new terms is incomprehensible gobbldey gook — "sloppy transposition of functional subunits...". Sloppy ideas and sloppy writing, more like.

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


text:
What is the main general difference between Mitosis and Meiosis?
I found such a clause:

The general principle is that mitosis creates somatic cells and
  meiosis creates germ cells.

However, I cannot agree. Each gametogonium needs to go through mitosis before it can enter meiosis I. So in that case mitosis is happening with germ cells so the clause is false.
I would rephrase the sentence to be

The general principle is that meiosis creates only germ cells with the possibility of a decrease in chromosome number, while mitosis can create both somatic and germ cells while the ploidy stays constant.

Ok, not perfect.
How would you say the main general difference between mitosis and meiosis?

In plants germ cells are created by mitosis and meiosis creates haploid cells that divide many times before producing gamets so both statements are not generally true.

@MartaCz-C Please, propose your own below. Can be many sentences. Can be in the form like: for this y and for that y. It helps me to think probably other way the problem.

@MartaCz-C Is my sentente, the second one, right for other species if we exclude plants from it? - Is it right for human?

If the question is about the one and only most important difference between mitosis and meiosis, then the answer "meiosis reduces ploidy" is probably correct. But if the list of important differences is open, it would be critical to add that mitosis generates identical cells (identical to each other and any ancestral cells, barring rare new mutations), while meiosis generates genetic diversity by creating cells, which are all different from each other and from any ancestral cells. It does so by independent segregation of homologs and by crossingover within chromosomes.

According to all I've learned and heard, the only thing consistent about meiosis is that it  reduces ploidy because homologous chromosomes are separated. (Not necessarily diploid to haploid - it can be polyploid as well, although odd ploidies usually seem to mess it up.)
Mitosis on the other hand mainly serves to separate two copies of a genome into different cells.

Meiosis is the specialized cell division that generates gametes. In
  contrast to mitosis, molecular mechanisms and regulation of meiosis
  are much less understood. Meiosis shares mechanisms and regulation
  with mitosis in many aspects, but also has critical differences from
  mitosis. This review highlights these differences between meiosis and
  mitosis. Recent studies using various model systems revealed
  differences in a surprisingly wide range of aspects, including
  cell-cycle regulation, recombination, postrecombination events,
  spindle assembly, chromosome–spindle interaction, and chromosome
  segregation. Although a great degree of diversity can be found among
  organisms, meiosis-specific processes, and regulation are generally
  conserved.

Meiosis: An Overview of Key Differences from Mitosis Published by Cold Spring Harbor Laboratory Press


text:
Measuring reverse transcriptase activity in E. coli
Goal: To quantify the HIV-1 reverse transcriptase (RT) activity for a number of mutated RTs.
Idea:

Put RT into a vector in E.coli.
Deliver GFP mRNA to E.coli.
RT will process the mRNA.
The resulting DNA will be integrated into E. coli.
RT activity correlates with the GFP we observe.

First question: Does this logic make sense?
Second question: An alternative procedure?

Wouldn't it be far, far easier to do the whole experiment in vitro instead of inside E. coli? You're introducing a whole lot of problems in your plan, and I'm having a had time understanding how you would get a quantitative result from it. You might want to add more detail about your specific goal.

the devil is in the details here - the logic is okay, but there is no experiment here. Too many unanswered questions.
Are you doing anything specific to see optimize RT activity?
How are you preventing your GFP mRNA from being turned into protein, producing much larger signal than you will ever see from RT activity?
Once its integrated into the chromosome, how will this gene be expressed when it has been suppressed in all these other stages?
How do you know that the plasmid isn't just being incorporated into the chromosome by some other means?
Where is the RT coming from ?  E coli doesn't have the gene. this experiment is very likely to give no results.
When/how does this RT work?  If its some sort of phage RT ( i don't know if there are such things) any sort of viral RT will probably kill the cell the way normally it would.
so many questions before this could work - need to do some homework here.

Thanks for the reply. (1) I should have mentioned that it is RT from HIV-1. (2) I would like to quantify the RT activity in a number of conformations of RT (mutant RTs).(3) I did not quite get why it may not be expressed after the integration? (4) I do not have any idea how frequent the incorporation into the plasmid by other means occurs - any estimate? (5) E.coli uptake of the RT is indeed an issue - but I suppose E.coli can handle the viral RT?

just because the GFP gene sequence is in the chromosome, does not mean it will be copied into mRNA.  You need to have a RNA polymerase binding site nearby upstream of the gene and an intact shine delgarno sequence 8 bp up from a start codon.  how will you get the HIV RT into the e coli?  expressed from a plasmid?  HIV cannot infect e coli - they will just sit in solution until the coli eats it, which probably wont do for your experiment.  Even if it did get inside the e coli, I doubt it would be active in a bacteria at all.... lots of little details to add to your question - feel free to edit.

I'm with @Mad Scientist. Save yourself the trouble and do this in an in vitro system. At the moment, you don't even know if the HIV-RT will express or will be active in E .coli.
Rather, express mutated HIV-RT in T-Cells or Rabbit Lysate. Purify.
Add in a RNA template with the appropriate primer.
Hydrolyze your RNA
Detect your cDNA.


text:
Determining if a Protein Model Contains a Backbone Clash
I have an ensemble of homology models of a protein, and I now wish to remove those models which have backbone clashes. I could obviously check by eye but this is subjective and probably will not be accepted for publication.
What is the best (reproducible) method to determine if a particular protein model contains a backbone clash?

The way to check for steric clashing between any two atoms, backbone or otherwise, is to compute their Euclidean distance. If a and b represent two atoms (with a_x being the X coordinate of atom a and so forth), you can calculate their Euclidean distance as follows.

d(a, b) = sqrt( (a_x - b_x)^2 + (a_y - b_y)^2 + (a_z - b_z)^2) )

So essentially the idea would be to calculate the pairwise distance between each of the backbone atoms. For any pair of atoms, there is steric clashing if the distance between them falls below a certain threshold. If I remember correctly, this threshold is the sum of the van der Waals radii of the two atoms.

I am assuming that the variables a and b represent atomic radii of the two respective atoms. So a_x is the atomic radii of a * the x co-ordinate? Wont this equation return an error if I try to square root a -ve number? To determine a steric clash I add the radii of atoms a and b and if this value is greater than the value from the equation I have a clash?

Yes, a and b are 3-dimensional vectors each containing the X, Y, and Z coordinates of the two atoms. However, the value inside the sqrt() will always be non-negative since each of the three differences is squared, so getting an undefined value shouldn't be a problem. I have updated the answer.

Using the Euclidean distance works if you assume that the proteins cannot invade each others surfaces. However, with current prediction software (I realise the post is 12 years old!) I have found predictions in which the volumes of the proteins intersect.
As an example, imagine you have two identical rings, and the circumference of one intersects in the center of the other. If their radii are larger than the maximal distance to consider a clash, they would be considered as OK with no clash with the Euclidean approach.

Is this a comment on the question or the answer. Let me know and I'll transfer it as appropriate. Use my handle "@David" in your reply so that I am alerted.

@David , I mistyped and meant to answer (for which I did not have the reputation. I have edited the answer to omit that sentence now) - thanks!


text:
Are there more descriptive ways of naming genes and gene interactions?
I couldn't help but notice just how non-descriptive the gene names that modern genetics is using. Currently I'm reading "The new science of Evo Devo" by Sean B. Carroll and here are some examples of gene names used:

Fzrb
Krox 20
Hoxa2, Hoxb4
ZPA
FGF8
sonic hedgehog

While these names identify genes uniquely, they do very little to express what and where the gene does, or how it is related to other genes (While FGF8 may be related to FGF7, it's relationship to XYZ10 is not obvious).
I get the need to uniquely identify genes , and the book is an example of just how hard it is to presently write about a lot of genes at once. The author creates a picture of what's going on, but the gene names get in the way. Even in cases where a gene has a semi-descriptive name, like "eyeless", the reader has to remember that it's actually the gene responsible for eye formation.
Are there are any efforts underway to systematize or name genes for a given organism in an expressive manner?
As a programmer, I write code for a living, and having descriptive names makes it easier to look at someone else's code, read about code and even discuss it with novices. For example:

initializeDataModel
createViewHierarchy
userDidSelectLayerAtIndex

Modern programming tools make using descriptive names easier, because of autocomplete - typing in the first few letters of a programming structure completes the rest. Even google has a list of autocomplete suggestions.
We are all familiar with the Internet, where biology.stackexchange.com/questionname resolves into a specific page. Stackexchange is the site we are visiting, and Biology is a subset of that site. There are other biology websites, but biology.stackexchange.com uniquely identifies this site. The use of "biology" in the address gives readers a general idea of what the site is about and relates it to other biology sites. Our web browsers resolve the address into a proper string of bytes and get the right page. What if we name genes like like

com.drosophila.eyeformation
com.chicken.limb.structure.ZPA
com.human.development.geometry/XYZ10

,and whatever technology we use would actually resolve that descriptive name into a gene or a series of gene interactions?

You are absolutely right and gene names are often horrid. Just wanted to point out that one of the genes on your list is actually quite descriptive: FGF8 is fibroblast growth factor 8, doesn't get any better than that.

@terdon Some have really huge full forms e.g. NEDD: Neuronal precursor Expressed Developmentally Downregulated; SNARE: Soluble N-ethyl maleimide-sensitive factor Activated protein REceptor ... :P

Many gene names are descriptive, e.g. DRD1: dopamine receptor D1, TOP2A: DNA topoisomerase 2-alpha, or PTGS1: prostaglandin G/H synthase 1. These are examples of genes that have a clearly defined main function.
The genes you listed are involved in development, and there describing the function of a gene becomes much more difficult. E.g. sonic hedgehog is involved in patterning many organs, from brain structures to teeth. How would you assign a descriptive name?
The analogy to (programming language) functions does not work for many genes, because they were not designed to fulfill one function, but evolved to do many different functions. For genes that have many functions, we just need a unique name. The multitude of functions is catalogued elsewhere.
(Bonus descriptive gene family name: MAPKKK: MAP kinase kinase kinase)

there are actually MAP4Ks as well - Mitogen Activated Protein Kinase Kinase Kinase Kinases :)

Maybe there's a higher level of abstraction then, like gene interactions or cycles that can be given descriptive name?

@AlexStone: there are pathways that can be given a nice name, e.g. http://www.genome.jp/kegg/pathway.html -- but even then there will be more functions to the pathway than what can be encapsulated in the name

In theory, your idea seems reasonable, but I can see at least to problems with implementing it.
First, the situation is complicated by the fact that genes often carry out multiple functions, and a single label is often insufficient to annotate the complete functional repertoire of a gene. @MichaelKuhn made an excellent point with regards to the evolution of gene function. When one stops thinking about a gene (and its protein products) as something that was designed to fulfill a specific purpose, but rather as something that has been adapted (often serendipitously), for better and for worse, to fulfill a particular set of functions, the difficulty with annotating gene function is a lot clearer.
Second, this idea is confounded by the fact that reliable functional annotations are really, really rare. Sure, lots of genes in human and yeast and Drosophila have been extensively studied for decades, and many of their functions are well understood (at least we think they are). But for the vast majority of genes for the vast majority of organisms that have been studied, functional annotations are inferred from sequence similarity to previously annotated genes, without any additional experimental validation. Of course, every genome project would love to functionally classify all of the genes for their pet genome, but this is really expensive, time consuming, and low-throughput. For every extensively studied, well annotated gene, there are literally hundreds of analogous genes in other organisms that have been annotated solely based on sequence similarity to this gene. As disappointing as this is, it doesn't seem like it's going to change any time in the near future (unless there are some drastic improvements in the throughput of gene function annotation). So any proposed nomenclature convention that does not address this reality is quite inadequate in my opinion.

Are there are any efforts underway to systematize or name genes for a given organism in an expressive manner?

As you observed, the genes are named by their discoverers and some genes usually have anecdotes behind their names. Since gene names have to be small it is difficult to systematically describe them completely. But gene nomenclature can adopt a certain way of classification and it has been used extensively in yeast; genes are named by their chromosomal locations (This was done in an age when cytogenetics was more developed than functional genetics. So you can understand why it so happened). Some genes were named after the processes they are involved in. For example cdc2, cdc48 etc (cell cycle control)
Check this site: it has some guidelines for gene nomenclature.
But I completely agree with you that there should be a standard way of nomenclature. Perhaps it shall happen when functional genomics gets saturated.

This is of only peripheral relevance, but I think that you have got the history of yeast genetic nomenclature backwards. For decades yeast genes were defined functionally and were named accordingly. So, for example, the CDC genes (uppercase = dominant form, usually wild-type, lowercase = recessive form, usually mutant) were described by Lee Hartwell in 1970, about 25 years before the yeast genome was sequenced. At this point ALL of the ORFs/genes were given a systematic name (e.g. CDC1 is YDR182W). The aim is, however, still for all genes to be given a name relating to function as well.

I think it seems like a good idea at first but...
You have to take into account that as has been said genes might have multiple roles, sometimes very different and for most of them functions are still unknown.
So It's very difficult to classify a constatly changing promiscuous set of things. Even the gene concept is changing (Hello, ENCODE :)).
To me It's a lot easier to leave names as short as possible with some hints of they role (just the way they are) and if you're interested in the specific function, a very quick visit to a database and using the list as input will provide you with the current description and/or function of the gene.


text:
What light intensity determines the start/end of a photoperiod in humans?
I'm reading this article, which discusses the influence of Long Photoperiod (LP) and Short Photoperiod (SP) on melatonin production:
HIOMT drives the photoperiodic changes in the amplitude of the melatonin peak of the Siberian hamster[1].
I'm interested in knowing what light intensity is interpreted as the onset and end of a light-dark photoperiod.
The referenced article indicates that animals were kept in cages, with a pre-set photoperiod duration, this sounds to me like it was done indoors. If it has been done indoors, then artificial lighting was involved, and I would guess it was an on-off affair, rather than gradual change or jumps in intensity.
The reason why I'm asking is that I'm trying to understand the implications of this article for humans, who may wake up before dawn, and spend some time under artificial lighting of various intensity before sunrise, and continue to function after sunset. For example a person may be looking at a TV or a monitor, and I would like to get an idea if this "presence of light" is enough to trigger photoperiod-related changes in the brain. Is there some "critical" density (or density at a specific wavelength) of light that signals the start/end of a photoperiod?

Ribelayga C, Pévet O, Simonneaux V. 2000. HIOMT drives the photoperiodic changes in the amplitude of the melatonin peak of the Siberian hamster. Regulatory, Integrative, and Comparative Physiology, 278(5), R1339-R1345.

The effects upon sleep of blue light exposure from screens is quite a current topic. Have a look at this blog post which points to a couple of recent studies:  http://www.marksdailyapple.com/how-light-affects-our-sleep/#axzz26uyWBa1R

Thank you! That article mentioned melanopsin as a pigment responsible for blue light detection in the eye. Since human eyes differ from hamster eyes, I would expect that the density of melanopsin in the eyes differs.  It would help to know what intensity of blue light triggers sleep-wake related changes in the brain.

It isn't really a specific light intensity that an organism will interpret as the start of a photoperiod. Maynard Johnson reported in 1939 that intensity of light used had an effect on the rate at which mice would shift their circadian rhythms. So, brighter light has a stronger effect, but there isn't a cutoff point that I'm aware of. Johnson was using illumination as low as 2.5 foot candles, which is pretty dim. Aschoff and Pittendrigh did some more work on light intensity in the 50s and 60s, but I don't think anyone ever found anything resembling a cutoff point, only the degree to which intensity had an effect.
Computer monitors are pretty bright. Luminance rating is typically 250-350 cd/m2, which, for comparison with Maynard's experiment, is eqivalent to 23-32 foot-candles. http://computer.howstuffworks.com/monitor6.htm
Johnson, Maynard S. "Effect of continuous light on periodic spontaneous activity of white‐footed mice (Peromyscus)." Journal of Experimental Zoology 82.2 (1939): 315-328.


text:
Accuracy of genome size estimation by flow cytometry
I'm working on a genome project and using an in silico k-mer analysis to estimate the size of our genome based on the available Illumina reads. The k-mer based estimate is consistent across a wide range of k values, but is substantially lower than the previous estimate based on flow cytometry (described in Experimental procedures of this paper). How accurate are estimations of genome size based on flow cytometry?

Could you please edit your question and provide information on how exactly the genome size was determined by flow cytometry?

If I understand the paper correctly, they are using fluorescence of nuclear DNA to estimate the genome size, presumably using a standard curve control, which is very clever and I guess if they do not have any saturation problems in signal detection and if their assumption about fluorescence to DNA size linear relationship holds true (presumably having done a standard curve), and if dense chromosomal areas don't make some kind of odd fluorescent effects then I don't see a major flaw in their work but very interesting and at the same time very simple and potentially high-throughput!

I don't think your results conflict. k-mer analysis is a measure of genome length, and flow cytometry is a raw measurement of DNA quantity. If I understand k-mer analysis correctly, a diploid or polyploid organism will give the genome length under k-mer analysis, and the genome length * the ploidy under flow cytometry. Are your results close to an integer multiple of their results?

@JeremyKemball No, it's not near an integer multiple, so it's not a ploidy issue. The reasoning behind the k-mer analysis is to identify a sequence that occurs once in the genome and count how many times it occurs as a proxy for coverage. Since that unique sequence is unknown, we instead examine k-mer distributions and look for the mode in those distributions.

Perhaps highly repetitive regions in the genome? Those should stand out in your k-mer analysis, though. If the reads have been filtered to remove hard-to-assemble repetitive regions, that might explain the discrepancy.

PI and DAPI can be used to approximate genome size. But you would need standards (known cells) and it is not accurate. I guess you can also estimate genome size by enzymatic digestion and capillary electrophoresis (it is just a guess).


text:
What Defines a Food as Edible?
With many foods today containing chemicals, agents and preservatives etc... What biological criteria must a new food and its constituent components satisfy biologically, to be defined as edible?
For example do they look at the chronic/acute affects of chemicals in the body?
This question is just limited to chemicals, if a new fruit was discovered, how would it be decided if it was edible or not?

As far as I know, edibility (wow, I'm surprised that passes the spell checker!) is not a strictly defined term, biologically or otherwise. Humans have been around eating and drinking stuff long before the scientific method was around to study this question rigorously, and before there were regulatory agencies charged with approving new products as "safe." As one might imagine, knowledge of what is and is not edible was likely passed down by oral tradition and personal experience.
Honestly, I'm not even sure designating a food (or a substance) as edible or inedible really makes much sense. Let's consider wild fruit, as mentioned in your question. If ingesting 5 or more berries of hypothetical fruit X causes your body to have a nasty reaction, then we could probably agree that fruit X is toxic and inedible (even if eating only 1 or 2 berries might not elicit the same reaction). On the other hand, ingesting berries of hypothetical fruit Y causes no reaction unless consumed in much larger quantities (maybe 100 or more berries). Although fruit Y does cause a reaction when ingested in excessive amounts, it would be a stretch to call it inedible. This principle applies to many foods that we typically consider edible but can be unhealthy or even dangerous when taken in excess.
So where do we draw the line? How much of a substance do you have to ingest without an adverse reaction to deem it edible? I don't think there is an objective answer to this question. It is complicated further by the vast amounts of variation in the human population: food allergies, differences in tolerance to certain substances, etc.

+1: it has to be noted, though, that there is a very big difference between edibility and suitable for human consumption, where the second one is simply defined according to local regulation. A food that is suitable for human consumption for instance in Europe may not be suitable for human consumption in the US and vice versa (and many examples of this exist)

@nico Indeed. But whatever any arbitrary group (government, social organization, etc) decides to term as "suitable" does nothing to change the underlying biology, which was the original question (and should be considering the scope of this site). One would expect and hope that such policy decisions be based on the underlying biology...

surely I totally agree although, alas, these laws are seldom made by listening to scientist...

Much like Daniel Standage suggests, I think "edible" is more inferried than defined, sort of like looking at a black hole - its absence is defined by the activity around it. Human bodies are capable of metabolizing lots of compounds that become poisonous pass some threshold.
In medical terms there are LDmin and MLD and LD50: miminum Lethal Dose, Median Lethal Dose, Lethal Dose for 50% of the Population respectively.
There are also compounds that aren't lethal, but are definitely harmful. Trans-Fats are one, where the FDA hasn't determined any safe levels of Trans-Fats in foods; they're always dangerous and harm your system.
Then there are materials or chemicals that will simply pass through your system without being absorbed or interferring with anything. Cellulose (refined wood pulp) is a popular additive in pre-made diet foods because it adds mass and texture while being completely indigestable since humans do not produce cellulase. The same can be said for silicone dioxide (sand), which is also very unreactive and passes through your digestive system benignly.
So I'd say as long as whatever is eaten is below the LDmin and/or can benignly pass through your system without damage, it is 'edible.'

+1 And since LDmin and related values must be tested a verified for each substance individually, it is clear why a concrete definition for "edible" is elusive.

Definitely. :-)

This is more a legal question, so I'll quote from what is lex in the EU:
Regulation (EC) No 178/2002 of the European Parliament and of the Council of 28 January 2002 laying down the general principles and requirements of food law, establishing the European Food Safety Authority and laying down procedures in matters of food safety

Article 2
Definition of "food"
For the purposes of this Regulation, "food" (or "foodstuff") means any
  substance or product, whether processed, partially processed or
  unprocessed, intended to be, or reasonably expected to be ingested by
  humans.
"Food" includes drink, chewing gum and any substance, including water,
  intentionally incorporated into the food during its manufacture,
  preparation or treatment. It includes water after the point of
  compliance as defined in Article 6 of Directive 98/83/EC and without
  prejudice to the requirements of Directives 80/778/EEC and 98/83/EC.
"Food" shall not include:
(a) feed;
(b) live animals unless they are prepared for placing on the market
  for human consumption;
(c) plants prior to harvesting;
(d) medicinal products within the meaning of Council Directives
  65/65/EEC(21) and 92/73/EEC(22);
(e) cosmetics within the meaning of Council Directive 76/768/EEC(23);
(f) tobacco and tobacco products within the meaning of Council
  Directive 89/622/EEC(24);
(g) narcotic or psychotropic substances within the meaning of the
  United Nations Single Convention on Narcotic Drugs, 1961, and the
  United Nations Convention on Psychotropic Substances, 1971;
(h) residues and contaminants.

http://eur-lex.europa.eu/LexUriServ/LexUriServ.do?uri=CELEX:32002R0178:EN:NOT

So if we rely on the legal definition (well, that in Europe at least), then "reasonably expected to be ingested by humans" is about as much detail as we're going to get.

Indeed, but I tried to answer the intended question (as perceived by me, mind you) rather than the "edible definition" part. Anyway, the OP should probably look up "food safety" in the Wikipedia.


text:
Number of spindle fibres during Metaphase?
During metaphase, the chromosomes are arranged on the equatorial plate and are attached to spindle fibres. After S phase, can the cell be said to attain the configuration of 4n?
Also, during metaphase, since two spindle fibres (one from say right centriole and other from say left centriole) are attached to one tetrad, so can it be said in a well defined pattern that for a human being, 46*2=92 spindle fibres are formed in order to proceed with mitosis? Also how would the number vary in case of Meiosis I and Meiosis II?

The number of spindle fibres is actually more than total number of kinetochore pairs. The fibres attached to kinetochores are called K-fibres and the others are called polar fibres. I cant surely say that there is exactly one K-fibre per kinetochore but as per its definition and from the microscopic images you can conclude that there is one per kinetochore.
In a normal mitotic metaphase there are 2n kinetochore pairs, and as you rightly calculated, there will be 96 K-fibres.
In meiosis-I there is a tetrad which has 2 kinetochore pairs but the ones in sister chromatids behave as a single unit. So there would be 23 fibres.
The fusion of kinetochores of sister chromatids is relaxed in meiosis-II and again a separation would require 23 fibres.
Please have a look at this article. Molecular biology of Meiosis nicely explained:
http://www.sciencedirect.com/science/article/pii/S0092867403000837
More about K-fibre formation:
http://link.springer.com/article/10.1007/s00412-005-0028-2/fulltext.html


text:
Does DNA contain information beyond protein synthesis?
It's well known that genetic information is stored in DNA.  As far as I know, DNA only has information at the protein level.  What about higher levels, such as organelles, cells, tissue, organs? Is there any known carrier of information at that level? If not, what guides those levels of structure?
Hypothesis: Above the protein level, there is no real genotype/phenotype.  Instead, it's all done through cell division.  So, there is no split between information and embodiment.  Instead, it's through a prototype-duplication model: cells grow and split, creating more cells.  As for differentation into different types of cells, and organization into tissue and organs: the information and control systems for that are currently unknown.

Excellent question. Welcome to Biology.SE!

What a timely question.

Does DNA contain information beyond protein synthesis?

Yes. In fact, protein-coding genes only constitute a tiny part – less than 2% – of the whole DNA. There are of course many other genes which aren’t protein coding: there are genes for ribosomal RNA and we find more and more genes which code for small RNAs, such as tRNA. But even if we count all those genes we won’t come above maybe 10% of the total DNA.
Most of the DNA is instead devoted to the regulation of gene expression, most importantly via the binding of transcription factors (but the picture is much more complex than that). With the conclusion of the ENCODE project, a whole slew of papers were published which show that in fact most of the DNA is actively implicated in the binding of various factors (although it’s not known how much of that actually contributed to the cell’s fitness).
But I’ve hijacked your question a bit here. So let’s come back to what you’re actually interested in:

What about higher levels, such as organelles, cells, tissue, organs?

There is no known mechanism (beyond the already mentioned regulation) which would encode such information in the DNA. Excluding its existence categorically may be hard but given that we haven’t found any machinery which would be necessary to read such information, we can be pretty confident that it doesn’t exist.

If not, what guides those levels of structure?

The higher levels of organisation are to all appearances emergent. That is, they are a consequence of the lower level organisation. For instance, take the cytoskeleton which carries much of the cell’s physical structure. It is composed of different protein complexes which form spontaneously through assembly of globular proteins (such as actin). The are several ways in which the process can be guided but strikingly it’s largely stochastic – i.e. mostly unguided, and it still succeeds in building a stable skeleton, simply by virtue of molecular properties encoded in the proteins.
I think this is a common theme of cell organisation: the elementary building blocks are encoded by the DNA, and their abundance is tightly regulated. Everything else, i.e. higher-level organisation – follows from that: abundance and localisation of the right proteins.

As for differentation into different types of cells, and organization into tissue and organs: the information and control systems for that are currently unknown.

In fact, much is known here, and it goes back to regulation on the level of DNA: we know that genes are differentially expressed depending on the cell type and stage of development (and the stage in the cell cycle). This regulation is highly complex and decoding it is a slow process. Nevertheless, the factors involved here are decoded one by one. This is the domain of developmental biology.

Thanks! Very helpful.  What about my hypothesis that not all biological information is split between genotype/information carrier and phenotype/embodiment, but some actually is closer to prototype + copier? Specifically, organelles and cells are never created ex nihlo from any type of information but always split from a preexisting one?

@S.RobertJames I don’t know. I would guess that most (though obviously not all, e.g. mitochondria / chloroplasts) organelles could also form de novo since their constituents are once again coded for in the nuclear genome and their assembly might again be either spontaneous or aided by other proteins. In fact, a friend just reminded me of things like centrioles which require a helper protein for assembly.

It really isn't correct to interpret the ENCODE data as showing that most of the DNA in the human genome is "actively implicated in the binding of various factors". According to ENCODE scientist Ewan Birney only 8% of the DNA functions in binding factors. Almost 60% of the DNA is intronic, classed by ENCODE as functional simply because it is transcribed.
http://genomeinformatician.blogspot.co.uk/2012/09/encode-my-own-thoughts.html

@Alan It absolutely is. The interaction is shown in vivo. The debate over whether this binding performs a function (and the definition thereof). Whether functional or not, it is, at some point or other, bound to – either by transcription factors or transcription machinery (i.e. transcribed). Ewan says exactly that in the blog post you linked, and he even qualifies his use of the word “functional”.

@Konrad This is a direct quotation: "using very strict, classical definitions of “functional” like bound motifs and DNaseI footprints; places where we are very confident that there is a specific DNA:protein contact, such as a transcription factor binding site to the actual bases – we see a cumulative occupation of 8% of the genome." I interpret this to mean that just 8% is "actively implicated in the biding of various factors".

@AlanBoyd No. Both I and Ewan would disagree. Ewan makes a clear distinction between the definition of “functional” which his detractors use, which would be under positive selection (and which would yield the 8% estimate, still way above classical estimates), and the one he uses, which yield 80% actively implicated in the binding of  factors (but which doesn’t necessarily contribute to the cell’s fitness, and which therefore maybe isn’t under selective pressure).

@AlanBoyd where did you see Ewan claiming that 60% is intronic? Don't you men intergenic but transcribed? Also, konrad, sorry to be a pedant but genes in the human genome are around ~5% of human DNA, protein coding exons are ~2%.

Ewan Birney: "...60% of the genome with the new detailed manually reviewed (GenCode) annotation is either exonic or intronic..."
As Konrad says, the generally quoted figure for coding (=exonic) DNA is "less than 2%" Therefore 58% of the genome is intronic: this is "almost 60%".

@AlanBoyd I see, sorry, I thought you meant protein coding genes.


text:
Is exon order always preserved in splicing?
Are there any cases in which the splicing machinery constructs an mRNA in which the exons are not in the 5' -> 3' genomic order? I'm interested any such cases, whether they involve constitutive or alternative splicing.

When you say order do you mean something like Exon 1 - Exon 3 - Exon 2 - Exon 4? or do you mean events such as exon skipping?

Exon skipping events preserve exon order. So...yeah, I mean something like your first example.

While this may not be what you are asking, given an exon sequence E1E2E3E4, if E2 and E4 have the exact same sequence, it will appear as if E1E2E3 and E1E3E2 can be generated from this gene.

I don't have any literature to back this up but I doubt that it occurs (at least frequently).
For example, imagine a simple three exon gene.  Upon splicing exon 1 to exon 3, exon 2 would be excised as part of the intron lariat and subsequently degraded.  So in order for exon 2 to be spliced to exon three you would need to either have splicing between exon 3 and exon 2 in the lariat or another copy of the pre-mRNA.  This is typically called trans-splicing but it only occurs in specialized systems such as spliced-leader sequences in C. elegans.

There are references in the literature to the phenomenon of "exon scrambling" which seems to be what you are asking about, but the prevailing view is that the evidence for this process, which comes from comparing EST sequences with genome sequences, can be explained by cloning artefacts occurring during EST characterisation. Certainly I agree that there is no evidence for a gene in which the rearrangement of exons is part of the normal pathway for mRNA generation.

Shao et al. (2006) Bioinformatic analysis of exon repetition, exon scrambling and trans-splicing in humans. Bioinformatics 22: 692-698

There is also more recent evidence from deep sequencing for rearrangement of exon order via circular RNAs:

Salzman et al. (2012), Circular RNAs Are the Predominant Transcript Isoform from Hundreds of Human Genes in Diverse Cell Types PLOS ONE 7: e30733   DOI: 10.1371/journal.pone.0030733
Most human pre-mRNAs are spliced into linear molecules that retain the exon order defined by the genomic sequence. By deep sequencing of RNA from a variety of normal and malignant human cells, we found RNA transcripts from many human genes in which the exons were arranged in a non-canonical order. Statistical estimates and biochemical assays provided strong evidence that a substantial fraction of the spliced transcripts from hundreds of genes are circular RNAs. Our results suggest that a non-canonical mode of RNA splicing, resulting in a circular RNA isoform, is a general feature of the gene expression program in human cells.

Incidentally it is perhaps worth mentioning that in the case of the lectin concanavalin A the equivalent effect is produced post-translationally when the protein rearranges.

Carrington et al. (1985) Polypeptide ligation occurs during post-translational modification of concanavalin A. Nature 313:64-67


text:
Why do DNA and RNA have the functions they have?
I know that there are two most important directions of genetic information transfer in living organisms: DNA->DNA and DNA->RNA. The first is replication, and the second is transcription. I wonder if there is a reason for this choice of directions. According to this article, all other directions are possible. Why do we use DNA for example? RNA is capable of self-replication since it happens in viruses. And why do we use RNA, not DNA, as messenger molecules? Is it just an accident or is it possible to explain why this is the right way of doing it?

One reason is surely that DNA is chemically more stable than RNA.

@nico Thank you, I didn't know that. That seems to explain why RNA is not used to store genetic information. Could you explain why RNA is used instead of DNA for communication? Is RNA easier to build?

On top of my head I cannot think of a reason. I will try to write an answer if I can find something about it.

RNA folds better than DNA.

For a reference of the RNA folding stability see http://biology.stackexchange.com/a/769/389

DNA is more chemically stable than RNA, which makes it ideal for long-term storage. RNA viruses like HIV have a short lifespan and must replicate to survive, which is why they can get by with a less chemically stable genome.
RNA is a useful format to transcribe since it has multiple forms and functions (e.g. rRNA, mRNA, tRNA, siRNA, snRNA, miRNA, etc.). RNA can sometimes function like a protein in which it carries out cellular actions without needing to be translated. It has been hypothesized that RNA were the first molecules as precursors to life since they can function for both storage and action. The theory is that RNA was the first molecule but was then able to be translated into proteins (which were more variable/useful) and able to be stored as DNA (which was more stable as a storage medium).

The first sentence of your second paragraph is essentially proof by intimidation: you’re not giving any reason here. Just because RNA can take on multiple forms doesn’t by itself say anything about the suitability of mRNA as an intermediary between DNA and proteins, especially since all the examples you’ve cited are noncoding.

True, I didn't mention any reason that it's a particularly good intermediary to be translated. I'm taking a different angle in answering the question by suggesting that maybe it has more to do with the sequence of origins instead of its usefulness as an intermediary.

Yes, in fact I’m convinced that sequence of origin is the real reason. The similarity with non-coding RNA is notable only insofar as much of the machinery for treating RNA (any RNA) is ancient and very well conserved, and thus the cell requires less innovation by relying on mRNA than it would by having some kind of mDNA.

@KonradRudolph, or RNA structure is simply more stable. see http://biology.stackexchange.com/a/769/389

@bobthejoe While that’s interesting in general (good answer!), here we are talking specifically about mRNA where structure plays no or only a very minor role.

@KonradRudolph, Well... that is a massive assumption that mRNA structure plays little to no role.

@bobthejoe Is it? Most of the mRNA seems to be unstructured, apart from cap, tail and maybe 3ʹ UTR. I admit that I haven’t read anything stating this definitely but I’ve also never read anything to the contrary (and a structure in the coding sequence sounds worth mentioning), and in fact the (electron scanning) photographs I’ve seen of transcription show elongated, unfolded mRNA tails.

I suggest going to the original refernces instead of wikipedia. Look up Gilbert (1986) in Nature for the RNA world.

If you had a complex life form which used only DNA or RNA, it would have no way to tell transcribed mXNA from genomic gXNA. This would cause problems during cellar replication, as you could also replicate your mXNA along with your gXNA. It would also cause problems repairing breaks in your gXNA, as you would run the risk of including mXNA during the repair process.
Therefore it seems advantageous to have a storage system for information which is not currently being translated into protein (i.e., DNA), as compared to just having RNA.
On the other hand a completely DNA organism would need RNA for functional ribosomes anyway. If RNA is being used for ribosomes, using it for mRNA as well to avoid confusion with genomic DNA seems advantageous.
In order to test this hypothesis, you would need to create a completely RNA/DNA based lifeform and investigate its properties. Short of starting life from scratch as RNA based and monitoring its evolution over a few million years, a conclusive proof as to why things are the way they are as opposed to being down to an evolutionary historical accident is difficult to obtain!

There are simpler ways to distinguish mXNA from gXNA. For example, single vs. double stranded, chaperone proteins or the simple absence of an origin of replication in the mXNA messenger.

https://www.quora.com/Why-do-cells-use-both-DNA-and-RNA also mentions that RNA is cheaper to replicate as it is less stable. While I don't know anything about this, I would guess that that is true.


text:
Are there verbs for "undergo mitosis" and "undergo meiosis"?
From my experience on SE sites, I believe this is the right site to ask this question under "terminology".
I've been trying to find out whether English has one-word verbs for "undergo mitosis" and "undergo meiosis". I haven't been able to find confirmation on Google, but my linguistic imagination is limited, and I may have failed to google the right things.
Could you tell me if there are such verbs in common use in biology? I mean, if such verbs exist, can I find them in modern biology books or papers?

How about "divide" or even "multiply" (if you include the entire cell cycle)? Those are generic terms, but the process is called cell division. And minor pet peeve of mine: "Google" isn't a verb...

What's wrong with "to undergo mitosis"?

@nico Nothing is wrong with that. I just wanted to know if there's a shorter way of saying this.

I'm voting to close this question as off-topic because it is about linguistics rather than biology. There is no real problem. If you are writing a paper you would write "undergoes mitosis".

I'm actually not sure myself. If I were to use something, I would go with "Mitos'd" and "Meios'd".
However, you may not win over many fans, depending on the audience. If it's with students or maybe a professor, you could get away with shortening the processes. If it's in any formal setting, be as precise and descriptive as possible. It's not a lot of trouble to be more accurate and add "underwent" to the sentence.

I agree - I do not recall seeing a verb for these actions, so in a paper or report use the actual terminology. But during discussions I'm sure people will get your meaning if you shorten the terms to "mitose" or "mitosed", or something.

Mitosis as a process does not have a verb form. However, as a process, there is an adjective; you could describe cells that undergo mitosis as mitotic.

Wiktionary suggests mitose: https://en.wiktionary.org/wiki/mitose.

The question asks “In common use in biology”, specifying books and papers. Wiktionary does not address that.

Was just researching your exact same question.  Self-replicate is the closest I could find or think of... but it's a very general verb, not even biology specific.
e.g. Please don't self-replicate, I'm already having trouble with just one of you -- said the programmer to his memory gobbling AI program.
https://en.wikipedia.org/wiki/Self-replication


text:
How can I pare down a PDB file in Python to only include specific residues?
I'm trying to make a script that will take a MTZ file (reflections), convert it into a CCP4 map, then pare that map down to only encompass a desired area to cut down on the size of my PyMol session files so they're email-able (a.k.a. not 200 MB) and ease the burden on my POS computer.
I currently have a Python script that can fft (CCP4) to create the map and mapmask to fix unit cell tiling issues.  What I want to add now is something that can take a PDB file and strip out most of it except, for example, residues within 10 Å of #123.
I've been looking at ProDy, but not quite sure where to start.  I would also be open to using something in the CCP4 toolkit.

@leonardo some sort of manual hack like that may work (as mapmask seems to expand a little anyway), but doesn't seem that optimal.  I'll beat on this for a while and let you know what I come up with.

Pymol has a selection operator that matches everthing in a specific distance around an atom, is should be possible to use that for this purpose.

@MadScientist from within a script running outside of PyMol?

I was thinking manually inside the program, but if you have to automate it, I believe you can use the pymol library from any python script.

Better fit for scicomp.se?

@David unfamiliar with that site, if you think it's better there, feel free to flag a mod down.

ProDy works quite well, especially from within an existing Python script.
The following code takes an existing PDB file, performs some selection query on it, then saves it to another file.
import prody

def pdbsubset(inpdb, outpdb, selection):
    with open(inpdb) as protf:
        prot = prody.parsePDBStream(protf)
    atoms = prot.select(selection)
    prody.writePDB(outpdb, atoms)

An example selection query builder

residues is a list e.g. ['A12', 'A39'] with each element in the form <chain><residue number>.  They were captured from the command line using argparse with
    parser.add_argument('-i', '--residues', nargs='+')

so you would specify -i A12 A39 or whatever.

pdb and outpdb are file paths
radius is the distance in angstroms to expand the selection by.

reslist = ["(chid {0} and resid {1})".format(res[0], res[1:]) for res in residues]
selector = 'within {0} of ({1})'.format(radius, ' or '.join(reslist))

# and running it:
pdbsubset(pdb, outpdb, selector)

The documentation on ProDy selection queries is not the most straightforward, but fairly analogous to PyMol, so doable.

With the program RasMol, you can select, as Mad Scientist explained it for PyMol, everything in a specific distance around an atom. RasMol can be run from command line, using a script (with the -script option under UNIX).