botany - Can any plant regenerate missing tissue?

In general, plant cells only undergo differentiation at special regions in the plant known as meristems. Two of the primary types of meristem are the root apical meristem (at the tips of roots) and the shoot apical meristem (at shoot tips)^. Within the shoot apical meristem the plant cells divide and begin to differentiate into different cell types (such as different cells of the leaf, or vascular cells). Later growth (of, say, a leaf) is largely a result of cell expansion (although cell division does still occur, but drops off as the leaf expands). Therefore, if you punch a hole in a leaf, it probably won't be filled in because the cells in that leaf have finished growing and dividing.

However, as a shoot grows, more meristems are created. These are found in the axillary buds, just above where the leaf meets the stem. The meristems in the axillary buds can grow to form branches. Different plants obviously make different numbers of branches, but there is a common control mechanism known as apical dominance, where the meristem at the tip of the shoot suppresses the growth of the lower axillary buds. This is why a shoot with no branches can be made to grow branches by cutting off the tip (gardeners often do this to make "leggy" plants more bushy).

All of that was a long explanation to say, no, a plant doesn't normally^^ regenerate in the sense of filling in cells that have gone missing. However, if you cut off a shoot, the next remaining bud might begin to grow and, in a sense, replace the part that was lost. In that case, an existing bud is recruited to form a new branch and replace lost functionality, but I wouldn't say that qualifies as regenerating missing tissue.

^There are other types of meristem as well.

^^If you torture plant cells enough you can force them to become "stem cells" and thereby make an entirely new plant, but this is rare in nature.

evolution - Is Behe's experiment (evolving the bacterial flagellum) plausible in the lab?

You may be interested in this paper and a video that summarizes it. It seems to be made quite clear that 1) effectively all of the parts of the flagellum are not original to it, and 2) there is a reasonable evolutionary path (one involving only increment/refine steps) that could have been responsible for it.

The video mentions but doesn't describe experiments that were in support of the proposed model. I assume they might involve refinement or statistical issues of the environment, not the whole-thing-at-once as Behe outlines. Obviously, if you can show that each step is independently adaptive, then the whole chain is shown to be possible evolutionarily, without trying to set up an experiment where you win the lottery n times simultaneously.

Personally I think the fact that the most awesome thing about the flagellum -- the rotation -- already exists in ATP synthase steals a lot of the flagellum's thunder. :)

Edit (Douglas S. Stones): Following the above references led me to this paper:

M.J. Pallen, N.J. Matzke "From The Origin of Species to the origin of bacterial flagella" Nature Reviews Microbiology 4 (2006), 784-790. (pdf)

In this article the authors discuss the possibility of designing a lab experiment to reproduce (steps of) the evolution of the flagellum.

Scott Minnich speculated in his testimony that studies on flagellar
evolution need not be restricted to sequence analysis or theoretical
models, but that instead this topic could become the subject of
laboratory-based experimental studies. But obviously, one cannot
model millions of years of evolution in a few weeks or months.

So how
might such studies be conducted? One option might be to look back in
time. It is feasible to use phylogenetic analyses to reconstruct
plausible ancestral sequences of modern-day proteins, and then
synthesize and investigate these ancestral proteins. Proof of
principle for this approach has already been demonstrated on several
NF proteins[69–75]. Similar studies could recreate plausible ancestors
for various flagellar components (for example, the common ancestor of
flagellins and HAP3 proteins). These proteins could then be reproduced
in the laboratory in order to examine their properties (for example,
how well they self-assemble into filaments and what those filaments
look like).

An alternative, more radical, option would be to model
flagellar evolution prospectively, for example, by creating random or
minimally constrained libraries and then iteratively selecting
proteins that assemble into ever more sophisticated artificial
analogues of the flagellar filament.

Another experimental option might
be to investigate the environmental conditions that favour or
disfavour bacterial motility. The fundamental physics involved
(diffusion due to Brownian motion) is mathematically tractable, and
has already been used to predict, for example, that powered motility
is useless in very small bacteria[76,77].

[For readability, I've added some line breaks to the above. There's too many cited references to list them all.]

bioinformatics - Displaying nucleotide at a single position from RNA-seq reads in a BAM file

How do I display a single nucleotide position from reads in a BAM file? I have been looking at variation using samtools mpileup, but I want to actually just display the nucleotide at the position I am interested in. This seems like you should be able to do it but I can't figure out how.

To be clear I have a BAM file of a bunch of reads. I'm looking to do something like samtools magic reads.bam chr3:10000 where I get back something like:

T T T T T T T T T T T T T T T T T T T A A A A A A A A A A A A A.

I just want to sanity check the output of bcftools by actually looking at the base calls.

evolution - Is extreme cladism a mainstream position in the species debate?

In the philosophy of biology it has been claimed many times that a popular position regarding the question of what species are, among biologists, is cladism. For my current purposes, the defining trait of cladism is captured in the following quote:

According to cladism, a species becomes extinct whenever it sends forth a new side species. (LaPorte 2004, 54)

So, for example, if Homo floresiensis is truly a species, and it derives, via a speciation event, from Homo sapiens, then, after the speciation, there is no Homo sapiens: there is Homo floresiensis and a new species, very similar to sapiens. In general, whenever there is speciation the mother species disappears.

I am under the impression that this description of the situation is not the one most mainstream biologists would endorse. I take it that a more common description would be one under which, if a number of Homo sapiens get isolated in an island and go on to form a new species, Homo sapiens exists both before and after this speciation event. I would like to know whether cladism, described as above, is really a popular position, or whether I am right about what most biologists would say about the relation between floresiensis and sapiens.

It might also be that biologists declare themselves cladists when explicitly theorizing about the nature of species, but fall back to a less extreme form of cladism in the actual practice. Evidence in favour of or against this possibility (coming from biology, not the philosophy of biology) would also be appreciated.

As Noah has pointed below, what I have called extreme cladism might be very far from cladism, as usually interpreted. This is precisely the kind of claim I would like to see substantiated.

LaPorte, Joseph. 2004. Natural Kinds and Conceptual Change. Cambridge University Press.

genetics - Do we get 1/4 of our genes from each grandparent?

I agree with the person above. But it might be more correct to say we get 1/4 of our total DNA from each of our grandparents, because though the genes are really important to code for specific proteins, there are tons of non-coding DNA in between them. In fact, 98% of our genome is non-coding! Although we are discovering awesome novel functions for this DNA slowly but surely. But it is important to think of it as 1/4 of your DNA and not genes because it is in this non-coding DNA where a lot of mutations can occur, and these mutations are what we inherit and make things like DNA fingerprinting for forensic analysis possible, like in CSI.

I just wanted to add three more thoughts:

Though it is true that 1/4 of your DNA would come from each grandparent, that is only true for your autosomal genes, not your necessarily for your sex chromosomes. The X chromosome does recombine regularly in the mother, but in the father the X and the Y do not recombine. (Actually I think part of the Y can recombine, but for the most part, the sex-determining part of the Y and its associated genes stay completely intact). This means that if you are a male, your father, and his father, and his father all share the same Y chromosome.

Additionally for the women, because the woman makes the egg, and thus all the early embryonic organelles and RNA's, the woman donates the mitochondrial DNA, which has its own sets of genes that are really important and have been linked to many diseases. So every child of a woman, shares their mother's mitochondrial DNA, as she shares her mother's and her mother's mother, etc.

If ~1/4 of our DNA comes each grandparent, then 1/8 of your DNA comes from each great-grandparent. So then 1/16 of our DNA comes from each great-great grandparent, which are your grandparent's grandparents. And thus it continues exponentially upward. The result is that there comes a point where your ancestors have contributed so little to your actual DNA, that it becomes almost negligible. So if you are an American, who most likely has ancestors from all over the world, even if you have 1 great-great-great-great grandparent who was a French immigrant while the rest of your ancestors were all British, the French DNA is only 1/64 of your total DNA. So even if you are a complete mix, there comes a point where so many different people have contributed to you being you, that you can establish a cut-off and just say, 3/4 of my ancestors were born in America, I'm American!

genetics - Which patterns do I have to avoid when modifying the 3'-UTR?

I want to change a pre-miRNA sequence (in my case the pre-miRNA is encoding in a 3'UTR of a gene) and then put it in a lentivirus to see if it is still processed.

After modification (permutation of ten regions of ~20 nt) which kind of newly appeared pattern I've to be careful about? I do not want to disturb the gene in which the miRNA is encoded