Sunday, December 24, 2006
Earlier this fall, Nakabachi et al. described a 160-Kilobase genome from the bacterial endosymbiont Carsonella in Science (PubMed). Now, Baker et al. describe acidophilic Archaea that may be the smallest cells yet observed (Science, PubMed). The authors themselves express this claim cautiously ("It has not escaped our attention that if the average cell size estimated from TEM observations is accurate, the ARMAN cells have volumes of <0.006>3, making them smaller than any other known cellular life form."), but it seems to me that even if this is some sort of artifact (perhaps these cells are larger, but extremely reticulate) it still bears on the controversy regarding microfossils in the martial meteorite ALH84001, which have been thought too small to be life.
Sunday, December 10, 2006
Today's New York Times reports (on the front page, in "DNA Gatherers Hit Snag: Tribes Don't Trust Them" by Amy Harmon) that the Genographic Project of National Geographic has been slowed by resistance from skeptical indigenous people, and a specific case involving "the Alaska review board" is highlighted. However, the same article also states that they have collected over 18,000 samples from remote places and 150,ooo samples from nonindigenous Americans interested in their roots. The picture is a screenshot from the National Geographic site.
Sunday, November 26, 2006
Two recent articles confirm that resveratrol can benefit health. Baur et al. report in Nature that mice on a high-calorie diet not only live longer if fed resveratrol, but also show increased insulin sensitivity, increased PGC-1 activity, increased mitochondrial number and improved motor function. Lagouge et al. report in Cell that resveratrol not only greatly increases mitochondrial function and endurance but that downstream effects on gene expression depend on SIRT1-dependent deacetylation of PGC-1. These results are all consistent with resveratrol acting through the same pathway by which caloric restriction extends lifespan. In just a few weeks, these results have been widely reported and are already well known. I recommend reading the original articles and the commentary by Kaeberlein and Rabinovitch in Nature, and following the reporting by Nicolas Wade in the New York Times. I expect this story to show considerable endurance.
Tuesday, October 24, 2006
When U12 introns were found in plants (Wu et al. 1996, "Non-canonical introns are at least [a billion] years old" PubMed, Nature Genetics) we knew that they must have been present in the ancestors of most unicellular eukaryotes, but none had been found until now (Russell et al. 2006; PubMed, Nature). Thus, this discovery of minor spliceosomal snRNAs proteins and introns in unicellular eukaryotes was anticipated, but it is still very exciting. It will provide tools for understanding the dynamics of U12 intron loss. In addition, the early indications are that the conservation observed between plants and animals is also retained in these species, making the divergence in insects (Schneider et al. 2004; PubMed, PNAS) all the more interesting.
Monday, September 18, 2006
The publication of "An RNA gene expressed during cortical development evolved rapidly in humans" by Pollard et al. (Nature, PubMed) is significant for several reasons. HAR1F appears to be one of those genes under selection in humans (see "From HapMap to Selection Map," May 12, 2006). Such genes, the methods for finding them, and their roles in human development, are all important. For me, however, there is special excitement because this study points to an important role for a spliced ("mRNA like") noncoding RNA. I have long been a fan of noncoding RNAs in general. I like to emphasize that not all exons are coding (see "Things that are not Exons," June 30, 2005) and that not all non-coding RNAs are of the class that associates with the RISC complex. This result does both.
Tuesday, September 05, 2006
The Washington Post describes a new study by Abraham Reichenberg and colleagues showing a significant effect of paternal age on autism rates (link). The author, Shankar Vedantam, ends with this:
While the link between older fathers and autistic children is likely to be genetic, the researchers who conducted the new study also acknowledged the possibility that unknown other factors could simultaneously be causing men to delay parenthood while independently increasing autism rates.It seems to me that, paradoxically, this is backwards. If paternal age itself somehow leads to autism, then the cause is less likely to be genetic (a father's genes don't change as he ages, but epigenetic factors could play a role). On the other hand, if there are factors that simultaneously delay parenthood and induce autism, those factors could be genetic. Under this hypothesis, fathers with certain alleles are more likely to be fathers late in life, and those same alleles, inherited by the child, could cause a predisposition towards autism.
Monday, September 04, 2006
Yes, I'm starting yet another blog! This one is devoted to quick comments on genetics news. I have developed the habit of bookmarking articles on Connotea. This blog a place where I can put my brief comments on news that interests me, and provide links to related sites of interest.