In Science this week, the University of Michigan, Ann Arbor's Patricia Wittkopp is first author on a paper that found that genes that code for color in fruit flies have an ancestral polymorphism. Two genes, ebony and tan, contribute to body color changes both within Drosophila americana and between this species and D. novamexicana, as they found that after sequencing multiple isolates, some strains of D. americana harbor alleles of tan and ebony that are more closely related to the D. novamexicana alleles than they are to other D. americana alleles. Their work suggests that genetic variation in a common ancestor gave rise to both inter- and intraspecies color differences.
Work out of David Bartel's lab at MIT shows that the mechanism of RNAi is not, actually, missing from all species of yeast, though up till now it has not been found in one of the most studied lab strains, Saccharomyces cerevisiae. In this paper, they found that RNAi is present in other budding yeast species, including Saccharomyces castellii and Candida albicans, and that by introducing Dicer and Argonaute of S. castellii into S. cerevisiae, they could restore RNAi. "These results identify a previously unknown class of Dicer proteins, bring the tool of RNAi to the study of budding yeasts, and bring the tools of budding yeast to the study of RNAi," says the abstract, while a perspective from Harvard Medical School's Danesh Moazed adds more.
A metagenomic study of oxygen-deficient ocean waters, or oceanic "dead zones," has revealed a deep-sea sensitivity to environmental changes. Scientists at the University of British Columbia, Vancouver, performed metagenomic analyses of an abundant microbe living in these dead zones that is both related to chemoautotrophic gill symbionts of deep-sea clams and mussels and was found to have genes that regulate "autotrophic carbon assimilation, sulfur oxidation, and nitrate respiration responsive to a wide range of water-column redox states," they say in the abstract.
Finally, work published online a few weeks ago found a possible viral link to chronic fatigue syndrome. Vincent Lombardi at the Whittemore Peterson Institute in Reno and Francis Ruscetti at NCI looked at peripheral blood mononuclear cells from CFS patients and discovered DNA from a human gammaretrovirus, xenotropic murine leukemia virus-related virus, in 68 out of 101 patients as compared to 8 out of 218 healthy controls. Further studies are needed to see if the virus actually causes the disease, offers a perspective written in part by Tufts University's John Coffin.