This week in PNAS, Rockefeller University's Amrita Basu is first author on a paper that looked at genome-wide patterns of acetylation substrate specificity. The scientists developed a prediction tool, PredMod, that combines experimental methods with clustering analysis of protein sequences to predict acetylation based on acetylated lysines within histones. Their method, they say, "combined with more traditional experimental methods, may be useful for identifying acetylated substrates proteome-wide."
Current human malaria strains have evolved from those that infect chimps, and not separately, says Stanford's Nathan Wolfe in a paper published this week. Taking blood samples from chimps in Cameroon and Côte d'Ivoire, his team discovered eight new strains of the parasite that infects chimps, Plasmodium reichenowi, all of which were very diverse. "There is a tremendous diversity of these parasites in chimpanzees, and it’s a diversity that completely encompasses a much more limited diversity in human malaria," he says in a story in Wired, adding that the chimp strain has been around a lot longer. Phylogenetic analysis showed that all P. falciparum strains originated from P. reichenowi and that this may have occurred as early as 2 million to 3 million years ago, or as recently as 10,000 years ago.
Work out of Carlos Bustamante's lab at Cornell studied the origins of the domestic dog, and the genetics behind small dog breeds. Ryan Boyko and Corin Boyko, two authors, led the blood sampling work from village dogs in Africa, collecting 318 samples from seven regions in Egypt, Uganda, and Namibia. To their surprise, they found that African village dogs are a blend of indigenous and non-native dogs. "We find similar mtDNA haplotype diversity in African and East Asian village dogs, potentially calling into question the hypothesis of an East Asian origin for dog domestication." The New York Times has the interesting back story to the work.
UCLA's Adam Sperling and Michael Grunstein studied the structure of yeast heterochromatin, namely how the H3 N-terminal tail interacts with Sir3 and Sir4 to silence gene expression. Using high-resolution genome-wide binding maps of heterochromatin proteins, they found that the H3 N terminus is not needed for either recruitment or spreading of Sir proteins at telomeres and the mating type (HM) loci, suggesting that "Sir proteins recruited by the H4 tail then interact with the H3 tail to form a higher order silent chromatin structure."