In a paper published online in advance in Nature this week, investigators at ETH Zürich's Institute of Molecular Biology and Biophysics report crystal structures for the Saccharomyces cerevisiae chromatin remodeling factor ISW1a "lacking its ATPase domain both alone and with DNA bound." In combining the composite X-ray and electron microscopy structures, and employing site-directed photocrosslinking analyses of these ISW1a complexes, the team found evidence that suggests "how a chromatin remodeling factor could set the spacing between two adjacent nucleosomes acting as a 'protein ruler.'"
A trio of researchers at the MRC Laboratory of Molecular Biology in Cambridge, England, reports a crystal structure for the U4 small nuclear ribonucleoprotein core domain and details "its implication for snRNP biogenesis." More specifically, the MRC Laboratory team shows that snRNA-dependent structural alterations "may facilitate the binding of particle-specific proteins that are crucial to biogenesis of spliceosomal snRNPs."
In a paper published online in advance in Nature Genetics this week, a team led by investigators at the Harvard School of Public Health reports its "use of whole-genome sequencing to estimate the mutation rate for Mycobacterium tuberculosis during latent infection" in cynomolgus macaques. By sequencing 33 Mtb isolates from nine animals at an average coverage of 93 percent and read depth of 117x, the researchers identified "a similar mutation rate during latency as during active disease or in a logarithmically growing culture over the same period of time," as well as a pattern of polymorphisms to suggest that "the mutational burden in vivo is because of oxidative DNA damage." Our sister publication, GenomeWeb Daily News, has more on this sequencing study.
Over in Nature Medicine, Xinyu Zhao and her colleagues at the University of New Mexico School of Medicine show that the ablation of fragile X mental retardation protein — FMRP — in neural stem and progenitor cells via inducible gene recombination "leads to reduced hippocampal neurogenesis in vitro and in vivo," and, in a mouse model, it "markedly" impairs hippocampus-dependent learning. In restoring Fmrp expression in neural stem and progenitor cells, the team rescued these learning deficits in null mice. Zhao et al. suggest that "adult neurogenesis may contribute to the learning impairment seen in FXS [fragile X syndrome]," and that it "can be rectified by delayed restoration of" Fmrp in neural stem and progenitor cells.