In a paper published online in Nature this week, a team led by investigators at the University of California, Los Angeles, reports its use of gene co-expression network analysis to identify "differences in transcriptome organization between autistic and normal brain." Furthermore, using RNA-seq and a published genome-wide association study for autism, the team found evidence to support the involvement of the neuronal specific splicing factor A2BP1 and other known susceptibility genes in autism. Our sister publication GenomeWeb Daily News has more on this study here .
Investigators in France show in a Nature advance online publication this week that "SAMHD1 is the dendritic- and myeloid-cell-specific HIV-1 restriction factor counteracted by Vpx," a primate lentivirus auxiliary protein. By silencing SAMHD1 in non-permissive cell lines, the team observed an alleviation of HIV-1 restriction — which it says is associated with an accumulation of viral DNA in infected cells. SAMHD1 silencing also showed an increase in the susceptibility of monocytic-derived dendritic cells to infection, the authors write.
A team led by researchers at the Max Planck Institute of Biochemistry in Martinsried, Germany, shows that in Saccharomyces cerevisiae alternative splicing of SRC1 pre-mRNA "is promoted by the conserved ubiquitin-like protein Hub1," as it reports in an advance online Nature paper. "Hub1 binding mildly alters spliceosomal protein interactions and barely affects general splicing in S. cerevisiae," the team writes, adding that "spliceosomes that lack Hub1 … cannot use certain non-canonical 5' splice sites and are defective in alternative SRC1 splicing." Overall, the team says that its study "indicates a novel mechanism for splice site utilization that is guided by non-covalent modification of the spliceosome by an unconventional ubiquitin-like modifier."
Finally, in this week's issue, researchers at the Stanford University School of Medicine, along with their colleague at Brigham Young University in Provo, Utah, discuss the "chromatin remodeling mechanisms … that govern nucleosome organization at promoters, regulatory elements, and other functional regions in the genome." Using deep sequencing to map nucleosome organization in three primary human cell types, the team found that most of "the genome showed substantial flexibility of nucleosome positions, whereas a small fraction showed reproducibly positioned nucleosomes," it reports in Nature.