In work appearing this week in PLoS Biology, scientists led by the University of Toronto's Charles Boone used a blend of phage display, yeast two-hybrid, and peptide array screening to scan billions of peptides in order to find SH3 domain binding partners in S. cerevisiae. After creating a "high-confidence yeast SH3 domain interaction map," they showed that the binding peptides were enriched for proteins involved in endocytosis.
A consortium of researchers performed a meta-analysis of GWAS studies linking a polymorphism of the INSIG2 gene to obesity, which has been "highly debated." Looking at 27 studies including a total of 66,000 Caucasian subjects, they found no overall association of this marker, rs7566605, with obesity. Instead, the data suggest an association with extreme obesity. "The importance of study design might be under-recognized in gene discovery and association replication so far," they write. The work was published in this week's PLoS Genetics.
In PLoS Pathogens, scientists performed the first large-scale rotavirus genomics project. Led by NIH's John Patton, they sequenced the genomes of 51 isolates from 1974 to 1991 from patients at Children's Hospital National Medical Center in Washington, DC, and found that "several distinct groups (clades) of rotaviruses co-circulated and caused disease in a single epidemic season." Contrasting with what they had thought, they discovered that few rotaviruses exchanged gene segments with each other. "Instead, the genome constellations of the viruses remained relatively stable," they say.
Finally, researchers used metabolomic profiling to identify biomarkers that are associated with idiopathic and LRRK2 Parkinson's disease. Led by Mikhail Bogdanov at Weill Medical College of Cornell University in New York, they found that the plasma metabolomic profiles of both idiopathic PD and LRRK2 PD subjects were separate from controls and that "LRRK2 PD patients had metabolomic profiles distinguishable from those with idiopathic PD, and the profiles could predict whether the PD was secondary to LRRK2 mutations or idiopathic," they write. Their work appears this week in PLoS One.