In a paper published online in advance in PNAS this week, investigators at The Scripps Research Institute in La Jolla, Calif., and their colleagues use whole-genome sequencing and microarray analysis data to show that a recent Peruvian Plasmodium vivax isolate — dubbed IQ07 — has one SNP per every 985 bases, which distinguish it from the reference strain of the malaria-causing parasite. They also show that "the genes containing the largest ratio of non-synonymous-to-synonymous SNPs include two AP2 transcription factors and the P. vivax multidrug resistance-associated protein," which, they write, has implications for future drug-resistance mapping studies.
The Food and Drug Adminstration's Alexander Neverov and Konstantin Chumakov suggest in PNAS this week that massively parallel sequencing is the "ultimate tool for monitoring genetic consistency of live viral vaccines," as it allows for the "sensitive detection and quantification of all mutations in the entire genome of attenuated viruses." The team's MPS-based data on a test set of vaccines was in "perfect agreement" with that generated by mutant analysis by PCR and restriction enzyme cleavage, though the former contained added information about mutations present at a low level, making it superior to the traditional MAPREC test, Neverov and Chumakov write.
Researchers at Harvard Medical School describe the "molecular architecture of the vesicular stomatitis virus RNA polymerase" in a paper published online in PNAS this week. The team suggests that phosphoprotein cofactor binding is "likely important for RNA synthesis," and shows that "because the arrangement of conserved regions involved in catalysis is homologous, the structural insights obtained for VSV L [large] likely extend to all NNS [non-segmented negative-strand] RNA viruses."
Harvard Medical Schools' Bo Li and Christopher Walsh identify the gene cluster involved in holomycin biosynthesis in Streptomyces clavuligerus. Li and Walsh examined the S. clavuligerus genome and found a candidate cluster in open-reading frams 3483-3492; in their subsequent analyses, the pair found that "deletions of ORF3488, the NRPS module, and ORF3489, a phosphopantothenoylcysteine decarboxylase homolog, abolished holomycin production both in wild-type and in a holomycin-overproducing mutant," they write in PNAS this week.