Human Genetic Variation Alters Anthrax Toxin Sensitivity
Martchenko, Candille et al., PNAS
Researchers at Stanford University School of Medicine show that genetic variation affecting capillary morphogenesis gene 2, or CMG2, dramatically alters toxin sensitivity in humans. In its analysis, the team reports on "a CMG2 single-nucleotide polymorphism occurring frequently in African and European populations [that they found] independently altered toxin uptake." The group goes on to suggest "testing of genomically characterized human cell populations may offer a broadly useful strategy for elucidating effects of genetic variation on infectious disease susceptibility."
This Week in PLoS
January 13, 2009
An international team of scientists used chIP-on-chip to map the chromosomal distribution of Drosophila Polycomb group (PcG) proteins, the N- and C-terminal fragments of the Trithorax (TRX) protein, and four candidate DNA-binding factors for PcG recruitment. They also mapped histone modifications associated with PcG-dependent silencing and TRX-mediated activation. Among their findings, they saw that PcG proteins co-localize in large regions, or polycomb domains, and co-localize with recruiters to form several hundreds of possible PcG response elements. "Strikingly, the majority of PcG recruiter binding sites are associated with H3K4me3 and not with PcG binding, suggesting that recruiter proteins have a dual function in activation as well as silencing," they say in the abstract, published in PLoS Biology.
In another paper in PLoS Computational Biology, a team led by scientists at SRI International used cross-genomic computational modeling to identify new peptide ligands for "orphan" G-protein-coupled receptors. To validate their method, they used it to identify a previously undiscovered neuropeptide that is found in certain brain regions and other organs.
A genome-wide association study published in PLoS Genetics this week has found new susceptibility loci for Kawasaki disease, a disease in children that damages the coronary arteries. Looking at a total of 893 KD cases, the scientists identified significant associations of 40 SNPs and six haplotypes, identifying 31 genes. NAALADL2 and ZFHX3 were found to be the most significantly associated. They also discovered that the associated genes are potentially related to inflammation, apoptosis, and cardiovascular pathology.