In this week's issue of Science, a Wellcome Trust Sanger Institute-led team describes its high-throughput, bulk bacterial sequencing approach for following methicillin-resistant Staphylococcus aureus or MRSA, evolution. By sequencing isolates collected around the world over many years and at a Thai hospital over several months, the researchers show that they can follow MRSA transmission between continents and within a single hospital. Scientific American reports on some of the implications of the work, while blogger Keith Robison delves into the team's methodology and the future of MRSA sequencing.
University of Toronto researcher Charles Boone and his team used synthetic genetic interaction data to come up with a genome-wide genetic interaction map for the budding yeast Saccharomyces cerevisiae, gaining insights into everything from gene function and regulation to drug targets in the model organism. "[G]enetic interaction maps provide a model for understanding the link between genotype and phenotype and for outlining the general principles of complex genetic interaction networks," they write, "which play a key role in governing inherited phenotypes, including human disease." For more information, check out a related news story in our sister publication GenomeWeb Daily News.
A group of researchers from Japan and the UK demonstrate that networks created by the slime mold Physarum polycephalum are comparable in efficiency, fault tolerance, and cost to the Tokyo rail network. In a perspectives article in Science, Wolfgang Marwan notes that self-organization, self-optimization, and self-repair in the slime mold may also inform mobile communication and computational networks. Meanwhile, The Economist says the work illustrates how simple principles can be used to come up solutions to complex problems.
In the early, online issue of the journal, researchers from Imperial College London explore the mechanism by which viruses spread from one cell to the next. Based on their experiments with vaccinia virus, they suggest two host cell surface proteins — called A33 and A36 — mark infected cells and prompt the cell's machinery to push infectious virions out toward uninfected cells through a process called superinfecting virion repulsion.