As a self-confessed prokaryotic chauvinist, I’m always on the lookout for new interesting papers aimed at understanding bacterial metabolism and regulation. A recent paper in Cell, entitled “Phenotypic Landscape of a Bacterial Cell” by a group of authors including Biology Professor Susan Lovett demonstrates the application of high-throughput screening to finding new bacterial phenotypes. Approximately 4000 E.coli mutant strains, representing deletions of individual non-essential genes, were plated on 324 different media representing a total of over 100 different stress conditions, and the growth followed by image analysis. Approximately half of the genes screened had one or more identifiable phenotypic repsonses. This approach allows the identification of genes that are conditionally essential, genes that are involved in multiple resistance, etc. This represents a new automated method for identifying phenotypes (hence “phenomics’) and understanding the roles of genes of as yet unidentified function in bacteria. The data set is publicly available at http://ecoliwiki.net/tools/chemgen/.
In a new study appearing in PNAS this week, Brandeis Molecular and Cell Biology graduate student Houra Merrikh and co-workers from the Lovett lab identified the E.coli gene iraD as a regulator of the response to oxidative DNA damage in exponentially growing bacteria. Interestingly, the mechanism seems to involve the alternative RNA polymerase sigma factor RpoS, previously characterized as a regulator of expression during the “stationary phase”. Merrikh et al. argue that this response works in parallel with the previously characterized SOS response in protecting growing bacteria from DNA damage.
The stringent response in E.coli is a response to nutrient (typically amino acid) starvation and is characterized by the accumulation of the small molecular regulator ppGpp, and a global response in transcriptional regulation. In a new paper in PLoS Genetics, Daniel Ferullo and Susan Lovett examine chromosome segregation during the stringent respons and discuss what appears to be a novel G1-like cell cycle checkpoint in bacteria that occurs as the result.