In PLOS One, researchers from the University of Maryland used RNA sequencing-based gene expression profiling to delve into Chlamydia trachomatis activities and host immune responses during chlamydial infections. Using a ribosomal RNA depletion method that made it possible to simultaneously sequence messenger RNA from C. trachomatis and host cells in an in vitro infection model, the group saw signs of pathogen and host expression responses kicking into gear early in the infection process. For instance, the pathogen appeared to dial up iron scavenging gene expression, while infected cells showed a jump in the expression of genes that seem to trigger a cascade of events suspected of contributing to the tissue scarring complications that sometimes occur in infected tissues.
GenomeWeb Daily News has more on the study.
More than 200 genes appear to contribute to fitness features of uropathogenic Escherichia coli, according to a PLOS Pathogens study by University of Michigan researchers. The team used transposon insertion mutagenesis and sequencing to look for genes that enhanced or diminished an uropathogenic E. coli strain's ability to infect mouse spleens. When they focused in on 11 of the 242 suspected fitness genes found in the screen, the investigators determined that at least nine of the 11 genes did affect the bug's vigor in infecting mouse spleens. That suggests approaches are unearthing authentic fitness genes, study authors say, noting that "fitness factors may represent targets for developing novel therapeutics against [uropathogenic E. coli]."
Through de novo assembly of genome sequences from a field isolate of Plasmodium vivax, a team from the US, Cambodia, and France identified almost 800 predicted protein-coding genes missing from the malaria-causing parasite's reference genome. As they reported in PLOS Neglected Tropical Diseases, the investigators tracked down 792 gene candidates within 3.8 million bases of sequence present in the Cambodian field strain in question, but absent in an existing reference genome sequenced with DNA from a monkey adapted version of the P. vivax strain Salvador I. These included several genes with sequences resembling those in genes used by other Plasmodium species to interact with and/or invade red blood cells.