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PNAS Studies on Pseudomonas Aeruginosa Virulence, Anti-CRISPR Proteins, More

A team from Northwestern University presents findings from a comparative genomic analysis aimed at identifying virulence genes related to pathogenicity in the accessory genome of the bacterial pathogen Pseudomonas aeruginosa. Using whole-genome sequencing, the researchers assessed core and accessory sequences from 100 clinical P. aeruginosa bloodstream isolates, which had their virulence features profiled in parallel in mouse bacteremia models of infection. Among the virulence factors found, the authors describe a contact-dependent growth inhibition (CDI) system that appeared to be over-represented in particularly virulent P. aeruginosa isolates. "Overall," they write, "our findings indicate that this P. aeruginosa CDI system functions as both an inter-bacterial inhibition system and a bacterial virulence factor against a mammalian host."

University of California, Berkeley, researchers describe "anti-CRISPR" (Acr) proteins in Staphylococcus aureus, since these inhibitors can damp down RNA-guided targeting by CRISPR-Cas enzymes, which could have gene editing applications. Using self-targeting CRISPR screens and other strategies, the team searched for Acr mobile genetic elements in S. aureus, uncovering three Cas9 inhibitors that were subsequently found to influence S. aureus Cas9-based editing in human cells to different degrees. "We believe that the search for more Acrs with potent and novel mechanisms of inhibition will continue to rapidly add new dimensions of control into the CRISPR toolbox," the authors conclude.

Imperial College London investigators identify an apparent role for the Plasmodium cell surface protein called PIMMS43 in dodging Anopheles coluzzii mosquito innate immune responses while setting up midgut infections on the way to mosquito salivary glands, where the malaria-causing parasites can be passed on to humans during mosquito bites. Starting from available Plasmodium falciparum transcriptome data generated for isolates from the mosquito midgut, the team focused in on PIMMS2, using array-based expression profiling and other approaches to pinpoint the PIMMS2 role in immune evasion. When the authors dialed down PIMMS2 expression in subsequent experiments, they saw more modest mosquito midgut infections by Plasmodium. "The discovery and characterization of PIMMS43 adds to our understanding of parasite immune evasion and malaria transmission through the vector," they write.