RT Journal Article SR Electronic T1 T3SS effector VopL inhibits the host ROS response, promoting the intracellular survival of Vibrio parahaemolyticus JF bioRxiv FD Cold Spring Harbor Laboratory SP 104315 DO 10.1101/104315 A1 Marcela de Souza Santos A1 Dor Salomon A1 Kim Orth YR 2017 UL http://biorxiv.org/content/early/2017/01/30/104315.abstract AB The production of antimicrobial reactive oxygen species by the nicotinamide dinucleotide phosphate (NADPH) oxidase complex is an important mechanism for control of invading pathogens. Herein, we show that the gastrointestinal pathogen Vibrio parahaemolyticus counteracts reactive oxygen species (ROS) production using the Type III Secretion System 2 (T3SS2) effector VopL. In the absence of VopL, intracellular V. parahaemolyticus undergo ROS-dependent filamentation, with concurrent limited growth. During infection, VopL assembles actin into non-functional filaments resulting in a dysfunctional actin cytoskeleton that can no longer mediate the assembly of the NADPH oxidase at the cell membrane, thereby limiting ROS production. This is the first example of how a T3SS2 effector contributes to the intracellular survival of V. parahaemolyticus to support the establishment of a protective intracellular replicative niche.