PARylation facilitates the DNA damage repair of Phytophthora sojae in response to host ROS stress.

Abstract

Host plants and various fungicides combat plant pathogens by triggering the release of excessive ROS, leading to DNA damage and subsequent cell death. The mechanisms by which the Phytophthora sojae mitigates ROS stress induced by plant immune responses and fungicides are not well understood. This study investigates the role of PsPARP1A-mediated poly (ADP-ribosylation) (PARylation) in ROS-induced DNA damage responses (DDR). Mechanistically, Phytophthora sojae poly (ADP-ribose) polymerase (PsPARP1A) interacts with meiotic recombination 11 (PsMRE11) to facilitate the accumulation of histone H2Ax phosphorylated on serine 137 (γH2Ax) in response to plant ROS-induced DNA damage. The PARylation of PsMRE11 by PsPARP1A at E5, D7, D8, and E12 is critical for the nuclear localization of PsMRE11 and the subsequent accumulation of γH2Ax during DNA damage induced by host defense-generated ROS stress in P. sojae. These findings underscore the pivotal role of the PsPARP1A-PsMRE11 axis in DNA damage repair and adaptation to ROS, thereby contributing to the virulence of P. sojae. Our study highlights the novel functions of PsPARP1/PsMRE11 in pathogenic oomycetes, linking PARylation-dependent DDR processes to their development and virulence.