The Pseudomonas syringae Type III Effector HopF2 Suppresses Arabidopsis Stomatal Immunity

• DOI: 10.1371/journal.pone.0114921
• Publication Date: 2014-12-11T19:15:15Z
• Authors: Brenden Hurley; Donghyuk Lee; Adam Mott; Michael Wilton; Jun Liu; Yulu C. Liu; Stephane Angers; Gitta Coaker; David S. Guttman; Darrell Desveaux
• Keywords: 580; ADP Ribose Transferases; Proteomics; 0301 basic medicine; 570; General Science & Technology; Science; Q; R; Arabidopsis; Pseudomonas syringae; Genetically Modified; Plants; Plants, Genetically Modified; 03 medical and health sciences; Bacterial Proteins; Host-Pathogen Interactions; Plant Stomata; Type III Secretion Systems; Medicine; Plant Immunity; Research Article

Pseudomonas syringae subverts plant immune signalling through injection of type III secreted effectors (T3SE) into host cells. The T3SE HopF2 can disable Arabidopsis immunity through Its ADP-ribosyltransferase activity. Proteomic analysis of HopF2 interacting proteins identified a protein complex containing ATPases required for regulating stomatal aperture, suggesting HopF2 may manipulate stomatal immunity. Here we report HopF2 can inhibit stomatal immunity independent of its ADP-ribosyltransferase activity. Transgenic expression of HopF2 in Arabidopsis inhibits stomatal closing in response to P. syringae and increases the virulence of surface inoculated P. syringae. Further, transgenic expression of HopF2 inhibits flg22 induced reactive oxygen species production. Intriguingly, ADP-ribosyltransferase activity is dispensable for inhibiting stomatal immunity and flg22 induced reactive oxygen species. Together, this implies HopF2 may be a bifunctional T3SE with ADP-ribosyltransferase activity required for inhibiting apoplastic immunity and an independent function required to inhibit stomatal immunity.