Open AccessThe Pseudomonas syringae Type III Effector HopF2 Suppresses Arabidopsis Stomatal Immunity
Author(s) -
Brenden A. Hurley,
Donghyuk Lee,
G. Adam Mott,
Michael Wilton,
Jun Li,
Yulu Cherry Liu,
Stéphane Angers,
Gitta Coaker,
David S. Guttman,
Darrell Desveaux
Publication year - 2014
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0114921
Subject(s) - pseudomonas syringae , arabidopsis , plant immunity , immunity , effector , biology , microbiology and biotechnology , plant defense against herbivory , apoplast , immune system , botany , biochemistry , pathogen , cell wall , immunology , gene , mutant
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.