Open AccessP seudomonas syringae pv. phaseolicola effector H opF1 inhibits pathogen‐associated molecular pattern‐triggered immunity in a RIN 4‐independent manner in common bean ( P haseolus vulgaris )
Author(s) -
Hou Shuguo,
Mu Ruimin,
Ma Guixia,
Xu Xiaoming,
Zhang Chao,
Yang Yifei,
Wu Daoji
Publication year - 2011
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.2011.02356.x
Subject(s) - pseudomonas syringae , phaseolus , effector , virulence , biology , pathogen , arabidopsis , gene silencing , nicotiana benthamiana , microbiology and biotechnology , hypersensitive response , plant immunity , plant disease resistance , gene , genetics , botany , mutant
Plant pathogens usually promote pathogenesis by secreting effector proteins into host plant cells. One of the secreted effectors of P seudomonas syringae pv. phaseolicola , the causative agent of halo‐blight disease in common bean ( P haseolus vulgaris ), H opF1, activates effector‐triggered immunity ( ETI ) in a bean cultivar containing R1 resistance gene, but displays virulence function in a bean cultivar without the R1 gene. The virulence mechanism of the effector remained unknown, although it was identified more than a decade ago. Here we demonstrated that H opF1 can inhibit pathogen‐associated molecular pattern‐triggered immunity ( PTI ) in a susceptible bean cultivar Tendergreen. H opF1 directly interacted with two RPM 1‐interacting protein 4 ( RIN 4) orthologs of bean, PvRIN 4a and PvRIN 4b. Like RIN 4 in A rabidopsis , both PvRIN 4 orthologs negatively regulated the PTI responses in bean. However, the virulence function of H opF1 was enhanced in Tendergreen silencing PvRIN 4 . Furthermore, silencing PvRIN 4a compromised the avrβ1‐induced hypersensitive response ( HR ), which previously was reported to be suppressed by H opF1. Together, these results demonstrated that PvRIN 4 orthologs were not the virulence target of H opF1 for inhibiting PTI , but probably for interfering with ETI .