P seudomonas syringae pv. phaseolicola effector HopF1 inhibits pathogen-associated molecular pattern-triggered immunity in a RIN4-independent manner in common bean ( P haseolus vulgaris).

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), HopF1, 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 HopF1 can inhibit pathogen-associated molecular pattern-triggered immunity ( PTI) in a susceptible bean cultivar Tendergreen. HopF1 directly interacted with two RPM1-interacting protein 4 ( RIN4) orthologs of bean, PvRIN4a and PvRIN4b. Like RIN4 in A rabidopsis, both PvRIN4 orthologs negatively regulated the PTI responses in bean. However, the virulence function of HopF1 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 HopF1. Together, these results demonstrated that PvRIN4 orthologs were not the virulence target of HopF1 for inhibiting PTI, but probably for interfering with ETI. [ABSTRACT FROM AUTHOR]