Objectives: It is known that many crops are destroyed by the destructive oomycetes and these pathogens secrete hundreds of RXLR effectors to manipulate host immunity.However,whether some conserved host protein families are targeted by the pathogen effectors remains unclear.This study is performed to identify the conserved host targets of Phytophthora RXLR effectors and investigate the underlying molecular mechanisms.Methods:We employed yeast two-hybrid system to identify the conserved host targets of RXLR effector Avr3a from Phytophthora infestans.BiFC was used to confirm interactions between Avr3a family effectors and the candidate proteins.The expression pattern of target genes during infection was assayed by using both qRT-PCR and GUS reporter.The mutant constructs of target genes were used to determine the relationship between the interaction sites and enzymatic activity sites of the target proteins by BiFC.The target gene was overexpressed in Arabidopsis and silenced in N.benthamiana to investigate its role in defense to Phytophthora attack.At last,agro-infiltration was used to study the relationship between target genes and Avr-R recognition.Results: We demonstrated that plant RIP1(RXLR-effector Interacting Protein 1)family proteins were targeted byPhytophthoraAvr3a family effectors.Phylogenetic analysis indicated that the RIP1 sub-family was fast evolving in host plant Solanum and Arabidopsis.Beside,RIP1 was heavily induced during the Arabidopsis-Phytophthora interaction.The interactions between RIP1 and Avr3a family effectors were independent ofthe enzymatic activity of RIP1.Inoculation analysis showed that RIP1 negatively regulated disease resistance of host plants to P.parasitica,P.capsici,and P.infestans.HR assays showed that silencing of RIP1 promotedINF1-triggered cell death,but inhibited Avr3a-R3a-triggeredcell death.Conclusions:Our results show that a conserved plant protein RIP1,which negatively regulates plant defense by inhibiting PAMPs-triggered immunity,is targeted by Avr3a family proteins.