The Mechanism Of Phytophthora Capsici RXLR Effector Pc210 In Suppression Of Tomato Immunity

Tomato(Solanum lycopersicum)is widely cultivated in China,and it is an important vegetable crop.Phytophthora capsici can infect tomato,causing roots,crowns and fruit rot,which seriously threatens tomato production.P.capsici suppresses crop immune response and promotes crop susceptibility by secreting RXLR effector.Therefore,the study of the immune mechanism of P.capsici RXLR effector regulating tomato immunity is of great significance for the analysis of the interaction mechanism between oomycete and host plant,and also provides resistance related gene resources for the cultivation of new tomato varieties resistant to P.capsici.We selected some highly expressed effector genes at the early stage of infection stage from the transcriptome data of P.capsici infested tomatoes for pathogenic screening.Among which the RXLR effector Pc210 can promote the infection of P.capsici in plants.In this study,we aim to unravel the mechanism of Pc210 in negative regulation of tomato immunity by verifying the function of Pc210 in P.capsici colonization,identifying host target of Pc210 and investigating the function of host target in tomato immunity.The specific results are as follows:(1)Pc210 without signal peptide is localized in the nucleus and cytoplasm,which promotes the infection of P.capsici to Nicotiana benthamiana.The signal peptide did not affect the virulent function of Pc210,but the Pc210 virulent function of intracellularly localized Pc210 was stronger than that of the intercellularly localized Pc210;(2)GFP-IP followed by LC/MS technology were used to screen the host target of Pc210.The candidate target genes SlGH31,SlPER12 and SlCa M3 in tomato were cloned.Through N.benthamiana transient expression assays,virus induced gene silencing(VIGS)and tomato genetic transformation,we show that SlGH31 inhibits the infection of P.capsici in tomato,enhances the expression of tomato salicylic acid responsive genes.Thus we conclude that SlGH31 positively regulats the resistance of tomato to P.capsici.The transient expression of SlPER12 promots the infection of P.capsici to the N.benthamiana,however,silenceing of PER12 had no obvious contribution to plant resistance.The transient expression of SlCa M3 does not alter plant response to P.capsici;(3)SlGH31 belongs to the glycoside hydrolase family with a signal peptide structure.The protein accumulation was detected by separating the apoplastic fluid,and the results showed that SlGH31 is not detected in the apoplastic fluid.Through Co-IP technology,the interaction between SlGH31 and Pc210 was proved;(4)The transient expression test showed that Pc210 degraded SlGH31.We speculate that the RXLR effector protein Pc210 inhibits the immune response of tomato by degrading SlGH31.