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Dissection of the APIP6-mediated ubiquitin-proteasome pathway in rice immunity against Magnaporthe oryzae Y. NING (1), X. Shi (1), R. Wang (1), J. Fan (2), C. Park (3), C. Zhang (1), T. Zhang (1), X. Ouyang (4), S. Li (4), G. Wang (5) (1) Institute of Plant Protection, Chinese Academy of Agricultural Sciences, China; (2) Institute of Plant Protection, Chinese Academy of Agricultural Sciences; Department of Plant Pathology, Ohio State University, China; (3) Department of Plant Pathology, Ohio State University, U.S.A.; (4) Rice Research Institute, Sichuan Agricultural University, China; (5) Institute of Plant Protection, Chinese Academy of Agricultural Sciences; Department of Plant Pathology, Ohio State University, U.S.A.
The ubiquitin-proteasome system (UPS) is one of the most important protein turnover mechanisms that regulate growth, development and responses to abiotic and biotic stresses. We previously found that the Magnaporthe oryzae effector AvrPiz-t suppresses the E3 ligase activity of the RING-type ligase APIP6 in rice. In return, APIP6 ubiquitinates and degrades AvrPiz-t. Genetic studies revealed that APIP6 is involved in the PAMP-triggered immunity (PTI) against M. oryzae. Recently, we found that APIP6 interacts with OsELF3-2 in rice, the ortholog of ELF3 in Arabidopsis. The expression of OsELF3-2 is induced in both incompatible and compatible rice–M. oryzae interactions. Compared with the wild type plants, the oself3-2 mutant and RNAi plants have a significant increase in flg22- and chitin-induced ROS generation, and confer enhanced resistance to a compatible M. oryzae isolate, which is similar with the phenotype of the AvrPiz-t ectopic expression lines in rice but opposite with that of the APIP6 RNAi plants. Co-expression assays in rice protoplasts and Nicotiana benthamiana leaves indicate that APIP6 promotes OsELF3-2 degradation, suggesting that OsELF3-2 is a substrate of APIP6. Taken together; these results demonstrate that the APIP6-mediated UPS plays an important role in rice immunity to M. oryzae.
Abstract Number:
S2-5 Session Type:
Special Session
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