UBP12/UBP13-mediated deubiquitination of salicylic acid receptor NPR3 suppresses plant immunity  

作　　者：Yu Zhou Su-Hyun Park Nam-Hai Chua 

机构地区：[1]Temasek Life Sciences Laboratory,National University of Singapore,1 Research Link,Singapore 117604,Singapore [2]Disruptive&Sustainable Technologies for Agricultural Precision,Singapore-MIT Alliance for Research and Technology,1 CREATE Way,Singapore 138602,Singapore

出　　处：《Molecular Plant》2023年第1期232-244,共13页分子植物（英文版）

基　　金：National Research Foundation(NRF),Prime Minister's Office,Singapore under its Campus for Research Excel-lence and Technological Enterprise(CREATE)program;The Disruptive and Sustainable Technologies for Agricultural Precision(DiSTAP)is an interdisciplinary research group(IRG)of the Singapore-MIT Alliance for Research and Technology Centre(SMART);National Research Foundation(NRF);Prime Minister's Office,Singapore,under its Campus for Research Excellence and Technological Enterprise(CREATE)program.

摘　　要：Salicylic acid(SA),a defense hormone produced after pathogen challenge,is critical for plant immunity.Arabidopsis NONEXPRESSER OF PR GENES 1(NPR1)and its paralogs NPR3 and NPR4 can bind SA and mediate SA signal transduction.NPR1 functions as a transcriptional co-activator to promote defense gene expression,whereas NPR3 and NPR4 have been shown to function as negative regulators in the SA signaling pathway.Although the mechanism about NPR1 regulation has been well studied,how NPR3/NPR4 proteins are regulated in immune responses remains largely unknown.Here,we show that the stability of NPR3/NPR4 is enhanced by SA.In the absence of pathogen challenge,NPR3/NPR4 are unstable and degraded by the 26S proteasome,whereas the increase in cellular SA levels upon pathogen infection suppresses NPR3/NPR4 degradation.We found that UBP12 and UBP13,two homologous deubiquitinases from a ubiquitin-specific protease subfamily,negatively regulate plant immunity by promoting NPR3/NPR4 stability.Our genetic results further showed that UBP12/UBP13-mediated immunity suppression is partially dependent on NPR3/NPR4 functions.By interacting with NPR3 in the nucleus in an SA-dependent manner,UBP12 and UBP13 remove ubiquitin from polyubiquitinated NPR3 to protect it from being degraded.The stabilization of NPR3/NPR4 promoted by UBP12/UBP13 is essential for negative regulation of basal and SA-induced immunity.

关 键 词：plant immunity salicylic acid NPR3 UBP12/UBP13 

分 类 号：O63[理学—高分子化学]