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 transd...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.展开更多
Arabidopsis NON-EXPRESSOR OF PR1 （NPR1） is a transcription co-activator that plays a central role in regulating the transcriptional response to plant pathogens. The NPR family consists of NPR1 and five NPRl-like gen...Arabidopsis NON-EXPRESSOR OF PR1 （NPR1） is a transcription co-activator that plays a central role in regulating the transcriptional response to plant pathogens. The NPR family consists of NPR1 and five NPRl-like genes. The NPR1 paralog NPR3 has recently been shown to function as a receptor of the plant hormone salicylic acid and to mediate proteosomal degradation of NPR1. The function of NPR3 protein during early flower development was revealed through a detailed molecular-genetic analysis including promoter transcriptional fusion analysis, phenotype characterization of npr3-3 mutants/overexpressors, and whole-plant fitness analysis. The physical interaction between NPR3 and NPR1/ TGA2 was explored using bimolecular fluorescence complementation analysis in onion epidermal cells, Here, we show that NPR3 expression was strongest in the petals and sepals of developing flowers and declined after flower opening. Consistently with this observation, an npr3 knockout mutant displayed enhanced resistance to Pseudomonas syringae infection of immature flowers, but not leaves. Developing npr3 flowers exhibited increased levels of basal and induced PR1 transcript accumulation. However, the npr3 mutant showed lower fitness compared to Col-0 in the absence of pathogen. Moreover, NPR3 was shown to interact with NPR1 and TGA2 in vivo. Our data suggest that NPR3 is a negative regulator of defense responses during early flower development and it may function through the association with both NPR1 and TGA2.展开更多
Plant immunity is controlled by both positive regulators such as PBS3 and EDS1 and negative regulators such as NPR3 and NPR4.However,the relationships among these important immune regulators remain elusive.In this stu...Plant immunity is controlled by both positive regulators such as PBS3 and EDS1 and negative regulators such as NPR3 and NPR4.However,the relationships among these important immune regulators remain elusive.In this study,we found that PBS3 interacts with EDS1 in both the cytoplasm and the nucleus,and is required for EDS1 protein accumulation?NPR3 and NPR4,which function as salicylic acid receptors and adaptors of Cullin3-based E3 ligase,interact with and mediate the degradation of EDS1 via the 26S proteasome.We further discovered that PBS3 inhibits the polyubiquitination and subsequent degradation of EDS1 by reducing the association of EDS1 with the Cullin3 adaptors NPR3 and NPR4.Furthermore,we showed that PBS3 and EDS1 also contribute to PAMP-triggered immunity in addition to effector-triggered immunity.Collectively,our study reveals a novel mechanism by which plants fine-tune defense resporises by inhibiting the degradation of a positive player in plant immunity.展开更多
基金National Research Foundation(NRF),Prime Minister's Office,Singapore under its Campus for Research Excel-lence and Technological Enterprise(CREATE)programThe 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)+1 种基金National Research Foundation(NRF)Prime Minister's Office,Singapore,under its Campus for Research Excellence and Technological Enterprise(CREATE)program.
文摘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.
文摘Arabidopsis NON-EXPRESSOR OF PR1 （NPR1） is a transcription co-activator that plays a central role in regulating the transcriptional response to plant pathogens. The NPR family consists of NPR1 and five NPRl-like genes. The NPR1 paralog NPR3 has recently been shown to function as a receptor of the plant hormone salicylic acid and to mediate proteosomal degradation of NPR1. The function of NPR3 protein during early flower development was revealed through a detailed molecular-genetic analysis including promoter transcriptional fusion analysis, phenotype characterization of npr3-3 mutants/overexpressors, and whole-plant fitness analysis. The physical interaction between NPR3 and NPR1/ TGA2 was explored using bimolecular fluorescence complementation analysis in onion epidermal cells, Here, we show that NPR3 expression was strongest in the petals and sepals of developing flowers and declined after flower opening. Consistently with this observation, an npr3 knockout mutant displayed enhanced resistance to Pseudomonas syringae infection of immature flowers, but not leaves. Developing npr3 flowers exhibited increased levels of basal and induced PR1 transcript accumulation. However, the npr3 mutant showed lower fitness compared to Col-0 in the absence of pathogen. Moreover, NPR3 was shown to interact with NPR1 and TGA2 in vivo. Our data suggest that NPR3 is a negative regulator of defense responses during early flower development and it may function through the association with both NPR1 and TGA2.
基金the National Natural Science Foundation of China(31701863)the University of South Carolina Office of Research(ASPIRE-I TrackllB,13010E244)the Postdoctoral Workstation of Jiangsu Academy of Agricultural Sciences.
文摘Plant immunity is controlled by both positive regulators such as PBS3 and EDS1 and negative regulators such as NPR3 and NPR4.However,the relationships among these important immune regulators remain elusive.In this study,we found that PBS3 interacts with EDS1 in both the cytoplasm and the nucleus,and is required for EDS1 protein accumulation?NPR3 and NPR4,which function as salicylic acid receptors and adaptors of Cullin3-based E3 ligase,interact with and mediate the degradation of EDS1 via the 26S proteasome.We further discovered that PBS3 inhibits the polyubiquitination and subsequent degradation of EDS1 by reducing the association of EDS1 with the Cullin3 adaptors NPR3 and NPR4.Furthermore,we showed that PBS3 and EDS1 also contribute to PAMP-triggered immunity in addition to effector-triggered immunity.Collectively,our study reveals a novel mechanism by which plants fine-tune defense resporises by inhibiting the degradation of a positive player in plant immunity.
