Leaf senescence can be triggered and promoted by various environmental stressors, developmental cues, and endogenous hormone signals. Several lines of evidence have suggested the involvement of WRKY transcription fact...Leaf senescence can be triggered and promoted by various environmental stressors, developmental cues, and endogenous hormone signals. Several lines of evidence have suggested the involvement of WRKY transcription factors in regulating leaf senescence, but the underlying mechanisms and signaling pathways involved remain elusive. In this study, we identified Arabidopsis thaliana WRKY DNA-binding protein 45 （WRKY45） as a positive regulator of age-triggered leaf senescence. Loss of W^KY45 function resulted in increased leaf longevity in age-triggered senescence, whereas overexpression of WRKY45 significantly accelerated age-triggered leaf senescence. Consistently, expression of SENESCENCE- ASSOCIATED GENEs （SAGs） was significantly reduced in wrky45 mutants but markedly enhanced in transgenic plants overexpressing WRKY45. Chromatin immunoprecipitation assays revealed that WRKY45 directly binds the promoters of several SAGs such as SAG12, SAG13, SAG113, and SEN4. Both in vivo and in vitro biochemical analyses demonstrated that WRKY45 interacts with the DELLA pro- tein RGA-LIKE1 （RGL1）, a repressor of the gibberellin （GA） signaling pathway. We found that RGL1 repressed the transcription activation function of WRKY45, thereby attenuating the expression of its reg- ulon. Consistent with this finding, overexpression of RGL1 resulted in significantly increased leaf longevity in age-triggered senescence. Taken together, our results provide compelling evidence that WRKY45 functions as a critical component of the GA-mediated signaling pathway to positively regulate age-triggered leaf senescence.展开更多
Plants maintain a dynamic balance between growth and defense,and optimize allocation of resources for survival under constant pathogen infections.However,the underlying molecular regulatory mechanisms,especially in re...Plants maintain a dynamic balance between growth and defense,and optimize allocation of resources for survival under constant pathogen infections.However,the underlying molecular regulatory mechanisms,especially in response to biotrophic bacterial infection,remain elusive.Here,we demonstrate that DELLA proteins and EDS1,an essential resistance regulator,form a central module modulating plant growth-defense tradeoffs via direct interaction.When infected by Pst DC3000,EDS1 rapidly promotes salicylic acid(SA)biosynthesis and resistance-related gene expression to prime defense response,while pathogen infection stabilizes DELLA proteins RGA and RGL3 to restrict growth in a partially EDS1-dependent manner,which facilitates plants to develop resistance to pathogens.However,the increasingly accumulated DELLAs interact with EDS1 to suppress SA overproduction and excessive resistance response.Taken together,our findings reveal a DELLA-EDS1-mediated feedback regulatory loop by which plants maintain the subtle balance between growth and defense to avoid excessive growth or defense in response to constant biotrophic pathogen attack.展开更多
文摘Leaf senescence can be triggered and promoted by various environmental stressors, developmental cues, and endogenous hormone signals. Several lines of evidence have suggested the involvement of WRKY transcription factors in regulating leaf senescence, but the underlying mechanisms and signaling pathways involved remain elusive. In this study, we identified Arabidopsis thaliana WRKY DNA-binding protein 45 （WRKY45） as a positive regulator of age-triggered leaf senescence. Loss of W^KY45 function resulted in increased leaf longevity in age-triggered senescence, whereas overexpression of WRKY45 significantly accelerated age-triggered leaf senescence. Consistently, expression of SENESCENCE- ASSOCIATED GENEs （SAGs） was significantly reduced in wrky45 mutants but markedly enhanced in transgenic plants overexpressing WRKY45. Chromatin immunoprecipitation assays revealed that WRKY45 directly binds the promoters of several SAGs such as SAG12, SAG13, SAG113, and SEN4. Both in vivo and in vitro biochemical analyses demonstrated that WRKY45 interacts with the DELLA pro- tein RGA-LIKE1 （RGL1）, a repressor of the gibberellin （GA） signaling pathway. We found that RGL1 repressed the transcription activation function of WRKY45, thereby attenuating the expression of its reg- ulon. Consistent with this finding, overexpression of RGL1 resulted in significantly increased leaf longevity in age-triggered senescence. Taken together, our results provide compelling evidence that WRKY45 functions as a critical component of the GA-mediated signaling pathway to positively regulate age-triggered leaf senescence.
基金This research was supported by grants from the "Strategic PriorityResearch Program " of the Chinese Academy of Sciences (no.XDA13020500)the National Natural Science Foundation of China (no.31300239)and the Natural Science Foundation of Guangdong Province(S2013040013147).
文摘Plants maintain a dynamic balance between growth and defense,and optimize allocation of resources for survival under constant pathogen infections.However,the underlying molecular regulatory mechanisms,especially in response to biotrophic bacterial infection,remain elusive.Here,we demonstrate that DELLA proteins and EDS1,an essential resistance regulator,form a central module modulating plant growth-defense tradeoffs via direct interaction.When infected by Pst DC3000,EDS1 rapidly promotes salicylic acid(SA)biosynthesis and resistance-related gene expression to prime defense response,while pathogen infection stabilizes DELLA proteins RGA and RGL3 to restrict growth in a partially EDS1-dependent manner,which facilitates plants to develop resistance to pathogens.However,the increasingly accumulated DELLAs interact with EDS1 to suppress SA overproduction and excessive resistance response.Taken together,our findings reveal a DELLA-EDS1-mediated feedback regulatory loop by which plants maintain the subtle balance between growth and defense to avoid excessive growth or defense in response to constant biotrophic pathogen attack.
