Hormonal crosstalk is central for tailoring plant responses to the nature of challenges encountered. The role of antagonism between the two major defense hormones, salicylic acid （SA） and jasmonic acid （JA）, and m...Hormonal crosstalk is central for tailoring plant responses to the nature of challenges encountered. The role of antagonism between the two major defense hormones, salicylic acid （SA） and jasmonic acid （JA）, and modulation of this interplay by ethylene （ET） in favor of JA signaling pathway in plant stress responses is well recognized, but the underlying mechanism is not fully understood. Here, we show the opposing function of two transcription factors, ethylene insensitive3 （EIN3） and EIN3-Like1 （EIL1）, in SA-mediated suppression and JA- mediated activation of PLANT DEFENSINI.2 （PDFI.2）. This functional duality is mediated via their effect on protein, not transcript levels of the PDF1.2 transcriptional activator octadecanoid-responsive Arabidopsis59 （ORA59）. Specifically, JA induces ORA59 protein levels independently of EIN3/EIL1, whereas SA reduces the protein levels dependently of EIN3/EIL1. Co-infiltration assays revealed nuclear co-localization of ORA59 and EIN3, and split- luciferase together with yeast-two-hybrid assays established their physical interaction. The functional ramification of the physical interaction is EIN3-dependent degradation of ORA59 by the 26S proteasome. These findings allude to SA-responsive reduction of ORA59 levels mediated by EIN3 binding to and targeting of ORA59 for degrada4tion, thus nominating ORA59 pool as a coordination node for the antagonistic function of ET/JA and SA.展开更多
The ethylene insensitive 3/ethylene insensitive3-like(EIN3/EIL)plays an indispensable role in fruit ripening.However,the regulatory mechanism that links post-translational modification of EIN3/EIL to fruit ripening is...The ethylene insensitive 3/ethylene insensitive3-like(EIN3/EIL)plays an indispensable role in fruit ripening.However,the regulatory mechanism that links post-translational modification of EIN3/EIL to fruit ripening is largely unknown.Here,we studied the expression of 13 MaE IL genes during banana fruit ripening,among which MaE IL9 displayed higher enhancement particularly in the ripening stage.Consistent with its transcript pattern,abundance of MaE IL9 protein gradually increased during the ripening process,with maximal enhancement in the ripening.DNA affinity purification(DAP)-seq analysis revealed that MaE IL9 directly targets a subset of genes related to fruit ripening,such as the starch hydrolytic genes MaA MY3D and MaB AM1.Stably overexpressing MaE IL9 in tomato fruit hastened fruit ripening,whereas transiently silencing this gene in banana fruit retarded the ripening process,supporting a positive role of MaEIL9 in fruit ripening.Moreover,oxidation of methionines(Met-129,Met-130,and Met-282)in MaEIL9 resulted in the loss of its DNA-binding capacity and transcriptional activation activity.Importantly,we identified MaEIL9 as a potential substrate protein of methionine sulfoxide reductase A MaMsrA4,and oxidation of Met-129,Met-130,and Met-282in MaEIL9 could be restored by MaMsrA4.Collectively,our findings reveal a novel regulatory network controlling banana fruit ripening,which involves MaMsrA4-mediated redox regulation of the ethylene signaling component MaEIL9.展开更多
基金supported by National Institutes of Health(R01GM107311)National Science Foundation(IOS-1036491and IOS1352478) grants awarded to K.D.
文摘Hormonal crosstalk is central for tailoring plant responses to the nature of challenges encountered. The role of antagonism between the two major defense hormones, salicylic acid （SA） and jasmonic acid （JA）, and modulation of this interplay by ethylene （ET） in favor of JA signaling pathway in plant stress responses is well recognized, but the underlying mechanism is not fully understood. Here, we show the opposing function of two transcription factors, ethylene insensitive3 （EIN3） and EIN3-Like1 （EIL1）, in SA-mediated suppression and JA- mediated activation of PLANT DEFENSINI.2 （PDFI.2）. This functional duality is mediated via their effect on protein, not transcript levels of the PDF1.2 transcriptional activator octadecanoid-responsive Arabidopsis59 （ORA59）. Specifically, JA induces ORA59 protein levels independently of EIN3/EIL1, whereas SA reduces the protein levels dependently of EIN3/EIL1. Co-infiltration assays revealed nuclear co-localization of ORA59 and EIN3, and split- luciferase together with yeast-two-hybrid assays established their physical interaction. The functional ramification of the physical interaction is EIN3-dependent degradation of ORA59 by the 26S proteasome. These findings allude to SA-responsive reduction of ORA59 levels mediated by EIN3 binding to and targeting of ORA59 for degrada4tion, thus nominating ORA59 pool as a coordination node for the antagonistic function of ET/JA and SA.
基金funded by the National Natural Science Foundation of China (31972116)Guangdong Special Support Program (2017TQ04N512)+1 种基金China Agriculture Research System of Ministry of Finance (MOF)and Ministry of Agriculture and Rural Affairs (MARA) (CARS-31)Guangdong Provincial Special Fund For Modern Agriculture Industry Technology Innovation Teams (2022KJ109)。
文摘The ethylene insensitive 3/ethylene insensitive3-like(EIN3/EIL)plays an indispensable role in fruit ripening.However,the regulatory mechanism that links post-translational modification of EIN3/EIL to fruit ripening is largely unknown.Here,we studied the expression of 13 MaE IL genes during banana fruit ripening,among which MaE IL9 displayed higher enhancement particularly in the ripening stage.Consistent with its transcript pattern,abundance of MaE IL9 protein gradually increased during the ripening process,with maximal enhancement in the ripening.DNA affinity purification(DAP)-seq analysis revealed that MaE IL9 directly targets a subset of genes related to fruit ripening,such as the starch hydrolytic genes MaA MY3D and MaB AM1.Stably overexpressing MaE IL9 in tomato fruit hastened fruit ripening,whereas transiently silencing this gene in banana fruit retarded the ripening process,supporting a positive role of MaEIL9 in fruit ripening.Moreover,oxidation of methionines(Met-129,Met-130,and Met-282)in MaEIL9 resulted in the loss of its DNA-binding capacity and transcriptional activation activity.Importantly,we identified MaEIL9 as a potential substrate protein of methionine sulfoxide reductase A MaMsrA4,and oxidation of Met-129,Met-130,and Met-282in MaEIL9 could be restored by MaMsrA4.Collectively,our findings reveal a novel regulatory network controlling banana fruit ripening,which involves MaMsrA4-mediated redox regulation of the ethylene signaling component MaEIL9.
