The anthracnose caused by Colletotrichum gloeosporioides poses a significant threat to the global mango(Mangifera indica L.)fruit industry.Although histone deacetylases(HDACs)are well recognized to be involved in plan...The anthracnose caused by Colletotrichum gloeosporioides poses a significant threat to the global mango(Mangifera indica L.)fruit industry.Although histone deacetylases(HDACs)are well recognized to be involved in plant immunity,the role of HDAC-mediated nonhistone deacetylation in the fruit immune response remains elusive.In the present study,MiHDA3,an HDAC from the RPD3/HDA1 subfamily,was identified as a candidate for regulating mango resistance based on the greatest induction of MiHDA3 in response to infection of C.gloeosporioides among the 19 tested HDAC genes.Transient overexpression of MiHDA3 in mango fruit strengthened the disease resistance by enhancing the activities of defense-related enzymes(phenylalanine ammonia-lyase(PAL)andβ-1,3-glucanase(GLU))and upregulating the expression levels of MiPAL and MiGLU.These increases occurred concomitantly with increased accumulation of local H_(2)O_(2),a critical signaling molecule.The opposite effects on resistance and H_(2)O_(2) production were observed in MiHDA3-silenced mango fruit.Physiological assays revealed that exogenous H_(2)O_(2) treatment suppressed anthracnose development in mango fruit after inoculation with C.gloeosporioides,whereas treatment with diphenylene iodonium,an inhibitor of endogenous H_(2)O_(2) generation,exacerbated disease symptoms.Furthermore,the mango catalase 1(MiCAT1),a redox homeostasis-related protein,was confirmed to negatively regulate the resistance of mango fruit to C.gloeosporioides by catalyzing the decomposition of H_(2)O_(2).Mechanistic investigations revealed that MiHDA3-mediated deacetylation of MiCAT1 at lysine residues K227 and K233 reduced the enzymatic activity and protein stability of MiCAT1,contributing to enhanced resistance in mango fruit.Collectively,these findings highlight that the functional interplay between HDACs and catalases can modulate the immune response in post-harvest fruits,and reveal a novel mechanism by which HDACs enhance mango disease resistance through the deacetylation of nonhistone proteins and the regulation of their biochemical functions.展开更多
基金financially supported by the Natural Science Foundation of Hainan Province,China(Grant No.324RC456)National Natural Science Foundation of China(Grant No.32460786)+2 种基金South China Botanical Garden,Chinese Academy of Sciences(Grant No.QNXM-202306)the Guangdong Science and Technology Plan Project(Grant No.2023B1212060046)the Foundation of Key Laboratory of South China Agricultural Plant Molecular Analysis and Genetic Improvement,South China Botanical Garden,Chinese Academy of Sciences(Guangzhou,China)。
文摘The anthracnose caused by Colletotrichum gloeosporioides poses a significant threat to the global mango(Mangifera indica L.)fruit industry.Although histone deacetylases(HDACs)are well recognized to be involved in plant immunity,the role of HDAC-mediated nonhistone deacetylation in the fruit immune response remains elusive.In the present study,MiHDA3,an HDAC from the RPD3/HDA1 subfamily,was identified as a candidate for regulating mango resistance based on the greatest induction of MiHDA3 in response to infection of C.gloeosporioides among the 19 tested HDAC genes.Transient overexpression of MiHDA3 in mango fruit strengthened the disease resistance by enhancing the activities of defense-related enzymes(phenylalanine ammonia-lyase(PAL)andβ-1,3-glucanase(GLU))and upregulating the expression levels of MiPAL and MiGLU.These increases occurred concomitantly with increased accumulation of local H_(2)O_(2),a critical signaling molecule.The opposite effects on resistance and H_(2)O_(2) production were observed in MiHDA3-silenced mango fruit.Physiological assays revealed that exogenous H_(2)O_(2) treatment suppressed anthracnose development in mango fruit after inoculation with C.gloeosporioides,whereas treatment with diphenylene iodonium,an inhibitor of endogenous H_(2)O_(2) generation,exacerbated disease symptoms.Furthermore,the mango catalase 1(MiCAT1),a redox homeostasis-related protein,was confirmed to negatively regulate the resistance of mango fruit to C.gloeosporioides by catalyzing the decomposition of H_(2)O_(2).Mechanistic investigations revealed that MiHDA3-mediated deacetylation of MiCAT1 at lysine residues K227 and K233 reduced the enzymatic activity and protein stability of MiCAT1,contributing to enhanced resistance in mango fruit.Collectively,these findings highlight that the functional interplay between HDACs and catalases can modulate the immune response in post-harvest fruits,and reveal a novel mechanism by which HDACs enhance mango disease resistance through the deacetylation of nonhistone proteins and the regulation of their biochemical functions.
