依赖叶黄素循环的热耗散是一种主要防御光破坏的机制。参与叶黄素循环的酶是紫黄质脱环氧化酶和玉米黄质环氧化酶 ,紫黄质脱环氧化酶已分离纯化 ,其 c DNA已被克隆 ,其活性主要受跨类囊体膜的 p H梯度和抗坏血酸浓度的调节 ;玉米黄质环...依赖叶黄素循环的热耗散是一种主要防御光破坏的机制。参与叶黄素循环的酶是紫黄质脱环氧化酶和玉米黄质环氧化酶 ,紫黄质脱环氧化酶已分离纯化 ,其 c DNA已被克隆 ,其活性主要受跨类囊体膜的 p H梯度和抗坏血酸浓度的调节 ;玉米黄质环氧化酶还没有被分离出来 ,但其 c DNA也已被克隆 ;其活性主要与NADPH的浓度、O2 及光等有关。展开更多
Reducing losses caused by pathogens is an effective strategy for stabilizing crop yields.Daunting challenges remain in cloning and characterizing genes that inhibit stripe rust,a devastating disease of wheat(Triticum ...Reducing losses caused by pathogens is an effective strategy for stabilizing crop yields.Daunting challenges remain in cloning and characterizing genes that inhibit stripe rust,a devastating disease of wheat(Triticum aestivum)caused by Puccinia striiformis f.sp.tritici(Pst).We found that suppression of wheat zeaxanthin epoxidase 1(ZEP1)increased wheat defense against Pst.We isolated the yellow rust slower 1(yrs1)mutant of tetraploid wheat in which a premature stop mutation in ZEP1-B underpins the phenotype.Genetic analyses revealed increased H_(2)O_(2) accumulation in zep1 mutants and demonstrated a correlation between ZEP1 dysfunction and slower Pst growth in wheat.Moreover,wheat kinase START 1.1(WKS1.1,Yr36)bound,phosphorylated,and suppressed the biochemical activity of ZEP1.A rare natural allele in the hexaploid wheat ZEP1-B promoter reduced its transcription and Pst growth.Our study thus identified a novel suppressor of Pst,characterized its mechanism of action,and revealed beneficial variants for wheat disease control.This work opens the door to stacking wheat ZEP1 variants with other known Pst resistance genes in future breeding programs to enhance wheat tolerance to pathogens.展开更多
Lesion mimic mutants(LMMs) are advantageous materials for studying programmed cell death(PCD).Although some rice LMM genes have been cloned, the diversity of functions of these genes indicates that the mechanism of ce...Lesion mimic mutants(LMMs) are advantageous materials for studying programmed cell death(PCD).Although some rice LMM genes have been cloned, the diversity of functions of these genes indicates that the mechanism of cell death regulation in LMMs needs further study. In this study, we identified a rice light-dependent leaf lesion mimic mutant 4(llm4) that showed abnormal chloroplast structure, photoinhibition, reduced photosynthetic protein levels, massive accumulation of reactive oxygen species(ROS), and PCD. Map-based cloning and complementation testing revealed that LLM4 encodes zeaxanthin epoxidase(ZEP), an enzyme involved in the xanthophyll cycle, which functions in plant photoprotection,ROS scavenging, and carotenoid and abscisic acid(ABA) biosynthesis. The ABA content was decreased,and the contents of 24 carotenoids differed between the llm4 mutant and the wild type(WT). The llm4mutant showed reduced dormancy and greater sensitive to ABA than the WT. We concluded that the mutation of LLM4 resulted in the failure of xanthophyll cycle, in turn causing ROS accumulation. The excessive ROS accumulation damaged chloroplast structure and induced PCD, leading eventually to the formation of lesion mimics.展开更多
文摘依赖叶黄素循环的热耗散是一种主要防御光破坏的机制。参与叶黄素循环的酶是紫黄质脱环氧化酶和玉米黄质环氧化酶 ,紫黄质脱环氧化酶已分离纯化 ,其 c DNA已被克隆 ,其活性主要受跨类囊体膜的 p H梯度和抗坏血酸浓度的调节 ;玉米黄质环氧化酶还没有被分离出来 ,但其 c DNA也已被克隆 ;其活性主要与NADPH的浓度、O2 及光等有关。
基金supported by the National Key Research and Development Program(2022YFF1001501)the National Natural Science Foundation of China(31972350)+1 种基金the Chinese Universities Scientific Fund(2022TC174)the financial support from an open project of the State Key Laboratory of Crop Stress Adaptation and Improvement in Henan University.
文摘Reducing losses caused by pathogens is an effective strategy for stabilizing crop yields.Daunting challenges remain in cloning and characterizing genes that inhibit stripe rust,a devastating disease of wheat(Triticum aestivum)caused by Puccinia striiformis f.sp.tritici(Pst).We found that suppression of wheat zeaxanthin epoxidase 1(ZEP1)increased wheat defense against Pst.We isolated the yellow rust slower 1(yrs1)mutant of tetraploid wheat in which a premature stop mutation in ZEP1-B underpins the phenotype.Genetic analyses revealed increased H_(2)O_(2) accumulation in zep1 mutants and demonstrated a correlation between ZEP1 dysfunction and slower Pst growth in wheat.Moreover,wheat kinase START 1.1(WKS1.1,Yr36)bound,phosphorylated,and suppressed the biochemical activity of ZEP1.A rare natural allele in the hexaploid wheat ZEP1-B promoter reduced its transcription and Pst growth.Our study thus identified a novel suppressor of Pst,characterized its mechanism of action,and revealed beneficial variants for wheat disease control.This work opens the door to stacking wheat ZEP1 variants with other known Pst resistance genes in future breeding programs to enhance wheat tolerance to pathogens.
基金the financial support of the National Natural Science Foundation of China (32060454, 32272109)Hainan Yazhou Bay Seed Laboratory (B21HJ0215)+1 种基金National Natural Science Foundation of China (32072048, U2004204)Specific Research Fund of The Innovation Platform for Academicians of Hainan Province。
文摘Lesion mimic mutants(LMMs) are advantageous materials for studying programmed cell death(PCD).Although some rice LMM genes have been cloned, the diversity of functions of these genes indicates that the mechanism of cell death regulation in LMMs needs further study. In this study, we identified a rice light-dependent leaf lesion mimic mutant 4(llm4) that showed abnormal chloroplast structure, photoinhibition, reduced photosynthetic protein levels, massive accumulation of reactive oxygen species(ROS), and PCD. Map-based cloning and complementation testing revealed that LLM4 encodes zeaxanthin epoxidase(ZEP), an enzyme involved in the xanthophyll cycle, which functions in plant photoprotection,ROS scavenging, and carotenoid and abscisic acid(ABA) biosynthesis. The ABA content was decreased,and the contents of 24 carotenoids differed between the llm4 mutant and the wild type(WT). The llm4mutant showed reduced dormancy and greater sensitive to ABA than the WT. We concluded that the mutation of LLM4 resulted in the failure of xanthophyll cycle, in turn causing ROS accumulation. The excessive ROS accumulation damaged chloroplast structure and induced PCD, leading eventually to the formation of lesion mimics.
