Plant Physiol:华南师范大学阳成伟教授课题组发现植物叶片衰老调
2017年3月1日，国际植物学顶级期刊《Plant Physiology》杂志上在线发表了华南师范大学生命科学学院阳成伟教授课题组题为《The mitochondrial protease FtSH4 regulates leaf senescence via WRKY-dependent salicylic acid signal》的研究成果。张盛春副教授为论文第一作者，阳成伟教授为论文通讯作者。
衰老是一个高度程序化的发育过程，是生物有机体发育的必经阶段。植物叶片衰老能够将衰老叶片中的营养物质重新分配给生长旺盛的果实或者种子，在很大程度上决定了作物的产量。植物过早启动衰老进程会对植物的正常生长发育产生不良影响，严重阻碍了各种农作物的生产量。因此，揭示植物衰老的分子调控机制是农业生产中亟需解决的重要生物学问题，具有重要的理论意义和应用价值。
线粒体是真核生物细胞的能量代谢中心，除给细胞供能外，线粒体还在衰老中起重要作用。一直以来人们认为植物线粒体所产生的活性氧(ROS)能够诱导细胞死亡并导致叶片衰老，但是线粒体产生的ROS调控叶片衰老的分子机制却一直不清楚。阳成伟教授课题组在前期研究基础上，发现模式植物拟南芥中一个定位于线粒体膜上的金属蛋白酶基因FtSH4突变后影响了线粒体呼吸链复合物的稳定性，导致了大量ROS的积累。突变体中积累的ROS能够诱导植物转录因子WRKY基因家族中WRKY75等成员的表达量上升，WRKY75等WRKY蛋白进入到细胞核后能够结合到植物衰老相关激素水杨酸(SA)合成基因SID2的启动子上并促进其表达，从而导致ftsh4突变体中SA含量升高;细胞中高水平的SA进一步激活了SA信号及细胞自噬信号，导致细胞进入衰老和自噬阶段并进一步引起了细胞死亡和叶片衰老。这一研究成果不仅在理论上加深了人们对ROS与SA相互作用调控植物叶片衰老机制的理解，也为线粒体逆向信号如何调控细胞核的生理功能提供了证据，同时也为其他作物生产上存在的叶片早衰问题提供了解决的可能途径。
线粒体FtSH4通过依赖于WRKY的SA信号调控自噬和衰老模型
原文链接：
The mitochondrial protease FtSH4 regulates leaf senescence via WRKY-dependent salicylic acid signal
原文摘要：
Mitochondria and autophagy play important roles in the networks that regulate plant leaf senescence and cell death. However, the molecular mechanisms underlying the interactions between mitochondrial signaling and autophagy are currently not well understood. This study characterized the function of the Arabidopsis mitochondrial AAA-protease gene AtFtSH4 in regulating autophagy and senescence,finding that AtFtSH4 mediates WRKY-dependent salicylic acid (SA) accumulation and signaling. Knock-out of FtSH4 in the ftsh4-4 mutant resulted in severe leaf senescence, cell death, and high autophagy levels. The level of SA increased dramatically in the ftsh4-4 mutant. expression of nahGin the ftsh4-4 mutant led to decreased SA levels and suppressed the leaf senescence and cell death phenotypes. The transcript levels of several SA synthesis and signaling genes, including SA INDUCTION DEFICIENT2 (SID2), NONRACE-SPECIFIC DISEASE RESISTANCE1 (NDR1), and NONEXPRESSOR OF PATHOGENESIS-RELATED PROTEINS1 (NPR1), increased significantly in the ftsh4-4 mutants compared with wild type. Loss-of-function of SID2, NDR1, or NPR1 in the ftsh4-1mutant reversed the ftsh4-1senescence and autophagy phenotypes. Furthermore, ftsh4-4 mutants had elevated levels of transcripts of several WRKY genes, including WRKY40, 46, 51, 60, 63, and 75; all of these WRKY proteins can bind to the promoter of SID2. Loss-of-function of WRKY75 in the ftsh4-4 mutants decreased the levels of SA and reversed the senescence phenotype. Taken together, these results suggest that the mitochondrial ATP-dependent proteaseFtSH4 may regulate the expression of WRKY genes by modifying the level of reactive oxygen species, and the WRKY transcription factors that control SA synthesis and signaling in autophagy and senescence.
作者：阳成伟
