光信号经由HY5与HDA6互作调控植物自噬的分子机制研究

Autophagy, a catabolic process mediating the degradation of abnormal proteins and cell organelles in vacuoles or lysosomes, plays essential roles in plant growth and stress responses. The important question in this research area is that how plants perceive external cues to activate or repress cellular autophagy to adapt ever-changing environments. Light as an important environmental factor whether and how to regulate plant autophagy is poorly understood. In our previous study, we demonstrated that plant autophagy is significantly activated in light to dark conversion process and found that ELONGATED HYPOCOTYL 5 (HY5), a core transcription factor in light signaling, interacts with HISTONE DEACETYLASE 6 (HDA6) to regulate gene expression of the important plant autophagy gene ATG5. Based on these results and literature review, this proposal intends to take a combination of biochemical, molecular cell and genetic approaches to uncover the molecular mechanism of plant autophagy regulated by light signaling. This project will determine the regularity of cellular autophagy controlled by light intensity, elucidate the roles of light signaling in regulating ATG5 gene expression via HY5, and clarify how HY5 recruits HDA6 to monitor ATG5 gene expression through histone deacetylation. Thus, this study will shed light on the coordinated regulation mechanism of light signaling and plant autophagy and uncover the epigenetic regulation mechanism of plant autophagy mediated by histone deacetylases.

自噬是细胞内依赖于液泡或溶酶体的蛋白质和细胞器降解途径，在植物生长发育及环境应答过程中发挥重要作用。其中重要的科学问题是植物如何感应外界信号并选择性开启或关闭细胞自噬过程而适应环境变化。光作为重要的环境因子，是否以及如何参与调控植物细胞自噬过程尚不清楚。我们的前期研究发现光照到黑暗的转变可以显著激活植物细胞自噬过程，并初步发现光信号的核心转录因子HY5与组蛋白去乙酰化酶HDA6互作调控重要自噬基因ATG5的表达。基于此，本项目拟从生化、分子细胞及遗传多个角度，重点研究光信号调控植物细胞自噬的分子基础，研究内容包括明确光照强度调控植物细胞自噬的内在规律，探索HY5介导光信号调控ATG5基因表达的功能，阐明HY5招募HDA6调控染色质组蛋白去乙酰化修饰而调控ATG5基因表达的功能。该研究将揭示光信号和植物细胞自噬的直接调控关系，并阐明组蛋白去乙酰化酶介导的植物自噬基因的表观遗传学调控机制。

自噬是细胞内依赖于液泡或溶酶体的蛋白质和细胞器降解途径，在植物生长发育及环境应答中发挥重要作用。其中重要的科学问题是植物如何感应外界信号并选择性开启或关闭细胞自噬过程而适应环境变化。本研究发现光照到黑暗的转变和氮饥饿可以显著激活植物细胞自噬。进一步研究发现，转录因子HY5可以和组蛋白去乙酰化酶HDA9互作，协同调控ATG5和ATG8e基因区域的H3K9ac和H3K27ac水平，从而负调控其基因转录和细胞自噬活性。此外，本项目研究发现调控植物开花的转录因子SOC1负调控ATG4b、ATG7和ATG18c的表达，从而抑制碳饥饿诱导的细胞自噬过程并调控植物碳饥饿胁迫耐受性。综上，本项目研究部分揭示了植物细胞自噬的转录调控机制。