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拟南芥PRL1与RPA2A协同调控植物衰老进程的分子机制

批准号:
32100291
项目类别:
青年科学基金项目(C类)
资助金额:
30.0 万元
负责人:
孟晶晶
依托单位:
学科分类:
植物生殖与发育
结题年份:
2024
批准年份:
2021
项目状态:
已结题
项目参与者:
孟晶晶

项目摘要

结项摘要

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中文摘要
衰老是植物生长发育的重要阶段。衰老过程伴随着基因组范围的转录重编程,大分子物质的降解和营养物质从衰老组织向新生组织和储藏器官的转移,对植物世代交替和作物产量形成具有重要意义。但是,目前对植物衰老调控机制的理解还很有限。本项目前期工作中发现,多效调控蛋白PRL1与复制蛋白RPA2A抑制黑暗碳饥饿胁迫诱导的衰老进程,PRL1与RPA2A存在直接互作,且两者均参与DNA损伤修复。在此基础上,本项目拟通过分析PRL1与RPA2A参与DNA损伤调控衰老的细胞与分子表征、明确PRL1与RPA2A参与DNA损伤修复调控衰老过程的遗传关系与解析PRL1-RPA2A互作调控黑暗碳饥饿胁迫诱导植物衰老的分子机制等三方面的工作,揭示PRL1与RPA2A参与调控植物衰老的生物学新功能,阐明DNA损伤修复与黑暗碳饥饿胁迫诱导植物衰老途径的相互调控关系,为人工改良作物衰老性状,提升作物产量与品质提供理论支撑。
英文摘要
Senescence is an important stage of the plant lifecycle. Senescence is accompanied by the genome-wide transcriptional reprogramming, degradation of macromolecules and the translocation of nutrients from senescent tissues to growing tissues and the storage organs, which are of great significance for plant generation alteration and crop yield formation. However, current understanding of the mechanism of plant senescence is still very limited. In our preliminary study, we have discovered that PRL1 and RPA2A inhibited the senescence process induced by dark and carbon deprivation. Moreover, we found that PRL1 interacted with RPA2A, and both of them were involved in DNA damage repair. Based on those findings, we proposed to explore the new biological functions of PRL1 and RPA2A and mechanism of PRL1 and RPA2A synergistically regulate plant senescence through the following three parts of works. First, analyze the cellular and molecule characterizations of PRL1 and RPA2A in DNA damage and regulation of senescence, second, elucidate the genetic relationship between PRL1 and RPA2A in the process of senescence induced by dark and carbon deprivation, and third, uncover the molecular mechanism of PRL1-RPA2A interaction element in regulating plant senescence. This work will reveal the new biological functions of PRL1 and RPA2A involved in regulating plant senescence, clarify the relationship between DNA damage repair and dark carbon starvation stress-induced plant senescence pathways, and provide theoretical support for artificially improving crop senescence traits and improving crop yield and quality.
植物衰老受到内源信号和外界环境因素的共同调控。光照缺乏等非生物胁迫诱导叶片早衰,影响作物产量与品质形成。然而,胁迫诱导衰老的分子机制尚不完全明确。在这项工作中,运用碳缺乏诱导植物幼苗衰老的实验体系,通过大规模遗传筛选衰老进程异常突变体,发现PRL1(Pleiotropic Regulatory Locus 1)功能缺失导致植物在碳缺乏胁迫下早衰,而过表达PRL1能够在碳缺乏和自然衰老过程中延缓植物衰老,说明PRL1是植物衰老的负调控因子。PRL1是真核生物中广泛保守的NTC复合体亚基,表型分析发现NTC复合体的其他亚基如AtCDC5和MAC3A/3B的缺失也导致植物在碳缺乏下的早衰。蛋白互作研究发现,PRL1与单链DNA结合蛋白RPA(Replication Protein A)复合体亚基RPA2A在细胞核内互作。RPA2A功能缺失突变体和过表达系的衰老表型分析发现RPA2A也具有抑制衰老的功能。遗传分析发现prl1-10 rpa2a-1双突变体衰老表型与rpa2a-1类似,并且在prl1-10背景下过表达RPA2A能够回复prl1-10的早衰表型,但是不能回复prl1-10的短根、糖敏感以及DNA损伤相关表型,而在rpa2a-1背景下过表达PRL1不能回复rpa2a-1的早衰表型,说明RPA2A与PRL1在同一衰老通路中发挥功能,并且RPA2A作用于PRL1的下游。进一步发现,碳缺乏条件下,PRL1通过增进RPA2A蛋白的稳定性抑制衰老。这些研究结果明确了PRL1和RPA2A是碳缺乏诱导植物衰老的负调控因子,揭示了PRL1-RPA2A功能模块在植物衰老调控中重要作用,为人工改造作物提供基因资源与遗传策略。
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