由于二氧化碳排放量的增加，地球温室效应的加剧，导致高温胁迫日益成为我国及世界现代农业生产体系所面临的严峻挑战。叶绿体是植物细胞进行光合作用的场所，也是高温逆境因子作用的敏感位点。高温胁迫导致叶绿体类囊体膜结构发生显著的改变，从而对光合作用和植物其他生理过程产生显著伤害。植物在高温胁迫条件下的热激反应是启动体内大量热激转录因子（HSF）和热激蛋白（HSP)基因的转录，而对于启动这些热激响应基因表达的信号来源并不清楚。
近日，国际遗传学权威期刊PLoS Genetics在线发表了我所郭房庆课题组的最新研究成果，该成果揭示高等植物叶绿体是细胞启动胞内热激反应的信号源，首次建立了叶绿体蛋白翻译效率和细胞核热胁迫响应转录因子HsfA2表达启动的遗传关系，证实了高等植物细胞存在热激反应的叶绿体逆向（retrograde）调控信号途径。上述的重要研究进展为细胞核-质体信号互做参与植物逆境胁迫适应机制提供了新的证据，为进一步研究高等植物的耐热性状形成机理开启了一个全新的视角。
鉴于叶绿体对于高温胁迫十分敏感这一事实，为了回答植物在高温胁迫下如何维持叶绿体稳定性这一关键科学问题，在郭房庆研究员的指导下，博士生于海东等开展了高通量的植物高温胁迫响应蛋白的筛选和鉴定工作。其中鉴定的一个热激响应蛋白为叶绿体核糖体蛋白RPS1（Ribosomal Protein S1）。研究表明RPS1参与类囊体膜蛋白的翻译，并且RPS1的表达水平以剂量依赖的方式调控类囊体膜结构的稳定性。尤为重要的是，RPS1表达水平下调导致拟南芥突变体对高温胁迫极度敏感，其原因是rps1突变体在高温胁迫条件下热激转录因子HsfA2及其下游靶基因的表达受到严重抑制。与以上结论相一致的是，组成型表达HsfA2可以将rps1类囊体膜稳定性和耐热性恢复至野生型水平。博士生杨小飞、陈思婷和王玉婷等参加了论文的部分研究工作。
综合论文的研究成果和前人对于细胞耐热性状形成机制的认识，研究者提出了以下的植物细胞热激反应逆向调控机制模型：RPS1作为叶绿体蛋白翻译调控的关键因子，其蛋白表达水平受高温胁迫的诱导；RPS1表达增强可以提高类囊体膜蛋白的翻译效率，对于维持高温胁迫下叶绿体的功能状态和产生质体逆向信号是必要的。产生的质体信号通过相关的热激信号转导组分传递到细胞核，从而启动HsfA2 和其下游靶基因的热激响应表达。而HsfA2下游靶基因编码的叶绿体定位的热激蛋白如HSP21等进入叶绿体，对高温胁迫下的叶绿体类囊体膜系统进行保护。以上发现同时也为通过调控质体翻译效率，增强农作物的耐高温胁迫能力提供了全新的遗传改良操作路径。
该工作得到了国家科技部、国家自然科学基金委员会和中国科学院等项目的资助。（生物谷Bioon.com）
doi:10.1371/journal.pgen.1002669
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Downregulation of Chloroplast RPS1 Negatively Modulates Nuclear Heat-Responsive Expression of HsfA2 and Its Target Genes in Arabidopsis
Hai-Dong Yu, Xiao-Fei Yang, Si-Ting Chen, Yu-Ting Wang, Ji-Kai Li, Qi Shen, Xun-Liang Liu, Fang-Qing Guo*
Heat stress commonly leads to inhibition of photosynthesis in higher plants. The transcriptional induction of heat stress-responsive genes represents the first line of inducible defense against imbalances in cellular homeostasis. Although heat stress transcription factor HsfA2 and its downstream target genes are well studied, the regulatory mechanisms by which HsfA2 is activated in response to heat stress remain elusive. Here, we show that chloroplast ribosomal protein S1 (RPS1) is a heat-responsive protein and functions in protein biosynthesis in chloroplast. Knockdown of RPS1 expression in the rps1 mutant nearly eliminates the heat stress-activated expression of HsfA2 and its target genes, leading to a considerable loss of heat tolerance. We further confirm the relationship existed between the downregulation of RPS1 expression and the loss of heat tolerance by generating RNA interference-transgenic lines of RPS1. Consistent with the notion that the inhibited activation of HsfA2 in response to heat stress in the rps1 mutant causes heat-susceptibility, we further demonstrate that overexpression of HsfA2 with a viral promoter leads to constitutive expressions of its target genes in the rps1 mutant, which is sufficient to reestablish lost heat tolerance and recovers heat-susceptible thylakoid stability to wild-type levels. Our findings reveal a heat-responsive retrograde pathway in which chloroplast translation capacity is a critical factor in heat-responsive activation of HsfA2 and its target genes required for cellular homeostasis under heat stress. Thus, RPS1 is an essential yet previously unknown determinant involved in retrograde activation of heat stress responses in higher plants.
