由于二氧化碳排放量的增加,，地球溫室效應(yīng)的加劇，導(dǎo)致高溫脅迫日益成為我國(guó)及世界現(xiàn)代農(nóng)業(yè)生產(chǎn)體系所面臨的嚴(yán)峻挑戰(zhàn),。葉綠體是植物細(xì)胞進(jìn)行光合作用的場(chǎng)所,，也是高溫逆境因子作用的敏感位點(diǎn),。高溫脅迫導(dǎo)致葉綠體類(lèi)囊體膜結(jié)構(gòu)發(fā)生顯著的改變,，從而對(duì)光合作用和植物其他生理過(guò)程產(chǎn)生顯著傷害,。植物在高溫脅迫條件下的熱激反應(yīng)是啟動(dòng)體內(nèi)大量熱激轉(zhuǎn)錄因子（HSF）和熱激蛋白（HSP)基因的轉(zhuǎn)錄，而對(duì)于啟動(dòng)這些熱激響應(yīng)基因表達(dá)的信號(hào)來(lái)源并不清楚,。
近日,，國(guó)際遺傳學(xué)權(quán)威期刊PLoS Genetics在線發(fā)表了我所郭房慶課題組的最新研究成果，該成果揭示高等植物葉綠體是細(xì)胞啟動(dòng)胞內(nèi)熱激反應(yīng)的信號(hào)源,，首次建立了葉綠體蛋白翻譯效率和細(xì)胞核熱脅迫響應(yīng)轉(zhuǎn)錄因子HsfA2表達(dá)啟動(dòng)的遺傳關(guān)系,，證實(shí)了高等植物細(xì)胞存在熱激反應(yīng)的葉綠體逆向（retrograde）調(diào)控信號(hào)途徑。上述的重要研究進(jìn)展為細(xì)胞核-質(zhì)體信號(hào)互做參與植物逆境脅迫適應(yīng)機(jī)制提供了新的證據(jù),，為進(jìn)一步研究高等植物的耐熱性狀形成機(jī)理開(kāi)啟了一個(gè)全新的視角,。
鑒于葉綠體對(duì)于高溫脅迫十分敏感這一事實(shí)，為了回答植物在高溫脅迫下如何維持葉綠體穩(wěn)定性這一關(guān)鍵科學(xué)問(wèn)題,，在郭房慶研究員的指導(dǎo)下,，博士生于海東等開(kāi)展了高通量的植物高溫脅迫響應(yīng)蛋白的篩選和鑒定工作。其中鑒定的一個(gè)熱激響應(yīng)蛋白為葉綠體核糖體蛋白R(shí)PS1（Ribosomal Protein S1）,。研究表明RPS1參與類(lèi)囊體膜蛋白的翻譯,，并且RPS1的表達(dá)水平以劑量依賴(lài)的方式調(diào)控類(lèi)囊體膜結(jié)構(gòu)的穩(wěn)定性。尤為重要的是,，RPS1表達(dá)水平下調(diào)導(dǎo)致擬南芥突變體對(duì)高溫脅迫極度敏感,，其原因是rps1突變體在高溫脅迫條件下熱激轉(zhuǎn)錄因子HsfA2及其下游靶基因的表達(dá)受到嚴(yán)重抑制。與以上結(jié)論相一致的是,，組成型表達(dá)HsfA2可以將rps1類(lèi)囊體膜穩(wěn)定性和耐熱性恢復(fù)至野生型水平,。博士生楊小飛、陳思婷和王玉婷等參加了論文的部分研究工作,。
綜合論文的研究成果和前人對(duì)于細(xì)胞耐熱性狀形成機(jī)制的認(rèn)識(shí),，研究者提出了以下的植物細(xì)胞熱激反應(yīng)逆向調(diào)控機(jī)制模型：RPS1作為葉綠體蛋白翻譯調(diào)控的關(guān)鍵因子，其蛋白表達(dá)水平受高溫脅迫的誘導(dǎo),；RPS1表達(dá)增強(qiáng)可以提高類(lèi)囊體膜蛋白的翻譯效率,，對(duì)于維持高溫脅迫下葉綠體的功能狀態(tài)和產(chǎn)生質(zhì)體逆向信號(hào)是必要的。產(chǎn)生的質(zhì)體信號(hào)通過(guò)相關(guān)的熱激信號(hào)轉(zhuǎn)導(dǎo)組分傳遞到細(xì)胞核,，從而啟動(dòng)HsfA2 和其下游靶基因的熱激響應(yīng)表達(dá),。而HsfA2下游靶基因編碼的葉綠體定位的熱激蛋白如HSP21等進(jìn)入葉綠體，對(duì)高溫脅迫下的葉綠體類(lèi)囊體膜系統(tǒng)進(jìn)行保護(hù),。以上發(fā)現(xiàn)同時(shí)也為通過(guò)調(diào)控質(zhì)體翻譯效率,，增強(qiáng)農(nóng)作物的耐高溫脅迫能力提供了全新的遺傳改良操作路徑。
該工作得到了國(guó)家科技部,、國(guó)家自然科學(xué)基金委員會(huì)和中國(guó)科學(xué)院等項(xiàng)目的資助,。（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.
