11月29日，PLoS Genetics?在線發(fā)表了中國科學(xué)院分子植物科學(xué)卓越創(chuàng)新中心/植物生理生態(tài)研究所薛紅衛(wèi)研究組題為SPOC domain-containing protein Leaf inclination3 interacts with LIP1 to regulate rice leaf inclination through auxin signaling?的研究論文。該研究發(fā)現(xiàn)水稻中的一個(gè)含有SPOC結(jié)構(gòu)域的蛋白Leaf inclination3 (LC3)通過結(jié)合轉(zhuǎn)錄因子LIP1共同調(diào)控生長素信號，從而調(diào)控水稻葉傾角。

水稻是重要的單子葉模式植物，也是我國乃至世界上最主要的糧食作物之一。株型對作物的生產(chǎn)和產(chǎn)量有著重要關(guān)系，而葉傾角又是水稻株型的關(guān)鍵組分之一。研究表明，適當(dāng)?shù)娜~傾角有利于提高水稻光合效率，通過合理密植，能夠有效提高產(chǎn)量。盡管早已發(fā)現(xiàn)植物激素生長素影響葉傾角大小，且其代謝調(diào)控因子GH3和信號通路的關(guān)鍵組分IAA、ARF等被報(bào)道參與了葉傾角的調(diào)控，但對相關(guān)上游調(diào)控因子及機(jī)制仍了解較少，有待進(jìn)一步闡明。研究組在前期工作中發(fā)現(xiàn)水稻缺失突變體LC3表現(xiàn)出葉傾角增大的表型。進(jìn)一步的遺傳學(xué)、細(xì)胞生物學(xué)等分析表明LC3蛋白作為一個(gè)轉(zhuǎn)錄抑制子通過與LC3互作的轉(zhuǎn)錄因子LIP1協(xié)同抑制下游基因OsIAA12和OsGH3.2表達(dá)，通過抑制生長素信號，最終調(diào)控水稻葉傾角。此外，OsIAA2通過與OsARF17互作抑制生長素信號，揭示了OsIAA2-OsARF17在葉傾角發(fā)育調(diào)控中的特定功能。

該研究有助于對生長素信號調(diào)控網(wǎng)絡(luò)的理解。也對研究植物中具有SPOC結(jié)構(gòu)域的蛋白的功能提供了借鑒。值得一提的是，這是首次發(fā)現(xiàn)的僅含有SPOC結(jié)構(gòu)域而不含RRM SPEN家族的成員。

博士生陳素卉和周莉娟為論文第一作者。相關(guān)工作得到國家自然科學(xué)基金項(xiàng)目(91535201)以及“萬人計(jì)劃”的資助。（來源：中國科學(xué)院植物生理生態(tài)研究所）

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SPOC domain-containing protein Leaf inclination3 interacts with LIP1 to regulate rice leaf inclination through auxin signaling

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Abstract??Leaf angle is an important agronomic trait and influences crop architecture and yield. Studies have demonstrated the roles of phytohormones, particularly auxin and brassinosteroids, and various factors in controlling leaf inclination. However, the underlying mechanism especially the upstream regulatory networks still need being clarified. Here we report the functional characterization of rice leaf inclination3 (LC3), a SPOC domain-containing transcription suppressor, in regulating leaf inclination through interacting with LIP1 (LC3-interacting protein 1), a HIT zinc finger domain-containing protein. LC3 deficiency results in increased leaf inclination and enhanced expressions of?OsIAA12?and?OsGH3.2. Being consistent, transgenic plants with?OsIAA12?overexpression or deficiency of OsARF17 which interacts with OsIAA12 do present enlarged leaf inclination. LIP1 directly binds to promoter regions of?OsIAA12?and?OsGH3.2, and interacts with LC3 to synergistically suppress auxin signaling. Our study demonstrate the distinct effects of IAA12-ARF17 interactions in leaf inclination regulation, and provide informative clues to elucidate the functional mechanism of SPOC domain-containing transcription suppressor and fine-controlled network of lamina joint development by LC3-regulated auxin homeostasis and auxin signaling through.

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原文鏈接：https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1007829