Salt stress adversely affects plant growth, development, and crop yield. Rice (Oryza sativa L.) is one of the most salt-sensitive cereal crops, especially at the early seedling stage. Mitogen-activated protein kinase (MAPK/MPK) cascades have been shown to play critical roles in salt response in Arabidopsis. However, the roles of the MPK cascade signaling in rice salt response and substrates of OsMPK remain largely unknown. Here, we report that the salt-induced OsMPK4-Ideal Plant Architecture 1 (IPA1) signaling pathway regulates the salt tolerance in rice. Under salt stress, OsMPK4 could interact with IPA1 and phosphorylate IPA1 at Thr180, leading to degradation of IPA1. Genetic evidence shows that IPA1 is a negative regulator of salt tolerance in rice, whereas OsMPK4 promotes salt response in an IPA1-dependent manner. Taken together, our results uncover an OsMPK4-IPA1 signal cascade that modulates the salt stress response in rice and sheds new light on the breeding of salt-tolerant rice varieties.
鹽脅迫是限制植物生長和作物產(chǎn)量的主要非生物脅迫之一，全球鹽漬土總面積高達(dá)8億公頃，嚴(yán)重危害糧食安全。水稻是我國最重要的糧食作物，但對鹽脅迫非常敏感，解析水稻鹽脅迫響應(yīng)的分子機(jī)制，對于改良水稻耐鹽性具有重要科學(xué)意義。
IPA1 (Ideal Plant Architecture 1)是此前中國科學(xué)院遺傳與發(fā)育生物學(xué)研究所李家洋團(tuán)隊(duì)鑒定到的一個(gè)水稻株型調(diào)控的主效基因，因其在調(diào)控水稻分蘗和籽粒大小方面發(fā)揮的重要作用，被廣泛用于高產(chǎn)水稻育種，但其參與水稻鹽脅迫響應(yīng)的機(jī)制并不清楚。近期，該團(tuán)隊(duì)通過對IPA1功能缺失突變體ipa1-10和功能獲得型ipa1-3D的幼苗進(jìn)行鹽處理，發(fā)現(xiàn)IPA1負(fù)調(diào)控水稻的耐鹽性，鹽脅迫處理30分鐘后IPA1的磷酸化水平升高但蛋白水平降低。為深入探究IPA1的上游調(diào)控因子，通過質(zhì)譜技術(shù)系統(tǒng)分析了鹽脅迫條件下IPA1的互作蛋白，鑒定到絲裂原活化蛋白激(MAPKs/MPKs)家族成員OsMPK4。進(jìn)一步的實(shí)驗(yàn)結(jié)果表明OsMPK4能夠與IPA1發(fā)生蛋白相互作用，并且在鹽脅迫條件下，OsMPK4被激活并磷酸化IPA1的Thr180位點(diǎn)，從而促進(jìn)IPA1的泛素化降解，降低IPA1的蛋白水平并最終提高水稻耐鹽性。遺傳結(jié)果表明，OsMPK4正調(diào)控水稻耐鹽性并與IPA1在耐鹽性調(diào)控上位于同一通路中。綜上，該項(xiàng)研究工作闡明了MPK4-IPA1模塊調(diào)控水稻鹽脅迫響應(yīng)的分子機(jī)制, 揭示了植物生長和脅迫之間的信號交互，為創(chuàng)制高產(chǎn)耐鹽水稻品種提供了新的分子機(jī)制與遺傳資源。