Sodium transporters play key roles in plant tolerance to salt stress. Here, we report that a member of the High-Affinity K+ Transporter (HKT) family, OsHKT1;1, in rice (Oryza sativa ‘Nipponbare’) plays an important role in reducing Na+ accumulation in shoots to cope with salt stress. The oshkt1;1 mutant plants displayed hypersensitivity to salt stress. They contained less Na+ in the phloem sap and accumulated more Na+ in the shoots compared with the wild type. OsHKT1;1 was expressed mainly in the phloem of leaf blades and up-regulated in response to salt stress. Using a yeast one-hybrid approach, a novel MYB coiled-coil type transcription factor, OsMYBc, was found to bind to the OsHKT1;1 promoter. In vivo chromatin immunoprecipitation and in vitro electrophoresis mobility shift assays demonstrated that OsMYBc binds to AAANATNC(C/T) fragments within the OsHKT1;1 promoter. Mutation of the OsMYBc-binding nucleotides resulted in a decrease in promoter activity of OsHKT1;1. Knockout of OsMYBc resulted in a reduction in NaCl-induced expression of OsHKT1;1 and salt sensitivity. Taken together, these results suggest that OsHKT1;1 has a role in controlling Na+ concentration and preventing sodium toxicity in leaf blades and is regulated by the OsMYBc transcription factor.
鈉離子轉(zhuǎn)運蛋白在植物的耐鹽性中發(fā)揮了關(guān)鍵作用，本文我們報道了一個高親和性K+轉(zhuǎn)運蛋白（HKT）家族成員OsHKT1;1，它在降低水稻地上部Na+積累以適應(yīng)鹽脅迫的過程中發(fā)揮重要作用。oshkt1;1突變體植株表現(xiàn)出對鹽脅迫超敏感。與野生型相比，突變體韌皮部汁液中含有較少的Na+，在莖部積累了較多的Na+。OsHKT1;1主要在葉片的韌皮部表達，鹽脅迫會誘導它的表達上調(diào)。利用酵母單雜的方法，發(fā)現(xiàn)一個新的MYB CC型轉(zhuǎn)錄因子OsMYBc，能夠與OsHKT1;1啟動子結(jié)合。體內(nèi)染色體免疫共沉淀以及體外凝膠遷移滯后實驗表明，OsMYBc與OsHKT1;1啟動子內(nèi)的AAANATNC(C/T)片段結(jié)合。結(jié)合OsMYBc的核苷酸的突變會導致OsHKT1;1啟動子活性降低。敲除OsMYBc會降低NaCl對OsHKT1;1表達的誘導作用以及鹽敏感性。綜合以上結(jié)果表明，OsHKT1;1在控制Na+含量以及抑制葉片中的鈉離子毒性過程中發(fā)揮作用，并受到OsMYBc轉(zhuǎn)錄因子的調(diào)控。