Drought is a recurring climatic hazard that reduces the crop yields. To avoid the negative effects of drought on crop production, extensive efforts have been devoted to investigating the complex mechanisms of gene expression and signal transduction during drought stress. Receptor-like kinases (RLKs) play important roles in perceiving extracellular stimuli and activating downstream signalling responses. The rice genome contains >1100 RLK genes, of which only two are reported to function in drought stress. A leucine-rich repeat (LRR)-RLK gene named Leaf Panicle 2 (LP2) was previously found to be strongly expressed in leaves and other photosynthetic tissues, but its function remains unclear. In the present study, it was shown that the expression of LP2 was down-regulated by drought and abscisic acid (ABA). Transgenic plants overexpressing LP2 accumulated less H2O2, had more open stomata in leaves, and showed hypersensitivity to drought stress. Further investigation revealed that transcription of LP2 was directly regulated by the zinc finger transcription factor DROUGHT AND SALT TOLERANCE (DST). In addition, LP2 was identified as a functional kinase localized to the plasma membrane and interacted with the drought-responsive aquaporin proteins OsPIP1;1, OsPIP1; 3, and OsPIP2; 3. Thus, the findings provided evidence that the LRR-RLK LP2, transcriptionally regulated by the drought-related transcription factor DST, served as a negative regulator in drought response.
干旱是一種經(jīng)常性的氣候?yàn)?zāi)害，會(huì)降低作物產(chǎn)量。為了避免干旱對(duì)作物生產(chǎn)的副作用，投入了大量工作對(duì)干旱脅迫過(guò)程中基因表達(dá)和信號(hào)傳導(dǎo)的復(fù)雜機(jī)理進(jìn)行研究。類受體激酶（RLKs）在識(shí)別胞外刺激和激活下游信號(hào)響應(yīng)過(guò)程中發(fā)揮了重要作用。水稻基因組含有超過(guò)1100個(gè)RLK基因，只有兩個(gè)RLK被報(bào)道在干旱脅迫中發(fā)揮功能。之前發(fā)現(xiàn)一個(gè)富含亮氨酸重復(fù)序列的RLK基因，Leaf Panicle 2(LP2)，在葉片和其它光合組織中強(qiáng)烈表達(dá)，但是它的功能仍不清楚。本文研究中，我們發(fā)現(xiàn)LP2表達(dá)受干旱和脫落酸（ABA）處理下調(diào)。LP2過(guò)表達(dá)轉(zhuǎn)基因植株積累更少的H202，葉片中有更多張開(kāi)的氣孔，表現(xiàn)出對(duì)干旱超敏感。進(jìn)一步研究表明，LP2的轉(zhuǎn)錄受到鋅指轉(zhuǎn)錄因子DROUGHT AND SALT TOLERANCE（DST）的直接調(diào)控。此外，LP2被鑒定是位于細(xì)胞膜的一個(gè)有功能的激酶，能與干旱應(yīng)答水通道蛋白OsPIP1;1、OsPIP1;3和OsPIP2;1互作。因而，我們的發(fā)現(xiàn)提供證據(jù)表明，LRR-RLK LP2，受到干旱相關(guān)轉(zhuǎn)錄因子DST的轉(zhuǎn)錄調(diào)控，作為干旱應(yīng)答的負(fù)調(diào)控因子發(fā)揮作用。