IDD16 negatively regulates stomatal initiation via trans-repression of SPCH in Arabidopsis
IDD16 negatively regulates stomatal initiation via trans-repression of SPCH in Arabidopsis
复制标题
IDD16 通过反式抑制拟南芥 SPCH 负调控气孔起始
DOI：
10.1111/pbi.13070
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发表时间：
2019-07-01
影响因子：
13.8
通讯作者：
Hua, Xue-Jun
中科院分区：
文献类型：
--
作者：
Qi, Shi-Lian;Lin, Qing-Fang;Hua, Xue-Jun
在拟南芥中，气孔谱系细胞的启动和增殖受SPEECHLESS（SPCH）控制。据报道，SPCH在翻译后水平的磷酸化调节气孔发育。在这里，我们报告IDD 16作为一个负调控气孔启动直接调节SPCH转录。在拟南芥中，IDD 16过表达以剂量依赖的方式降低远轴气孔密度。时间进程分析表明，IDD 16-OE植株气孔前体细胞的启动受到严重抑制。与这些发现一致，SPCH的转录在IDD 16-OE植物中被极大地抑制。而IDD 16-RNAi转基因植株气孔密度增加，表明IDD 16基因是气孔发育的内在调节因子。ChIP分析表明IDD 16可直接与SPCH启动子结合。此外，过表达IDD 16的拟南芥表现出显著增加的耐旱性和较高的综合水分利用效率（WUE），由于减少叶片蒸腾。总的来说，我们的研究结果表明，IDD 16负调控气孔启动通过反式阻遏SPCH，从而提供了一个实用的工具，通过操纵IDD 16的表达增加植物WUE。
In Arabidopsis, the initiation and proliferation of stomatal lineage cells is controlled by SPEECHLESS (SPCH). Phosphorylation of SPCH at the post-translational level has been reported to regulate stomatal development. Here we report that IDD16 acts as a negative regulator for stomatal initiation by directly regulating SPCH transcription. In Arabidopsis, IDD16 overexpression decreased abaxial stomatal density in a dose-dependent manner. Time course analysis revealed that the initiation of stomatal precursor cells in the IDD16-OE plants was severely inhibited. Consistent with these findings, the transcription of SPCH was greatly repressed in the IDD16-OE plants. In contrast, IDD16-RNAi transgenic line resulted in enhanced stomatal density, suggesting that IDD16 is an intrinsic regulator of stomatal development. ChIP analysis indicated that IDD16 could directly bind to the SPCH promoter. Furthermore, Arabidopsis plants overexpressing IDD16 exhibited significantly increased drought tolerance and higher integrated water use efficiency (WUE) due to reduction in leaf transpiration. Collectively, our results established that IDD16 negatively regulates stomatal initiation via trans-repression of SPCH, and thus provide a practical tool for increasing plant WUE through the manipulation of IDD16 expression.