Key Laboratory of Plant Molecular Physiology, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China.
Plant Physiol. 2013 Jun;162(2):1030-41. doi: 10.1104/pp.113.215798. Epub 2013 May 8.
Arabidopsis (Arabidopsis thaliana) CYCLIN-DEPENDENT KINASE Ds (CDKDs) phosphorylate the C-terminal domain of the largest subunit of RNA polymerase II. Arabidopsis CYCLIN H;1 (CYCH;1) interacts with and activates CDKDs; however, the physiological function of CYCH;1 has not been determined. Here, we report that CYCH;1, which is localized to the nucleus, positively regulates blue light-induced stomatal opening. Reduced-function cych;1 RNA interference (cych;1 RNAi) plants exhibited a drought tolerance phenotype. CYCH;1 is predominantly expressed in guard cells, and its expression was substantially down-regulated by dehydration. Transpiration of intact leaves was reduced in cych;1 RNAi plants compared with the wild-type control in light but not in darkness. CYCH;1 down-regulation impaired blue light-induced stomatal opening but did not affect guard cell development or abscisic acid-mediated stomatal closure. Microarray and real-time polymerase chain reaction analyses indicated that CYCH;1 did not regulate the expression of abscisic acid-responsive genes or light-induced stomatal opening signaling determinants, such as MYB60, MYB61, Hypersensitive to red and blue1, and Protein phosphatase7. CYCH;1 down-regulation induced the expression of redox homeostasis genes, such as LIPOXYGENASE3 (LOX3), LOX4, ARABIDOPSIS GLUTATHIONE PEROXIDASE 7 (ATGPX7), EARLY LIGHT-INDUCIBLE PROTEIN1 (ELIP1), and ELIP2, and increased hydrogen peroxide production in guard cells. Furthermore, loss-of-function mutations in CDKD;2 or CDKD;3 did not affect responsiveness to drought stress, suggesting that CYCH;1 regulates the drought stress response in a CDKD-independent manner. We propose that CYCH;1 regulates blue light-mediated stomatal opening by controlling reactive oxygen species homeostasis.
拟南芥(Arabidopsis thaliana)细胞周期蛋白依赖性激酶 Ds(CDKDs)磷酸化 RNA 聚合酶 II 大亚基的 C 端结构域。拟南芥细胞周期蛋白 H;1(CYCH;1)与 CDKDs 相互作用并激活它们;然而,CYCH;1 的生理功能尚未确定。在这里,我们报告说,定位于细胞核的 CYCH;1 正向调控蓝光诱导的气孔开放。功能降低的 cych;1 RNA 干扰(cych;1 RNAi)植物表现出耐旱表型。CYCH;1 在保卫细胞中主要表达,其表达在脱水时显著下调。与野生型对照相比,cych;1 RNAi 植物在光照下但不在黑暗下的完整叶片蒸腾减少。CYCH;1 的下调抑制了蓝光诱导的气孔开放,但不影响保卫细胞发育或脱落酸介导的气孔关闭。微阵列和实时聚合酶链反应分析表明,CYCH;1 不调控脱落酸反应基因或蓝光诱导的气孔开放信号决定因素的表达,如 MYB60、MYB61、Hypersensitive to red and blue1 和 Protein phosphatase7。CYCH;1 的下调诱导了氧化还原稳态基因的表达,如脂氧合酶 3(LOX3)、LOX4、拟南芥谷胱甘肽过氧化物酶 7(ATGPX7)、早期光诱导蛋白 1(ELIP1)和 ELIP2,并增加了保卫细胞中过氧化氢的产生。此外,CDKD;2 或 CDKD;3 的功能丧失突变不影响对干旱胁迫的响应,表明 CYCH;1 以 CDKD 非依赖性方式调节干旱胁迫响应。我们提出,CYCH;1 通过控制活性氧稳态来调节蓝光介导的气孔开放。