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拟南芥 ANGUSTIFOLIA3(AN3)与 CONSTITUTIVE PHOTOMORPHOGENIC1(COP1)启动子相关,以调节光介导的气孔发育。

Arabidopsis ANGUSTIFOLIA3 (AN3) is associated with the promoter of CONSTITUTIVE PHOTOMORPHOGENIC1 (COP1) to regulate light-mediated stomatal development.

机构信息

The Key Laboratory of Biotechnology for Medicinal Plant of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou, Jiangsu, 221116, People's Republic of China.

Public Technical Service Center, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan, 650223, People's Republic of China.

出版信息

Plant Cell Environ. 2018 Jul;41(7):1645-1656. doi: 10.1111/pce.13212. Epub 2018 May 10.

DOI:10.1111/pce.13212
PMID:29645276
Abstract

Light signals are perceived by multiple photoreceptors that converge to suppress the RING E3 ubiquitin ligase CONSTITUTIVE PHOTOMORPHOGENIC1 (COP1) for the regulation of stomatal development. Thus, COP1 is a point of integration between light signaling and stomatal patterning. However, how light signaling is collected into COP1 for the production and spacing of stomata is still unknown. Here, we report that the loss-of-function mutant of ANGUSTIFOLIA3 (AN3) delays asymmetric cell division, which leads to decreased stomatal index. Furthermore, overexpression of AN3 accelerates asymmetric cell division, which results in clusters of stomata. In addition, the stomatal development through AN3 regulation is mediated by light signaling. Finally, we find that an3 is a light-signaling mutant, and that AN3 protein is light regulated. Self-activation by AN3 contributes to the control of AN3 expression. Thus, AN3 is a point of collection between light signaling and stomatal patterning. Target-gene analysis indicates that AN3 is associated with COP1 promoter for the regulation of light-controlling stomatal development. Together, these components for regulating stomatal development form an AN3-COP1-E3 ubiquitin ligase complex, allowing the integration of light signaling into the production and spacing of stomata.

摘要

光信号被多个光感受器感知,这些感受器汇聚在一起抑制 RING E3 泛素连接酶 CONSTITUTIVE PHOTOMORPHOGENIC1(COP1),从而调节气孔发育。因此,COP1 是光信号和气孔模式之间的整合点。然而,光信号如何被收集到 COP1 中以产生和间隔气孔仍然未知。在这里,我们报告说 ANGUSTIFOLIA3(AN3)的功能丧失突变体延迟不对称细胞分裂,导致气孔指数降低。此外,过表达 AN3 会加速不对称细胞分裂,导致气孔簇的形成。此外,通过 AN3 调节的气孔发育是由光信号介导的。最后,我们发现 an3 是一个光信号突变体,并且 AN3 蛋白是光调控的。AN3 的自我激活有助于控制 AN3 的表达。因此,AN3 是光信号和气孔模式之间的一个收集点。靶基因分析表明,AN3 与 COP1 启动子相关,用于调节光控制的气孔发育。总之,这些调节气孔发育的成分形成了一个 AN3-COP1-E3 泛素连接酶复合物,允许光信号整合到气孔的产生和间隔中。

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