AUXIN RESPONSE FACTOR17 Directly Regulates MYB108 for Anther Dehiscence
AUXIN RESPONSE FACTOR17 Directly Regulates MYB108 for Anther Dehiscence
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生长素反应因子 17 直接调节 MYB108 导致花药开裂
DOI：
10.1104/pp.19.00576
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发表时间：
2019-10-01
期刊：
影响因子：
7.4
通讯作者：
Yang, Zhong-Nan
中科院分区：
文献类型：
--
作者：
Xu, Xiao-Feng;Wang, Bo;Yang, Zhong-Nan
花药开裂后成熟花粉的及时释放对开花植物的繁殖至关重要。生长素反应因子17（ARF 17）在花药中花粉壁图案形成、绒毡层发育和生长素信号转导中起着重要作用。在这里，我们发现ARF 17也参与花药开裂。拟南芥（Arabidopsis thaliana）arf 17突变体表现出有缺陷的药室内壁木质化，这导致花药开裂的缺陷。MYB 108的表达，它编码一个重要的花药开裂的转录因子，显着下调arf 17的花蕾。染色质免疫沉淀分析和电泳迁移率变动分析表明，ARF 17直接结合MYB 108启动子。在ARF 17-GFP转基因系中，其中ARF 17-GFP完全补充了arf 17表型，在花药阶段11的内皮中观察到ARF 17-GFP。在转MYB 108：：GUS启动子的转基因植株中，在花药后期的内皮细胞中也检测到由MYB 108启动子驱动的GUS信号。因此，ARF 17和MYB 108的表达模式与这些基因在花药开裂中的功能一致。此外，由ARF 17启动子驱动的MYB 108的表达成功地恢复了arf 17的花药开裂缺陷。这些结果表明，ARF 17调控MYB 108的表达，花药开裂。与其在小细胞和绒毡层中的功能一起，ARF 17可能协调花药中不同孢子体细胞层的发育。本文还讨论了ARF 17-MYB 108信号通路在花药开裂调控中的作用。
The timely release of mature pollen following anther dehiscence is essential for reproduction in flowering plants. AUXIN RESPONSE FACTOR17 (ARF17) plays a crucial role in pollen wall pattern formation, tapetum development, and auxin signal transduction in anthers. Here, we showed that ARF17 is also involved in anther dehiscence. The Arabidopsis (Arabidopsis thaliana) arf17 mutant exhibits defective endothecium lignification, which leads to defects in anther dehiscence. The expression of MYB108, which encodes a transcription factor important for anther dehiscence, was dramatically downregulated in the flower buds of arf17. Chromatin immunoprecipitation assays and electrophoretic mobility shift assays showed ARF17 directly binds to the MYB108 promoter. In an ARF17-GFP transgenic line, in which ARF17-GFP fully complements the arf17 phenotype, ARF17-GFP was observed in the endothecia at anther stage 11. The GUS signal driven by the MYB108 promoter was also detected in endothecia at late anther stages in transgenic plants expressing promoterMYB108::GUS. Thus, the expression pattern of both ARF17 and MYB108 is consistent with the function of these genes in anther dehiscence. Furthermore, the expression of MYB108 driven by the ARF17 promoter successfully restored the defects in anther dehiscence of arf17. These results demonstrated that ARF17 regulates the expression of MYB108 for anther dehiscence. Together with its function in microcytes and tapeta, ARF17 likely coordinates the development of different sporophytic cell layers in anthers. The ARF17-MYB108 pathway involved in regulating anther dehiscence is also discussed.