DYT1 directly regulates the expression of TDF1 for tapetum development and pollen wall formation in Arabidopsis

DYT1 directly regulates the expression of TDF1 for tapetum development and pollen wall formation in Arabidopsis
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DYT1直接调节拟南芥绒毡层发育和花粉壁形成中TDF1的表达

DOI:
10.1111/tpj.12694
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发表时间:
2014-12-01
期刊:
影响因子:
7.2
通讯作者:
Yang, Zhong-Nan
Yang, Zhong-Nan
中科院分区:
生物学1区
文献类型:
--
作者:
Gu, Jing-Nan;Zhu, Jun;Yang, Zhong-Nan

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绒毡层在小孢子的发育和成熟过程中起着至关重要的作用。功能失调的绒毡层 1 (DYT1) 对于早期绒毡层发育至关重要。在这里,我们确定启动子区域(-550 至 -463bp)包含 DYT1 表达不可或缺的顺式元件。虽然 DYT1 转录本可以在性母细胞和绒毡层细胞中检测到,但 DYT1-GFP 的定位表明 DYT1 在小孢子发生过程中严格定位于绒毡层细胞中。染色质免疫沉淀 (ChIP) 分析显示 DYT1 直接结合绒毡层发育和功能缺陷 1 (TDF1) 的启动子区域,TDF1 是绒毡层发育所必需的转录因子。当 DYT1 启动子驱动的 TDF1 在 dyt1 突变体中表达时,转录因子 AMS、MS188/MYB80、TEK 和 MS1 以及花粉壁相关基因的表达得到恢复。尽管花粉壁未形成且小孢子破裂,但DIOC2染色显示转基因品系中合成了脂肪酸(花粉壁的前体)。这些结果表明,DYT1 主要通过 TDF1 调节 AMS、MS188/MYB80、TEK 和 MS1 的表达,从而促进花粉壁的形成。
The tapetum plays a critical role during the development and maturation of microspores. DYSFUNCTIONAL TAPETUM 1 (DYT1) is essential for early tapetal development. Here, we determined that the promoter region (-550 to -463bp) contains indispensable cis-elements for DYT1 expression. Although DYT1 transcripts can be detected in both meiocytes and tapetal cells, localization of DYT1-GFP demonstrated that DYT1 is strictly located in tapetal cells during microsporogenesis. Chromatin immunoprecipitation (ChIP) analysis revealed that DYT1 directly binds the promoter region of Defective in Tapetal Development and Function 1 (TDF1), a transcription factor essential for tapetum development. When TDF1 driven by the DYT1 promoter is expressed in a dyt1 mutant, the expression of the transcription factors AMS, MS188/MYB80, TEK and MS1 and the pollen wall-related genes are restored. Although the pollen wall is not formed and the microspores are ruptured, DIOC2 staining showed that fatty acids, the precursors of the pollen wall, were synthesized in the transgenic lines. These results indicate that DYT1 regulates the expression of AMS, MS188/MYB80, TEK and MS1 for pollen wall formation, primarily via TDF1.