Key Message

The mutation of FAX1 (Fatty Acid Export 1) disrupts ROS homeostasis and suppresses transcription activity of DYT1-TDF1-AMS-MS188 genetic network, leading to atypical tapetum PCD and defective pollen formation in Arabidopsis.

Abstract

Fatty acids (FAs) have multiple important biological functions and exert diverse cellular effects through modulating Reactive Oxygen Species (ROS) homeostasis. Arabidopsis FAX1 (Fatty Acid Export 1) mediates the export of de novo synthesized FA from chloroplast and loss of function of FAX1 impairs male fertility. However, mechanisms underlying the association of FAX1-mediated FA export with male sterility remain enigmatic. In this study, by using an integrated approach that included morphological, cytological, histological, and molecular analyses, we revealed that loss of function of FAX1 breaks cellular FA/lipid homeostasis, which disrupts ROS homeostasis and suppresses transcriptional activation of the DYT1-TDF1-AMS-MS188 genetic network of anther development, impairing tapetum development and pollen wall formation, and resulting in male sterility. This study provides new insights into the regulatory network for male reproduction in plants, highlighting an important role of FA export-mediated ROS homeostasis in the process.

中文翻译：

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拟南芥 FAX1 介导的脂肪酸输出是花药发育和花粉壁形成的转录调控所必需的。

关键信息

FAX1 ( Fatty Acid Export 1 )的突变破坏了 ROS 稳态并抑制了DYT1-TDF1-AMS-MS188遗传网络的转录活性，导致拟南芥中的非典型绒毡层 PCD 和花粉形成缺陷。

抽象的

脂肪酸 (FAs) 具有多种重要的生物学功能，并通过调节活性氧 (ROS) 稳态发挥多种细胞作用。拟南芥 FAX1 (Fatty Acid Export 1) 介导叶绿体从头合成的 FA 的输出，FAX1的功能丧失会损害雄性生育能力。然而， FAX1介导的 FA 输出与雄性不育之间的关联机制仍然是个谜。在这项研究中，通过使用包括形态学、细胞学、组织学和分子分析在内的综合方法，我们揭示了FAX1的功能丧失破坏细胞 FA/脂质稳态，破坏 ROS 稳态并抑制花药发育的 DYT1-TDF1-AMS-MS188 遗传网络的转录激活，损害绒毡层发育和花粉壁形成，并导致雄性不育。这项研究为植物雄性繁殖的调控网络提供了新的见解，强调了 FA 输出介导的 ROS 稳态在该过程中的重要作用。