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AP1G 在受助细胞控制的花粉管接收过程中介导液泡酸化。

AP1G mediates vacuolar acidification during synergid-controlled pollen tube reception.

机构信息

State Key Laboratory of Crop Biology, College of Life Sciences, Shandong Agricultural University, Tai'an, 271018, China.

State Key Laboratory of Crop Biology, College of Life Sciences, Shandong Agricultural University, Tai'an, 271018, China

出版信息

Proc Natl Acad Sci U S A. 2017 Jun 13;114(24):E4877-E4883. doi: 10.1073/pnas.1617967114. Epub 2017 May 30.

Abstract

Double fertilization in angiosperms requires the delivery of immotile sperm through pollen tubes, which enter embryo sacs to initiate synergid degeneration and to discharge. This fascinating process, called pollen tube reception, involves extensive communications between pollen tubes and synergids, within which few intracellular regulators involved have been revealed. Here, we report that vacuolar acidification in synergids mediated by AP1G and V-ATPases might be critical for pollen tube reception. Functional loss of or , encoding the γ subunit of adaptor protein 1 or the shared component of two endomembrane V-ATPases, respectively, impaired synergid-controlled pollen tube reception and caused partial female sterility. AP1G works in parallel to the plasma membrane-associated receptor FERONIA in synergids, suggesting that synergid-mediated pollen tube reception requires proper sorting of vacuolar cargos by AP1G. Although AP1G did not mediate the targeting of V-ATPases, loss of function or the expression of AP1G-RNAi compromised vacuolar acidification mediated by V-ATPases, implying their genetic interaction. We propose that vacuolar acidification might represent a distinct cell-death mechanism specifically adopted by the plant phylum, which is critical for synergid degeneration during pollen tube reception.

摘要

被子植物的双受精过程需要将不活动的精子通过花粉管输送到胚囊中,以启动助细胞退化和排出。这个引人入胜的过程被称为花粉管接收,涉及花粉管和助细胞之间的广泛交流,其中很少有涉及的细胞内调节剂被揭示。在这里,我们报告说,AP1G 和 V-ATPases 介导的助细胞中的液泡酸化对于花粉管接收可能是至关重要的。 或 ,分别编码衔接蛋白 1 的 γ 亚基或两种内质网膜 V-ATPases 的共享组件的功能丧失,损害了助细胞控制的花粉管接收并导致部分雌性不育。AP1G 在助细胞中与质膜相关的受体 FERONIA 平行工作,表明助细胞介导的花粉管接收需要 AP1G 对液泡货物进行适当的分拣。尽管 AP1G 不介导 V-ATPases 的靶向,但 功能丧失或 AP1G-RNAi 的表达削弱了 V-ATPases 介导的液泡酸化,暗示它们的遗传相互作用。我们提出,液泡酸化可能代表植物门特有的一种独特的细胞死亡机制,对于花粉管接收过程中助细胞的退化至关重要。

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