AP1G mediates vacuolar acidification during synergid-controlled pollen tube reception

AP1G mediates vacuolar acidification during synergid-controlled pollen tube reception
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DOI:
10.1073/pnas.1617967114
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发表时间:
2017-05
期刊:
Proceedings of the National Academy of Sciences
影响因子:
--
通讯作者:
Jia-Gang Wang;Chong Feng;Hai-Hong Liu;Qiang-Nan Feng;Sha Li;Yan Zhang
Jia-Gang Wang;Chong Feng;Hai-Hong Liu;Qiang-Nan Feng;Sha Li;Yan Zhang
中科院分区:
其他
文献类型:
--
作者:
Jia-Gang Wang;Chong Feng;Hai-Hong Liu;Qiang-Nan Feng;Sha Li;Yan Zhang

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被子植物的双受精是在配子体细胞死亡之前:两个助细胞退化,为受精创造一个微环境,而花粉管破裂,排出精细胞。这一过程被称为花粉管接受,其中一些助细胞表面蛋白已被鉴定,但涉及的细胞内活动尚不清楚。我们在这里报告的V-ATP酶和衔接蛋白1介导的液泡酸化,可能是一个重要的机制,助细胞退化在花粉管接收。这项研究为植物门特别采用的细胞死亡机制提供了见解。被子植物的双受精需要不动的精子通过花粉管进入胚囊,启动助细胞的退化并排出。这个迷人的过程,被称为花粉管接收,涉及花粉管和助细胞之间的广泛通信,其中涉及的细胞内调节因子很少被发现。在这里,我们报告,液泡酸化的助细胞介导的AP 1G和V-ATP酶可能是至关重要的花粉管接收。AP 1G或VHA-A分别编码衔接蛋白1的γ亚基或两种内膜V-ATP酶的共有组分,其功能的丧失损害了协同控制的花粉管接受,并导致部分雌性不育。AP 1G在助细胞中与质膜相关受体FERONIA平行发挥作用,表明助细胞介导的花粉管接收需要AP 1G对液泡中的货物进行适当的分选。虽然AP 1G不介导V-ATP酶的靶向,但AP 1G功能的丧失或AP 1G-RNAi的表达损害了V-ATP酶介导的液泡酸化,这意味着它们的遗传相互作用。我们认为,液泡酸化可能代表了一种独特的细胞死亡机制,特别是通过植物门,这是至关重要的助细胞退化过程中花粉管接收。
Significance Double fertilization of angiosperms is preceded by the death of gametophytic cells: Two synergid cells degenerate to create a microenvironment for fertilization, whereas the pollen tube bursts to discharge sperm cells. This process is called pollen tube reception, in which a few synergid surface proteins have been identified, but intracellular activities involved are obscure. We report here that vacuolar acidification, mediated by V-ATPases and adaptor protein 1, might be an important mechanism for synergid degeneration during pollen tube reception. The study provides insights into a cell-death mechanism specifically adopted by the plant phylum. 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 AP1G or VHA-A, 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, AP1G 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.