AP1G mediates vacuolar acidification during synergid-controlled pollen tube reception.
basic_science · Level V
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- Record sourced from PubMed, PMID 28559348.
- Also identified by DOI 10.1073/pnas.1617967114 and PMC identifier 5474829.
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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 <i>AP1G</i> or <i>VHA-A</i>, 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, <i>AP1G</i> 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.
Medical subject headings
- Adaptor Proteins, Signal Transducing
- Arabidopsis Proteins
- Pollen Tube
- Vacuolar Proton-Translocating ATPases