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CELL DEATH1 salvaguarda la determinación del destino del microsporo reprimiendo la muerte celular programada
Yiming Wang1, Yixuan Feng1, Tengwei Yu1
1State Key Laboratory of Forage Breeding-by-Design and Utilization, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China; College of Life Science, University of Chinese Academy of Sciences, Beijing 100049, China; China National Botanical Garden, Beijing 100093, China.
Abstract:
During flowering plant reproduction, microspores develop a prominent vacuole before entering pollen mitosis I (PMI), a critical checkpoint where defective microspores are selectively eliminated via programmed cell death (PCD). However, the mechanism governing the vacuole-driven PCD remains enigmatic. Here, we identify CELL DEATH1 (CED1), a fasciclin I (FAS1)-domain-containing protein, as a suppressor of premature microspore PCD. CED1 is predominantly expressed in pollen mother cells (PMCs) and tetrads, with the encoded protein localizing to the plasma membrane and endomembranes. ced1 microspores exhibit defective vacuole biogenesis, vesicle deacidification, nuclear arrest, and cell clearance with hallmarks of PCD. CED1 physically interacts with the subunit c of vacuolar H+-ATPase (VHA-c), where it sustains V-ATPase activity, and the overexpression of VHA-c decreases pollen viability. Our work reveals that CED1 safeguards pollen development and may suppress vacuole-driven PCD in association with VHA regulation, elucidating a quality control mechanism in pollen development.
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