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CELL DEATH1 safeguards microspore fate determination by repressing vacuole-executed programmed cell death
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.
Insights
Scientists discovered CELL DEATH1 (CED1), a protein that prevents premature cell death in developing plant pollen. CED1 regulates vacuole function, ensuring proper pollen development and quality control.
Area of Science:
- Plant reproductive biology
- Molecular genetics
- Cellular quality control
Background:
- Microspore development involves vacuole formation and programmed cell death (PCD) for quality control.
- The precise mechanisms of vacuole-mediated PCD during pollen development are not fully understood.
Purpose of the Study:
- To identify factors regulating vacuole-driven PCD during microspore development.
- To elucidate the role of CELL DEATH1 (CED1) in safeguarding pollen viability.
Main Methods:
- Gene expression analysis of CED1 in pollen mother cells and tetrads.
- Protein localization studies of CED1.
- Analysis of microspore development in ced1 mutants.
- Investigating CED1 interaction with vacuolar H+-ATPase (VHA-c).
Main Results:
- CED1 acts as a suppressor of premature microspore PCD.
- ced1 mutants display defects in vacuole biogenesis, nuclear progression, and PCD.
- CED1 interacts with VHA-c, sustaining V-ATPase activity crucial for pollen development.
- VHA-c overexpression negatively impacts pollen viability.
Conclusions:
- CED1 is essential for preventing premature PCD and ensuring proper vacuole function during pollen development.
- CED1-mediated regulation of VHA-ATPase activity represents a key quality control mechanism in plant reproduction.
- This study uncovers a novel role for CED1 in safeguarding microspore development through vacuole and VHA regulation.
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