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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.
Cell Reports
|December 25, 2025
Summary
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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