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Updated: Jun 14, 2025

Use of Time-Lapse Microscopy and Stage-Specific Nuclear Depletion of Proteins to Study Meiosis in S. cerevisiae
Published on: October 11, 2022
A chromosome-coupled ubiquitin-proteasome pathway is required for meiotic surveillance
Ruirui Zhang1, Bohan Liu1, Yuqi Tian1
1Center for Cell Structure and Function, College of Life Sciences, Shandong Provincial Key Laboratory of Animal Resistance Biology, Collaborative Innovation Center of Cell Biology in Universities of Shandong, Shandong Normal University, Jinan, 250358, China.
Abstract:
Defects in meiotic prophase can cause meiotic chromosome missegregation and aneuploid gamete formation. Meiotic checkpoints are activated in germ cells with meiotic defects, and cells with unfixed errors are eliminated by apoptosis. How such a surveillance process is regulated remains elusive. Here, we report that a chromosome-coupled ubiquitin-proteasome pathway (UPP) regulates meiotic checkpoint activation and promotes germ cell apoptosis in C. elegans meiosis-defective mutants. We identified an F-box protein, FBXL-2, that functions as a core component within the pathway. This chromosome-coupled UPP regulates meiotic DSB repair kinetics and chromosome dynamic behaviors in synapsis defective mutants. Disrupted UPP impairs the axial recruitment of the HORMA domain protein HIM-3, which is required for efficient germ cell apoptosis in synapsis defective mutants. Our data suggest that an efficient chromosome-coupled UPP functions as a part of the meiotic surveillance system by enhancing the integrity of the meiotic chromosome axis.
Insights
A ubiquitin-proteasome pathway (UPP) involving FBXL-2 regulates meiotic surveillance in C. elegans. This pathway ensures germ cell apoptosis by maintaining meiotic chromosome axis integrity, preventing aneuploidy.
Area of Science:
- Cell Biology
- Genetics
- Developmental Biology
Background:
- Meiotic prophase defects can lead to chromosome missegregation and aneuploidy.
- Meiotic checkpoints activate in response to defects, eliminating abnormal cells via apoptosis.
- The regulation of this meiotic surveillance process remains poorly understood.
Purpose of the Study:
- To investigate the regulatory mechanisms of meiotic surveillance in C. elegans.
- To identify components involved in germ cell apoptosis following meiotic defects.
Main Methods:
- Utilized C. elegans meiosis-defective mutants.
- Investigated a chromosome-coupled ubiquitin-proteasome pathway (UPP).
- Identified the F-box protein FBXL-2 as a key component of the UPP.
Main Results:
- The chromosome-coupled UPP regulates meiotic checkpoint activation and germ cell apoptosis.
- FBXL-2 is crucial for the UPP's function in meiosis.
- UPP disruption impairs double-strand break repair kinetics and chromosome synapsis, affecting HIM-3 recruitment and germ cell apoptosis.
Conclusions:
- An efficient chromosome-coupled UPP is integral to the meiotic surveillance system.
- This pathway enhances meiotic chromosome axis integrity, promoting germ cell elimination.
- FBXL-2 and the UPP are critical for preventing aneuploid gamete formation.
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