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Preparation of Meiotic Chromosome Spreads from Mouse Oocytes for Assessment of Synapsis and Recombination
Published on: July 18, 2025
Synaptonemal complex protein SYCP3 impairs mitotic recombination by interfering with BRCA2
Noriko Hosoya1, Miyuki Okajima, Aiko Kinomura
1Laboratory of Molecular Radiology, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, University of Tokyo, Tokyo 113-0033, Japan. nhosoya-tky@umin.ac.jp
EMBO Reports
|November 26, 2011
Summary
Synaptonemal complex protein 3 (SYCP3) is found in tumors and disrupts chromosomal integrity in dividing cells. This impairs DNA repair, potentially making tumors sensitive to PARP inhibitors.
Area of Science:
- Cancer Biology
- Molecular Oncology
- Genetics
Background:
- The meiosis-specific protein SYCP3 has a known role in chromosome pairing during meiosis.
- Its function in mitotic cells, particularly in cancer, remains largely uncharacterized.
Purpose of the Study:
- To investigate the role of SYCP3 in mitotic cells within primary tumors.
- To determine the impact of SYCP3 expression on chromosomal integrity and DNA repair pathways.
Main Methods:
- Analysis of SYCP3 expression in various primary tumors.
- Functional assays to assess the effect of SYCP3 on homologous recombination (HR) mediated by RAD51.
- Investigation of SYCP3 interaction with BRCA2.
- Assessment of cellular response to DNA-damaging agents, including PARP inhibitors.
Main Results:
- SYCP3 is expressed in a variety of primary tumors.
- SYCP3 expression in mitotic cells impairs chromosomal integrity.
- SYCP3 inhibits the RAD51-mediated homologous recombination pathway.
- SYCP3 forms a complex with BRCA2, hindering its HR function.
- SYCP3 expression leads to hypersensitivity to DNA-damaging agents and chromosomal instability.
Conclusions:
- SYCP3 plays a novel role in promoting chromosomal instability in cancer cells.
- Inhibition of HR by SYCP3 provides a new mechanism for cancer development.
- Tumors expressing SYCP3 may represent a distinct subset sensitive to PARP inhibitors.
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