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Updated: May 26, 2026
A Modified Technique for Inducing Polycystic Ovary Syndrome in Mice
Published on: July 5, 2024
Effects of ubiquitin C-terminal hydrolase L1 deficiency on mouse ova
Sayaka Koyanagi1, Hiroko Hamasaki, Satoshi Sekiguchi
1Department of Biomedical Science, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Yayoi 1-1-1, Bunkyo-ku, Tokyo 113-8657, Japan.
Abstract:
Maternal proteins are rapidly degraded by the ubiquitin-proteasome system during oocyte maturation in mice. Ubiquitin C-terminal hydrolase L1 (UCHL1) is highly and specifically expressed in mouse ova and is involved in the polyspermy block. However, the role of UCHL1 in the underlying mechanism of polyspermy block is poorly understood. To address this issue, we performed a comprehensive proteomic analysis to identify maternal proteins that were relevant to the role of UCHL1 in mouse ova using UCHL1-deficient gad. Furthermore, we assessed morphological features in gad mouse ova using transmission electron microscopy. NACHT, LRR, and PYD domain-containing (NALP) family proteins and endoplasmic reticulum (ER) chaperones were identified by proteomic analysis. We also found that the 'maternal antigen that embryos require' (NLRP5 (MATER)) protein level increased significantly in gad mouse ova compared with that in wild-type mice. In an ultrastructural study, gad mouse ova contained less ER in the cortex than in wild-type mice. These results provide new insights into the role of UCHL1 in the mechanism of polyspermy block in mouse ova.
Insights
Ubiquitin C-terminal hydrolase L1 (UCHL1) deficiency in mice affects oocyte maturation and the polyspermy block. Proteomic analysis revealed altered maternal protein levels and endoplasmic reticulum structures in UCHL1-deficient ova.
Area of Science:
- Reproductive biology
- Cellular and molecular biology
- Developmental biology
Background:
- Maternal proteins are crucial for oocyte maturation and are degraded by the ubiquitin-proteasome system.
- Ubiquitin C-terminal hydrolase L1 (UCHL1) is vital for the polyspermy block in mouse ova, but its precise role is unclear.
- Understanding UCHL1's function is key to elucidating mechanisms preventing multiple sperm fertilizations.
Purpose of the Study:
- To investigate the role of UCHL1 in the polyspermy block by identifying associated maternal proteins in mouse ova.
- To analyze the impact of UCHL1 deficiency on the proteome and ultrastructure of mouse ova.
- To gain new insights into the molecular mechanisms underlying UCHL1's function in preventing polyspermy.
Main Methods:
- Comprehensive proteomic analysis of UCHL1-deficient (gad) mouse ova.
- Transmission electron microscopy (TEM) to assess morphological features of gad mouse ova.
- Comparison of protein expression profiles and ultrastructural characteristics between gad and wild-type mouse ova.
Main Results:
- Proteomic analysis identified NACHT, LRR, and PYD domain-containing (NALP) proteins and endoplasmic reticulum (ER) chaperones in UCHL1-deficient ova.
- A significant increase in the 'maternal antigen that embryos require' (NLRP5 (MATER)) protein level was observed in gad mouse ova compared to wild-type.
- Ultrastructural studies revealed reduced cortical ER in gad mouse ova compared to wild-type controls.
Conclusions:
- UCHL1 plays a significant role in regulating maternal protein levels and ER structure in mouse ova.
- The findings suggest UCHL1 influences the polyspermy block through modulation of specific protein families and cellular components.
- This study provides novel insights into the complex mechanisms governing polyspermy prevention in mammalian oocytes.
