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Adult Apaf-1-deficient mice exhibit male infertility
N Honarpour1, C Du, J A Richardson
1Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, Texas 75235, USA.
Developmental Biology
|February 5, 2000
Summary
Apoptotic protease-activating factor-1 (Apaf-1) is crucial for development, but not essential for neural development. Apaf-1 knockout mice reveal its critical role in male spermatogenesis, suggesting alternative apoptosis pathways.
Area of Science:
- Cell Biology
- Developmental Biology
- Genetics
Background:
- Cytochrome c release from mitochondria and binding to Apaf-1 initiates apoptosis.
- Apaf-1, dATP, and cytochrome c form a complex activating caspases for programmed cell death.
Purpose of the Study:
- To investigate the role of Apaf-1 in mouse development and apoptosis.
- To characterize the phenotype of Apaf-1 knockout mice.
Main Methods:
- Gene disruption of Apaf-1 in mice.
- Phenotypic analysis of Apaf-1 knockout embryos and adults.
Main Results:
- Most Apaf-1 mutants die perinatally with neural defects (exencephaly, cranioschesis) due to excess neural progenitors.
- 5% of mutants survive to adulthood with normal brain development but male sterility due to spermatogonia degeneration.
- Cytochrome c-mediated apoptosis is not essential for neural development but is critical for spermatogenesis.
Conclusions:
- Apaf-1 is essential for normal spermatogenesis but not absolutely required for neural development.
- Alternative apoptotic pathways function in parallel to Apaf-1, influencing programmed cell death outcomes.