Related Experiment Videos
Functional analysis of sperm from c-mos(-/-) mice
Vera S Gross1, Geoffrey M Cooper
1Department of Biology, Boston University, Boston, Massachusetts 02215, USA.
Abstract:
The c-mos protooncogene, which is expressed predominantly in male and female germ cells, is crucial for normal oocyte meiosis and female fertility in mice. Inactivation of c-mos results in abnormal oocyte development and leads to ovarian cysts and tumors in vivo. In contrast to the severe effects of c-mos ablation in females, targeted inactivation of c-mos has not been reported to affect spermatogenesis in male mice. However, previously reported studies of male c-mos(-/-) mice have been limited to histological analyses of testes and in vivo matings, both of which are relatively insensitive indicators of sperm production and function. Therefore, we assayed sperm function of c-mos(-/-) males under in vitro conditions to determine whether the absence of Mos during development affected sperm production or fertilizing ability. We found no significant differences between the number of sperm collected from c-mos(-/-) and wild type mice. Additionally, sperm from c-mos(-/-) and c-mos(+/+) males performed equally well in assays of in vitro fertilization (IVF) and fertilization-associated events including zona pellucida (ZP) penetration, sperm/egg plasma membrane fusion, and sperm chromatin remodeling. Therefore, we suggest that the function of Mos in spermatogenesis is either not related to the ultimate fertilizing potential of the sperm, or else the absence of Mos is masked by a redundant kinase.
Insights
The c-mos protooncogene is essential for female fertility but does not impact male sperm production or fertilizing ability in mice. Studies show male mice lacking c-mos exhibit normal sperm function and in vitro fertilization rates.
Area of Science:
- Reproductive Biology
- Molecular Genetics
- Oncology
Background:
- The c-mos protooncogene is vital for oocyte meiosis and female fertility in mice.
- c-mos inactivation leads to ovarian abnormalities, including cysts and tumors.
- Previous studies indicated c-mos deficiency does not affect male spermatogenesis, but relied on limited analyses.
Purpose of the Study:
- To comprehensively assess sperm function and fertilizing ability in male mice lacking the c-mos protooncogene under in vitro conditions.
- To determine if the absence of Mos impacts sperm production or function despite previous histological findings.
Main Methods:
- Sperm was collected from c-mos knockout (c-mos(-/-)) and wild-type (c-mos(+/+)) male mice.
- Sperm counts were compared between groups.
- In vitro fertilization (IVF) assays were performed, including zona pellucida penetration, sperm-egg fusion, and chromatin remodeling assessments.
Main Results:
- No significant difference in sperm count was observed between c-mos(-/-) and wild-type mice.
- Sperm from c-mos(-/-) males demonstrated equivalent performance in IVF assays compared to wild-type.
- Fertilization-associated events, including zona pellucida penetration and sperm chromatin remodeling, were unaffected by the absence of c-mos.
Conclusions:
- The c-mos protooncogene is not essential for male mouse sperm production or fertilizing potential.
- The function of Mos in spermatogenesis may be unrelated to the final fertilizing capacity of sperm.
- Alternatively, the absence of Mos's role in spermatogenesis could be compensated for by a redundant kinase pathway.