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c-mos proto-oncogene product is partly degraded after release from meiotic arrest and persists during interphase in
M Weber1, J Z Kubiak, R B Arlinghaus
1Laboratoire de Physiologie du Développement, Université Paris VII, France.
Abstract:
Recently, it has been shown that the product of the c-mos proto-oncogene is a component of cytostatic factor, an activity present in unfertilized eggs from vertebrates that arrests the cell cycle in metaphase of the second meiotic division (metaphase II) possibly by stabilizing maturation-promoting factor (MPF). We have studied the behavior of the c-mos product in metaphase II mouse oocytes and soon after activation. The amount of c-mos in the oocyte was still very high after second polar body extrusion, when cyclin B has been degraded and MPF activity had decreased dramatically. Degradation of c-mos takes place later, during the G1 phase of the first cell cycle and a residual amount of c-mos is detectable during the first zygotic interphase. Our data show that the degradation of c-mos is not involved in the release from the metaphase arrest.
Insights
The c-mos proto-oncogene product remains high in mouse oocytes after metaphase II arrest release, even as cell cycle factors degrade. Its later degradation indicates c-mos is not involved in exiting metaphase II arrest.
Area of Science:
- Cell Biology
- Molecular Biology
- Developmental Biology
Background:
- Cytostatic factor (CSF) arrests the cell cycle at metaphase II in vertebrate oocytes.
- CSF activity may involve stabilizing maturation-promoting factor (MPF).
- The c-mos proto-oncogene product is a known component of CSF.
Purpose of the Study:
- To investigate the behavior and degradation timing of the c-mos product in mouse oocytes.
- To determine if c-mos degradation is linked to the release from metaphase II arrest.
Main Methods:
- Analysis of c-mos protein levels in metaphase II oocytes and post-activation.
- Monitoring cyclin B degradation and MPF activity.
- Tracking c-mos presence during the first cell cycle.
Main Results:
- High levels of c-mos persist in oocytes after the second polar body extrusion and MPF degradation.
- Cyclin B is degraded, and MPF activity decreases significantly before c-mos degradation.
- c-mos degradation occurs later, during the G1 phase of the first cell cycle, with residual amounts in the zygote.
Conclusions:
- The degradation of c-mos is not the trigger for the release from metaphase II arrest.
- c-mos functions independently of MPF degradation in exiting meiotic arrest.
- The timing of c-mos degradation suggests a role beyond maintaining metaphase II arrest.