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Updated: Aug 18, 2026
Detection of DNA Double-Stranded Breaks in Mouse Oocytes
Published on: June 23, 2023
p90Rsk is not involved in cytostatic factor arrest in mouse oocytes
Julien Dumont1, Muriel Umbhauer, Pascale Rassinier
1Equipe Divisions Méiotiques chez la souris, UMR7622, Centre National de la Recherche Scientifique/Université Pierre et Marie Curie, Paris, France.
Abstract:
Vertebrate oocytes arrest in metaphase of the second meiotic division (MII), where they maintain a high cdc2/cyclin B activity and a stable, bipolar spindle because of cytostatic factor (CSF) activity. The Mos-MAPK pathway is essential for establishing CSF. Indeed, oocytes from the mos-/- strain do not arrest in MII and activate without fertilization, as do Xenopus laevis oocytes injected with morpholino oligonucleotides directed against Mos. In Xenopus oocytes, p90Rsk (ribosomal S6 kinase), a MAPK substrate, is the main mediator of CSF activity. We show here that this is not the case in mouse oocytes. The injection of constitutively active mutant forms of Rsk1 and Rsk2 does not induce a cell cycle arrest in two-cell mouse embryos. Moreover, these two mutant forms do not restore MII arrest after their injection into mos-/- oocytes. Eventually, oocytes from the triple Rsk (1, 2, 3) knockout present a normal CSF arrest. We demonstrate that p90Rsk is not involved in the MII arrest of mouse oocytes.
Insights
Mouse oocytes arrest in metaphase II (MII) due to cytostatic factor (CSF). Researchers found that p90 ribosomal S6 kinase (Rsk) is not the key mediator of this crucial cell cycle arrest in mice, unlike in Xenopus.
Area of Science:
- Developmental Biology
- Cell Cycle Regulation
- Meiosis
Background:
- Vertebrate oocytes arrest at metaphase II (MII) via cytostatic factor (CSF) activity, maintaining high cdc2/cyclin B and a stable spindle.
- The Mos-MAPK pathway is critical for establishing CSF, with p90 ribosomal S6 kinase (Rsk) identified as a key mediator in Xenopus oocytes.
Purpose of the Study:
- To investigate the role of p90 Rsk in mediating cytostatic factor (CSF) activity and MII arrest in mouse oocytes.
- To determine if p90 Rsk is essential for maintaining the MII cell cycle arrest in mouse oocytes.
Main Methods:
- Injection of constitutively active mutant forms of Rsk1 and Rsk2 into two-cell mouse embryos.
- Injection of constitutively active mutant Rsk forms into mos-/- mouse oocytes.
- Analysis of oocytes from a triple Rsk (1, 2, 3) knockout mouse strain.
Main Results:
- Constitutively active Rsk1 and Rsk2 mutants did not induce cell cycle arrest in mouse embryos.
- These Rsk mutants failed to restore MII arrest in mos-/- oocytes.
- Oocytes from the triple Rsk knockout exhibited normal CSF-mediated MII arrest.
Conclusions:
- Contrary to findings in Xenopus, p90 Rsk is not the primary mediator of CSF activity in mouse oocytes.
- p90 Rsk is not involved in the establishment or maintenance of the MII cell cycle arrest in mouse oocytes.
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