From progesterone to active Cdc2 in <i>Xenopus</i> oocytes: a puzzling signalling pathway

Karaı̈skou, Anthi; Dupré, Aude; Haccard, Olivier; Jessus, Catherine

doi:10.1016/s0248-4900(01)01126-1

Cited by 42 publications

(34 citation statements)

References 120 publications

(156 reference statements)

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“…Meiotic maturation resembles a G 2 /M transition. This transition is controlled by the activity of the Cdc2/cyclinB complex (M-phase promoting factor, MPF), a universal regulator of the G 2 /M transition (Ferrell, 1999;Nebreda and Ferby, 2000;Karaiskou et al, 2001;Dekel, 2005). Throughout the cell cycle, the activity of MPF is mainly regulated by phosphorylation of two highly conserved residues, Thr14 and Tyr15 of Cdc2 (Malumbres and Barbacid, 2005).…”

Section: Introductionmentioning

confidence: 99%

Protein kinase a modulates Cdc25B activity during meiotic resumption of mouse oocytes

Zhang

et al. 2008

Developmental Dynamics

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Protein kinase A (PKA) play a critical role in maintaining the meiotic arrest. However, the steps downstream of PKA remain largely unknown. In this study, we investigated the regulation of meiotic resumption by PKA/Cdc25B pathway in mouse oocytes. Injection of mRNA coding for Cdc25b-S321A had a more potent maturation-inducing ability than Cdc25b-WT. When co-injected with PKA inhibitor, Cdc25B-WT had similar activities with Cdc25B-S321A. Meanwhile, the phosphorylation of Cdc25B-S321 was detected in germinal vesicle (GV) oocytes by Western blotting with a phospho-Ser321-specific antibody and the band disappeared when oocytes reenter into the meiotic cell cycle. Furthermore, Cdc25B-WT translocated to the nucleus shortly before GV breakdown (GVBD), whereas phosphorylated Cdc25B-S321 expressed exclusively in the cytoplasm and the signal could not be detected in GVBD oocytes. Taken together, these data indicate that Cdc25B-Serine321 is the potential PKA target and Cdc25B subcellular localization determines its function during the process of maintaining GV arrest in mouse oocytes. Developmental Dynamics 237: 3777-3786, 2008.

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Section: Introductionmentioning

confidence: 99%

Protein kinase a modulates Cdc25B activity during meiotic resumption of mouse oocytes

Zhang

et al. 2008

Developmental Dynamics

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“…To account for MPF activation during meiotic maturation, simple models were proposed whereby progesterone stimulation triggered a series of events leading to the conversion of stockpiled preMPF into active MPF via the inactivation of Myt1 and/or the activation of Cdc25. 5 Since it was well established that inhibition of the cAMP-dependent protein kinase (PKA) and protein synthesis were the two main requirements for MPF activation promoted by progesterone, 5 this hormone was proposed to induce inhibition of adenylyl cyclase, resulting in a drop of cAMP concentration and a subsequent inhibition of PKA. The next key step appeared to be the translation of Mos, a protein kinase that indirectly activates Mitogen-Activated protein Kinase (MAPK), resulting in the activation of the ribosomal S6 kinase, p90 Rsk (see below).…”

Section: Introductionmentioning

confidence: 99%

Oocyte Maturation, Mos and Cyclins—A Matter of Synthesis: Two Functionally Redundant Ways to Induce Meiotic Maturation

Haccard

Jessus²

2006

Cell Cycle

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The development of an immature oocyte into a fertilizable gamete is a process known as meiotic maturation. In vertebrates, it corresponds to the transition from the prophase arrest of the first meiotic division (usually considered as a late G 2 phase) to the metaphase arrest of the second meiotic division. This transition is controlled by modulating the activity of the cyclin B-Cdc2 complex, MPF (M-phase promoting factor), the universal regulator of the G 2 /M transition. Meiotic maturation of frog oocytes is triggered by steroid hormones through a rapid, necessary and sufficient suppression of PKA and requires ongoing protein synthesis. A long-standing question has been to identify key protein(s) required to trigger the activation of MPF in response to the hormonal signal. Here we will discuss data supporting the view that steroids bring about meiotic maturation through functionally redundant pathways involving synthesis of Mos or of cyclin proteins, reinforcing the robustness of the system.

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“…This block is released by progesterone, triggering the activation of the cdc2-Cyclin B complex or MPF (M phase Promoting Factor) in a post-transcriptional manner. The oocyte completes the first meiotic division and then arrests again in metaphase of the second meiotic cell division (Metaphase II), a process known as meiotic maturation (for review, see Karaiskou et al, 2001). Progesterone addition induces a drop in cAMP concentration, leading to the inhibition of the cAMPdependent protein kinase (PKA) activity, and subsequently to the synthesis of new proteins, among them Cyclin B1/B4 and the serine/threonine kinase Mos, product of the c-mos proto-oncogene (Frank-Vaillant et al, 1999;Hochegger et al, 2001;Matten et al, 1994;Sagata et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

“…Progesterone addition induces a drop in cAMP concentration, leading to the inhibition of the cAMPdependent protein kinase (PKA) activity, and subsequently to the synthesis of new proteins, among them Cyclin B1/B4 and the serine/threonine kinase Mos, product of the c-mos proto-oncogene (Frank-Vaillant et al, 1999;Hochegger et al, 2001;Matten et al, 1994;Sagata et al, 1988). Mos accumulates at the time of germinal vesicle breakdown (GVBD), leading indirectly to p42 MAPK activation, which ultimately phosphorylates RSK (Ribosomal S6 Kinase) (Karaiskou et al, 2001). Major objectives in the understanding of the progesterone signaling pathway are, first, to identify which proteins could mediate the early steps of the progesterone pathway and second, to understand the relationship between the p42 MAPK pathway and cdc2 activation.…”

Section: Introductionmentioning

confidence: 99%

Xenopus H-RasV12 promotes entry into meiotic M phase and cdc2 activation independently of Mos and p42MAPK

et al. 2002

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In the Xenopus oocyte, progesterone triggers M phase Promoting Factor (MPF) activation in a protein synthesis dependent manner. Although the synthesis of the p42 MAPK activator Mos appears to be required for MPF activation, p42 MAPK activity has been shown to be dispensable. To clarify this paradox, we attempted to activate the p42 MAPK pathway independently of Mos synthesis by cloning and using Xenopus H-Ras in the oocyte. We demonstrate that the injection of the constitutively active Xe H-RasV12 mutant induces p42 MAPK and MPF activation through two independent pathways. Xe H-RasV12 induces only a partial activation of p42 MAPK when protein synthesis and MPF activation are prevented. A full level of p42 MAPK activation is reached when MPF is activated and Mos is present. In contrast, MPF activation induced by Xe HRasV12 is achieved independently of Mos synthesis and p42 MAPK activation but still depends on protein synthesis. Therefore, the amphibian oocyte represents a new model system to analyse an original H-Ras pathway ending to MPF activation and distinct from the p42 MAPK pathway. The identification of the proteins synthesized in response to Xe H-RasV12 and required for MPF activation, represents an important clue in understanding the mechanism of progesterone action.

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From progesterone to active Cdc2 in Xenopus oocytes: a puzzling signalling pathway

Cited by 42 publications

References 120 publications

Protein kinase a modulates Cdc25B activity during meiotic resumption of mouse oocytes

Protein kinase a modulates Cdc25B activity during meiotic resumption of mouse oocytes

Oocyte Maturation, Mos and Cyclins—A Matter of Synthesis: Two Functionally Redundant Ways to Induce Meiotic Maturation

Xenopus H-RasV12 promotes entry into meiotic M phase and cdc2 activation independently of Mos and p42MAPK

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