Protein Synthesis Controls Cyclin Stability in Metaphase I-Arrested Oocytes of Patella vulgata

Colas, Pierre; Launay, Caroline; Loon, André E. van; Galle, P.

doi:10.1006/excr.1993.1275

Cited by 17 publications

(6 citation statements)

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“…It can be asked how the calcium transient observed during fertilization of the metaphase I-arrested oocytes of Ruditapes and Crassostrea is able to release oocytes from the metaphase I block? It has been suggested that, in Ruditapes and other molluscs, calcium may act via a calcium calmodulin-kinase since calcium calmodulin antagonists were able to prevent the metaphase I release and cyclin degradation upon fertilization (Dubé and Dufresne, 1990;Abdelmajid et al, 1993;Colas et al, 1993;Néant et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

Role of dihydropyridine‐sensitive calcium channels in meiosis and fertilization in the bivalve molluscs Ruditapes philippinarum and Crassostrea gigas

Leclerc

Galle

Moreau

2000

Biology of the Cell

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Prophase-arrested oocytes of Ruditapes philippinarum can not be fertilized or stimulated by a depolarizing agent such as an excess of KCl, in contrast to the situation found in Crassostrea gigas. We have performed a comparative study between the two situations found in these species. In vitro, both of these oocytes can be triggered to reinitiate meiosis following a treatment by serotonin which promotes an intracellular calcium surge. Ruditapes and Crassostrea oocytes further arrest in metaphase I, at which stage they can be either activated by sperm or by excess KCl. These treatments trigger an intracellular calcium increase. This suggests that functional voltage-operated Ca2+ channels are expressed in Ruditapes during the course of maturation between prophase and metaphase I. Results obtained using pharmacological tools and direct binding of specific dihydropyridines, strongly suggest that these channels are dihydropyridine-sensitive calcium channels. In Ruditapes they become functional after 5-HT stimulation, their number increasing before GVBD. In Crassostrea the dihydropyridine-sensitive Ca2+ channels are already present at prophase stage and their density is constant from prophase to metaphase I. Moreover, we have shown for Ruditapes and Crassostrea that: 1) the addition of 10 microM of S(-)BayK8644, an agonist of dihydropyridine-sensitive calcium channels to metaphase-arrested oocytes releases them from metaphase block; and 2) incubating these oocytes with nicardipine, a potent blocker of dihydropyridine-sensitive Ca2+ channels, inhibits both their activation by excess KCl or fertilization. Taken together these data suggest that the absence of dihydropyridine-sensitive Ca2+ channels in the membrane of prophase-arrested oocytes of Ruditapes may account for their inability to be fertilized at this stage, while the presence of dihydropyridine-sensitive Ca2+ channels in prophase-arrested oocytes of Crassostrea may explain their fertilizability at this stage.

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Section: Discussionmentioning

confidence: 99%

Role of dihydropyridine‐sensitive calcium channels in meiosis and fertilization in the bivalve molluscs Ruditapes philippinarum and Crassostrea gigas

Leclerc

Galle

Moreau

2000

Biology of the Cell

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“…This technique was used to look at the control of release from metaphase I by following the chromosomal material with the dye during the addition of protein synthesis inhibitors. Looking at the control of metaphase arrest using Hoechst dyes has also been carried out on Patella vulgata oocytes (Colas et al, 1993). The properties of these dyes has given them a wide range of uses, and they are likely to be of continued value in the investigation of oocyte cytology, especially when maturational stages are difficult to visualise with normal microscopic techniques.…”

Section: Discussionmentioning

confidence: 99%

Evidence for a coelomic maturation factor controlling oocyte maturation in the polychaeteArenicola marina(L.)

Watson¹,

Bentley²

1997

Invertebrate Reproduction & Development

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Invertebrate Reproduction and Development, 3 1 : 1-3 (1 997) 297-305 Balaban, PhiladelphialRehovot 0 168-8 170/97/$05 . OO Q 1997 Balaban SummaryPrevious studies on Arenicola marina suggested that oocyte maturation was induced by a single maturation hormone fiom the prostomiurn. This maturation hormone was thought to act directly on the oocyte (Meijer and Durchon, 1977). A recently described species, Arenicola defodiens (Cadman and Nelson-Smith, 1993), morphologically very similar to A. marina, has been found at the sampling sites described by Meijer and Durchon (1977). Results presented here fiom studies on British populations of Arenicola marina show that in this species, oocyte maturation is controlled by two hormonal steps. The first step involves the prostomial maturation hormone. The second step depends on a maturation inducing substance in the coelornic fluid. We will refer to this as the coelomic maturation factor (CMF). A reliable in vitro assay for oocyte maturation in the lugworm Arenicola marina has been adopted. It utilizes fluorescence staining of the chromosome material with DNA labelling dyes (Hoechst 33342 and 33258). Maturation of oocytes in A. marina involves germinal vesicle breakdown (GVBD). This is accompanied by the movement of chromosomes fiom late prophase to metaphase of meiosis I and chromosome condensation. The chromosomes are stained brightly by the dyes and their relative positions can be easily identified so that mature and immature eggs can be distinguished by the differences in chromosome position and form. The development of the in vitro fluorescence assay has enabled us to demonstrate that there are two endocrine steps involved in the induction of oocyte maturation. We have begun the characterization of CMF, and data show this to be a thermolabile molecule with a molecular mass greater than 10 kd.

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“…This is the case for some molluscs as Patella, Mytilus and Ruditapes, in which metaphase I arrest also depends on a continuous protein synthesis [4] for maintaining a high level of MPF activity [1,34]. It may be envisaged that in different species different strategies were adopted to stabilize a metaphase spindle; a strategy may involve the continuous synthesis of cyclins as in mouse [16,24,40], another could depend on the synthesis of putative intermediaries required to stabilize cyclins as in molluscs [2].…”

Section: Discussionmentioning

confidence: 99%

Microinjection of Cdc25 protein phosphatase into Xenopus prophase oocyte activates MPF and arrests meiosis at metaphase I

Rime

Huchon

Smedt³

et al. 1994

Biology of the Cell

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Microinjection of bacterially expressed human cdc25A protein into Xenopus prophase oocytes provokes the activation of p34cdc2 kinase and the tyrosine dephosphorylation of p34cdc2 in the presence or absence of protein synthesis. The level of p34cdc2 kinase activity then drops in parallel with the degradation of cyclin B2 and finally increases again to stabilize at a high level. Cdc25 microinjection induces the assembly of a metaphase I spindle which is abnormally located in the deep cytoplasm. Moreover, oocytes arrest at the metaphase I stage and do not reach metaphase II even 10 h after cdc25 microinjection. The extended metaphase I period observed in cdc25-injected oocytes results from an equilibrium between degradation of cyclins and synthesis of new cyclins. This is in contrast with progesterone-stimulated oocytes where cyclin degradation is turned off when oocytes enter metaphase II. During metaphase I, the reactivation of MPF activity can be disrupted in two different ways: 1) cycloheximide, an inhibitor of protein synthesis, by preventing the synthesis of new cyclins, provokes the disappearance of MPF kinase activity and the reformation of a nucleus; 2) when the cAMP level is increased during the metaphase I period in cdc25-injected oocytes, MPF kinase activity drops following a rephosphorylation of tyrosine 15 of p34cdc2, while the cyclin turn-over remains unaffected. Moreover, increasing the cAMP level in prophase oocytes totally prevents the action of cdc25. Our results indicate that in Xenopus oocytes, the PKA pathway negatively regulates the activation of MPF and the activity of p34cdc2/cyclin B complex through tyrosine phosphorylation of p34cdc2 during metaphase I.

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Protein Synthesis Controls Cyclin Stability in Metaphase I-Arrested Oocytes of Patella vulgata

Cited by 17 publications

References 0 publications

Role of dihydropyridine‐sensitive calcium channels in meiosis and fertilization in the bivalve molluscs Ruditapes philippinarum and Crassostrea gigas

Role of dihydropyridine‐sensitive calcium channels in meiosis and fertilization in the bivalve molluscs Ruditapes philippinarum and Crassostrea gigas

Evidence for a coelomic maturation factor controlling oocyte maturation in the polychaeteArenicola marina(L.)

Microinjection of Cdc25 protein phosphatase into Xenopus prophase oocyte activates MPF and arrests meiosis at metaphase I

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