Signaling pathways in ascidian oocyte maturation: The role of cyclic AMP and follicle cells in germinal vesicle breakdown
Article first published online: 27 FEB 2008
© 2008 The Author
Development, Growth & Differentiation
Volume 50, Issue 3, pages 181–188, April 2008
How to Cite
Lambert, C. C. (2008), Signaling pathways in ascidian oocyte maturation: The role of cyclic AMP and follicle cells in germinal vesicle breakdown. Development, Growth & Differentiation, 50: 181–188. doi: 10.1111/j.1440-169X.2008.00983.x
- Issue published online: 3 MAR 2008
- Article first published online: 27 FEB 2008
- Received 18 October 2007; revised 19 November 2007; accepted 27 November 2007.
- cyclic AMP;
- follicle cell;
- germinal vesicle;
Many ascidian oocytes undergo ‘spontaneous’ germinal vesicle breakdown (GVBD) when transferred from the ovary to normal pH 8.2 sea water (SW); however, low pH inhibits GVBD, which can then be stimulated while remaining in the low pH SW. Oocytes of Boltenia villosa blocked from GVBD by pH 4 SW undergo GVBD in response to permeant cyclic AMP (8-bromo-cyclic AMP), phosphodiesterase inhibitors (isobutylmethylxanthine and theophylline) or the adenylyl cyclase activator forskolin. This suggests that cAMP increases during GVBD. Removal of the follicle cells or addition of a protease inhibitor inhibits GVBD in response to raised pH but not to forskolin, theophylline or 8 bromo-cAMP. Isolated follicle cells in low pH SW release protease activity in response to an increase in pH. These studies imply that the follicle cells release protease activity, which either itself stimulates an increase in oocyte cAMP level or reacts with other molecules to stimulate this process. Studies with the mitogen-activated protein (MAP) kinase inhibitors U0126 and CI 1040 suggest that MAP kinase is not involved in GVBD. The Cdc25 inhibitor NSC 95397 inhibits GVBD at 200 nm in a reversible manner.