Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 393, Issue 1-2, Pages 109-119Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2014.06.008
Keywords
Zebrafish; Insulin; Oocyte; cAMP/PKA; MAPK (ERK1/2); Okadaic acid
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Funding
- Department of Biotechnology, Govt. of India [BT/29/NE/TBP/2010]
- University Grants Commission, New Delhi, India [39-681/2010 (SR)]
- INSPIRE Program
- Department of Science and Technology, Govt. of India
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High intra-cellular cyclic nucleotide (cAMP) ensures prophase-I arrest and prevent steroid-induced meiotic G2-M1 transition in full-grown oocytes; however, relatively less information is available for CAMP regulation of growth factor-stimulated signalling events in the oocyte model. Here using zebrafish oocytes, we show that priming with dibutyryl cAMP (dbcAMP) or cAMP modulators, e.g. adenylate cyclase activator, forskolin or phosphodiesterase inhibitors (IBMX/cilostamide) block insulin action on germinal vesicle breakdown (GVBD) and histone H1 kinase activation. Though high cAMP priming attenuates insulin-induced MAPK3/1 (ERK1/2) phosphorylation (activation), following 2 h of insulin stimulation it fails to block MAPK activation and GVBD. Further, insulin stimulation promotes down regulation of phospho-PKAc (inactivation) and PICA inhibition by H89/PKI-(6-22)-amide overcomes negative regulation by CAMP and induces GVBD and MAPK activation. Moreover, MEK1/2 inhibitor U0126 has no influence on H89-induced GVBD; however, it delays GVBD response in insulin-stimulated oocytes. MAPK activation by okadaic acid (OA) promotes GVBD; however, high dbcAMP abrogates OA action suggesting cross-talk between cAMP/PKA and MAPK-mediated signalling pathways may contribute significantly in maturing zebrafish oocyte. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
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