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Title: INSULIN-LIKE GROWTH FACTOR-I INDUCES OOCYTE MATURATIONAL COMPETENCE BUT NOT MEIOTIC RESUMPTION IN WHITE BASS (MORONE CHRYSOPS) FOLLICLES IN VITRO: EVIDENCE FOR THE RAPID EVOLUTION OF INSULIN-LIKE GROWTH FACTOR ACTION

Author
item Weber, Gregory - Greg
item SULLIVAN, CRAIG - NC STATE UNIV

Submitted to: Biology of Reproduction
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/6/2005
Publication Date: 1/12/2005
Citation: Weber, G.M., Sullivan, C.V. 2005. Insulin-like growth factor-i induces oocyte maturational competence but not meiotic resumption in white bass (morone chrysops) follicles in vitro: evidence for the rapid evolution of insulin-like growth factor action. Biology of Reproduction. 72:1177-1186.

Interpretive Summary: Fully grown eggs must undergo a maturational process before they can be fertilized. This process has two stages. We have discovered that a hormone called insulin-like growth factor-I is involved in the regulation of this maturational process. In white bass, insulin-like growth factor-I regulates only the first stage; whereas in a closely related species, the striped bass, insulin-like growth factor-I has been found to induce only the second stage. There are also differences in the way these two species of fish spawn. One produces eggs that float and the other produces eggs that sink. In addition, one releases all of its eggs at once and the other produces eggs in batches. The differences in the actions of insulin-like growth factor-I between the two fish might contribute to these differences in the way the fish spawn. In addition, we may be able to use what we discovered about the actions of insulin-like growth factor-I to develop better methods to control spawning of the white bass.

Technical Abstract: A combination of recombinant human (rh) insulin-like growth factor-I (IGF-I) (25 nM) and the maturation-inducing hormone (MIH), 17,20',21-trihydroxy-4-pregnen-3-one (20'-S; 72.5 nM), induced germinal vesicle breakdown (GVBD) in ovarian follicles of white bass incubated in vitro, whereas a four times greater concentration of each hormone was ineffective alone. These results indicate that IGF-I induces oocyte maturational competence (OMC) but not meiotic resumption in white bass. Culture medium concentrations of 20'-S remained below detection limits for ovarian fragments incubated with rhIGF-I. Actinomycin D blocked GVBD in response to human chorionic gonadotropin (hCG) but not to rhIGF-I plus 20'-S, suggesting that IGF-I requires de novo translation but not transcription to induce OMC. Gap junction uncouplers, 1-octanol and 1-heptanol, and the phosphatidylinositiol 3-kinase (PI 3-K) inhibitors, wortmannin and LY 294002, attenuated hCG-, 20'-S-, and rhIGF-I plus 20'-S-induced GVBD. Although these inhibitors reduced hCG-induced progestin release, PI 3-K inhibitors did not alter MIH synthesis in some incubations and addition of 20'-S to the incubations did not fully overcome the effects of either class of inhibitors, suggesting that decreasing MIH production is not their only inhibitory effect on GtH action. Our data suggest that functional gap junctions and PI 3-K activity are necessary for GtH and IGF-I to induce and maintain OMC in white bass.