This proposal on """"""""Electrical Control of Sperm-Egg Fusion"""""""" involves an investigation of three questions: 1. How does fertilization cause the egg's membrane potential to change? 2. How does the egg's membrane potential regulate sperm-egg fusion? 3. Does the sperm's membrane participate in regulation of sperm-egg fusion? The methodology involves electrophysiological techniques for intracellular microelectrode and patch electrode recording. 1) We will analyze the conductance increase that occurs at fertilization in the frog egg, measuring the whole cell and single-channel currents, and examining the roles of membrane addition and removal and of calcium in regulating the conductance. 2) We will use cross-species fertilization to determine whether the sperm or the egg contributes the potential-sensitive component involved in sperm-egg fusion. We will begin a project to examine the mechanism of voltage-sensitive fusion by developing procedures for isolating the fusogenic region of the sperm and fusing it with eggs. 3) We will measure the membrane potential at various positions on the guinea pig sperm, and then modify the potential while examining the effects on events leading to sperm-egg fusion. The long-term objectives are to contribute to our understanding of the regulation of sperm-egg fusion and to our general knowledge of fertilization.

Agency
National Institute of Health (NIH)
Institute
Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD)
Type
Research Project (R01)
Project #
3R01HD014939-06S1
Application #
3312874
Study Section
Reproductive Biology Study Section (REB)
Project Start
1981-03-01
Project End
1987-11-30
Budget Start
1987-07-01
Budget End
1987-11-30
Support Year
6
Fiscal Year
1987
Total Cost
Indirect Cost
Name
University of Connecticut
Department
Type
School of Medicine & Dentistry
DUNS #
City
Farmington
State
CT
Country
United States
Zip Code
06030
Lee, Kyung-Bon; Zhang, Meijia; Sugiura, Koji et al. (2013) Hormonal coordination of natriuretic peptide type C and natriuretic peptide receptor 3 expression in mouse granulosa cells. Biol Reprod 88:42
Robinson, Jerid W; Zhang, Meijia; Shuhaibar, Leia C et al. (2012) Luteinizing hormone reduces the activity of the NPR2 guanylyl cyclase in mouse ovarian follicles, contributing to the cyclic GMP decrease that promotes resumption of meiosis in oocytes. Dev Biol 366:308-16
Norris, Rachael P; Freudzon, Marina; Nikolaev, Viacheslav O et al. (2010) Epidermal growth factor receptor kinase activity is required for gap junction closure and for part of the decrease in ovarian follicle cGMP in response to LH. Reproduction 140:655-62
Norris, Rachael P; Ratzan, William J; Freudzon, Marina et al. (2009) Cyclic GMP from the surrounding somatic cells regulates cyclic AMP and meiosis in the mouse oocyte. Development 136:1869-78
Jaffe, Laurinda A; Norris, Rachael P; Freudzon, Marina et al. (2009) Microinjection of follicle-enclosed mouse oocytes. Methods Mol Biol 518:157-73
Norris, Rachael P; Freudzon, Marina; Mehlmann, Lisa M et al. (2008) Luteinizing hormone causes MAP kinase-dependent phosphorylation and closure of connexin 43 gap junctions in mouse ovarian follicles: one of two paths to meiotic resumption. Development 135:3229-38
Norris, Rachael P; Freudzon, Leon; Freudzon, Marina et al. (2007) A G(s)-linked receptor maintains meiotic arrest in mouse oocytes, but luteinizing hormone does not cause meiotic resumption by terminating receptor-G(s) signaling. Dev Biol 310:240-9
Mehlmann, Lisa M; Kalinowski, Rebecca R; Ross, Lavinia F et al. (2006) Meiotic resumption in response to luteinizing hormone is independent of a Gi family G protein or calcium in the mouse oocyte. Dev Biol 299:345-55
Mehlmann, Lisa M; Jaffe, Laurinda A (2005) SH2 domain-mediated activation of an SRC family kinase is not required to initiate Ca2+ release at fertilization in mouse eggs. Reproduction 129:557-64
Mehlmann, Lisa M (2005) Oocyte-specific expression of Gpr3 is required for the maintenance of meiotic arrest in mouse oocytes. Dev Biol 288:397-404

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