Disginguished University Professor Emeritus;
Adjunct Professor of Physiology and Pharmacology
PH.D. Yale University
B.Sc. Hiram College
Office: Victoria Research Labs A5-144
Phone: (519) 685-8500 Ext. 55427
Fax: (519) 661-3827 or (519) 850-2562
E-mail: gerald.kidder@schulich.uwo.ca
See Publications by Gerald Kidder on PubMed
Research in the Kidder lab is aimed at understanding the roles of intercellular communication in mammalian gametogenesis. We are interested in the direct exchange of molecules via gap junction channels as well as signaling via secreted paracrine factors, and the interaction between these two modes of intercellular communication. We use a range of approaches in cellular and molecular biology and genetics to study gametogenesis in mice. We also model human connexin mutations in mice to study their effects on reproductive and other organs.
Publications:
Wang, H.-X., Gillio-Meina, C., Chen, S., Gong, X.-Q, Li, T.Y., Bai, D., and Kidder, G.M. (2013) The canonical WNT2 pathway and FSH interact to regulate gap junction assembly in mouse granulosa cells. Biol. Reprod. 89: 39, 1-7.
Li, D., Sekhon, P., Barr, K.J., Márquez-Rosado, L., Lampe, P.D., and Kidder, G.M. (2013) Connexins and steroidogenesis in mouse Leydig cells. Can. J. Physiol. Pharmacol. 91: 157-164.
Dyce, P.W., Norris, R.P., Lampe, P.D., and Kidder, G.M. (2012) Phosphorylation of serine residues in the C-terminal cytoplasmic tail of connexin43 regulates proliferation of ovarian granulosa cells. J. Membr. Biol. 245: 291-301.
Gregory, M., Kahiri, C.N., Barr, K.J., Smith, C.E., Hermo, L., Cyr, D.G., and Kidder, G.M.(2011). Male reproductive system defects and subfertility in a mutant mouse model of oculodentodigital dysplasia. Int. J. Androl. 34: e630–e641.
Wang, H.-X., Li, T.Y., and Kidder, G.M. (2010). WNT2 regulates DNA synthesis in mouse granulosa cells through β-catenin. Biol. Reprod. 82: 865-875.
Wang, H.-X., Tong, D., El-Gehani, F., Tekpetey, F.R., and Kidder, G.M. (2009). Connexin expression and gap junctional coupling in human cumulus cells: contribution to embryo quality. J. Cell. Molec. Med. 13: 972-984.
Tong, D., Lu, X., Wang, H.-X., Plante, I., Lui, E., Laird, D.W., Bai, D., and Kidder, G.M. (2009). A dominant loss-of-function Gja1 (Cx43) mutant impairs parturition in the mouse. Biol. Reprod. 80: 1099-1106.
Tong, D., Colley, D., Thoo, R., Li, T.Y., Plante, I., Laird, D.W., Bai, D., and Kidder, G.M.(2009). Oogenesis defects in a mutant mouse model of oculodentodigital dysplasia. Dis. Model. Mech. 2: 157-167.
Li, T.Y., Colley, D., Barr, K.J., Yee, S.-P., and Kidder, G.M. (2007). Rescue of oogenesis in Cx37 null mutant mice by oocyte-specific replacement with Cx43. J. Cell Sci. 120: 4117-4125.
Tong, D., Li, T.Y., Naus, K.E., Bai, D., and Kidder, G.M. (2007). In vivo analysis of undocked connexin43 gap junction hemichannels in ovarian granulosa cells. J. Cell Sci.120: 4016-4024.
Kahiri, C.N., Khalil, M.W., Tekpetey, F., and Kidder, G.M. (2006). Leydig cell function in mice lacking connexin43. Reproduction 132: 607-616. Gittens, J.E. I, Barr, K. J., Vanderhyden, B.C., and Kidder, G. M. (2005). Interplay between paracrine signalling and gap junctional communication in ovarian follicles. J. Cell Sci. 118: 113-122
