Gerald M. Kidder, Ph.D.


Children’s Health Research Institute
Scientist and Chair, Developmental Biology Program


Lawson Health Research Institute
Scientist, Children’s Health Research Institute


University of Western Ontario
Associate Vice President (Research)
Professor, Departments of Physiology and Pharmacology, Obstetrics and Gynaecology, and Paediatrics

Contact Information
Tel: (519) 661-3132
Fax: (519) 850-2562
E-mail: gerald.kidder@schulich.uwo.ca
Web: http://www.physpharm.fmd.uwo.ca/research/research.html


Brief Biography

Dr. Kidder earned a bachelor's degree in biology from Hiram College in 1966 and a doctorate in developmental biology from Yale University in 1971. He received postdoctoral training in developmental biology at Reed College (1971-72) before moving to Canada to take up an Assistant Professorship at The University of Western Ontario in the Department of Zoology, Faculty of Science. He rose through the ranks in that department to become Professor of Zoology. In 1996, he moved to the Department of Physiology and Pharmacology in Western’s Schulich School of Medicine and Dentistry. During his career at Western he has held visiting or adjunct appointments at the University of California, San Francisco (1979-80), the Massachusetts Institute of Technology (1986-87), the University of Guelph (1991-95) and The Jackson Laboratory in Bar Harbor, Maine (1994 and 1997).


Research Interests

• The roles of gap junctional intercellular communication in gametogenesis and early stages of embryogenesis
• Genetic factors in infertility studied using genetically modified mice
• Modeling human connexin diseases in mice

• Improving pregnancy outcome in assisted conception


Research Activities

The Kidder laboratory uses genetically modified mice to investigate cellular and molecular mechanisms of gonad development, gametogenesis, and early embryogenesis, with particular emphasis on the roles of gap junctional intercellular communication. Mice carrying loss-of-function or gain-of-function mutations in connexin genes, which encode the subunits of gap junction channels, are analyzed for the developmental and physiological consequences of perturbing gap junctional communication. A newly emerging direction of the laboratory is modeling congenital abnormalities using connexin mutant mice, based on the growing list of such abnormalities caused by human connexin gene mutations. In collaboration with the Reproductive Endocrinology and Infertility Program of the LHSC, they are translating their knowledge of the roles of gap junctional communication during oogenesis into improving the health of babies conceived through in vitro fertilization. Dr. Kidder has trained over 30 graduate students and postdoctoral fellows.

 

Awards and Recognition

J.J. Turner Society Award for Excellence in the Life Sciences - Awarded by Hiram College

 

Discovery Grant - Awarded by Natural Science and Engineering Research Council of Canada  

                                                                 
Operating Grant - Awarded by Canadian Institute of Health Research

      

Operating Grant - Awarded by Canadian Institute of Health Research
        

Innovation Fund - Awarded by University of Western Ontario

 

Patents

  1. Kidder, G.M., Wang, H.-X., Tong, D., and Tekpetey, F.R. Method of assessing embryo quality. US patent application filed 5 March, 2008

Publications

  1. Wang, H.-X., Tekpetey, F.R., and Kidder, G.M. "Exploration of the WNT/$-CATENIN signaling pathway in human cumulus cells". Submitted for publication
  2. Tong, D., Lu, X., Wang, H.-X., Plante, I., Lui, E., Laird, D.W., Bai, D., and Kidder, G.M.  "A dominant loss-of-function Cx43 mutant impairs parturition in the mouse". Submitted for publication.
  3. Tong, D., Colley, D., Thoo, R., Plante, I., Laird, D.W., Bai, D., and Kidder, G.M. "Oogenesis defects in a mutant mouse model of oculodentodigital dysplasia". Submitted for publication
  4. McKinnon, R.L., Bolon, M.L., Kidder, G.M., Simon, A.M., and Tyml, K. "Reduction of electrical coupling between endothelial cells by NO depends on connexin37". Submitted for publication.
  5. Wang, H.-X., Tong, D., El-Gehani, F., Tekpetey, F.R., and Kidder, G.M. (2008). "Connexin expression and gap junctional coupling in human cumulus cells: contribution to embryo quality". J. Cell. Molec. Med., in press.
  6. Bolon, M.L., Peng, T., Kidder, G.M., and Tyml, K. (2008). "Lipopolysaccharide plus hypoxia and reoxygenation synergistically reduce electrical coupling between microvascular endothelial cells by dephosphorylating connexin40". J. Cell. Phys. 217: 350-359.
  7. Kidder, G.M.  (2008). "Towards a new nomenclature for connexin genes". In: Connexins: A Guide (A.L. Harris and D.A. Locke, eds.). Totowa, New Jersey: The Humana Press Inc., pp 537-539.
  8. Kidder, G.M. and Winterhager, E. (2008). "Roles of connexins in female reproduction". In: Connexins: A Guide (A.L. Harris and D.A. Locke, eds.). Totowa, New Jersey: The Humana Press Inc., pp 475-487
  9. McLachlan, E., Shao, Q., Gillingham, E., Tong, D., Kidder, G.M., Bernier, S.M., and Laird, D.W.  (2008). "ODDD-linked Cx43 mutants reduce endogenous Cx43 expression and function in osteoblasts and inhibit late stage differentiation". J. Bone Mineral Res.23: 928-938.
  10. 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.
  11. 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
  12. Langlois, S., Maher, A.C., Manias, J.L., Shao, Q., Kidder, G.M. and Laird, D.W. (2007). "Connexin levels regulate keratinocyte differentiation in the epidermis". J. Biol. Chem. 282: 30171-30180.
  13. Roscoe, W.A., Kidder, G.M., and Karlik, S.J. (2007). "Experimental allergic encephalomyelitis in connexin43 heterozygous mice". Cell  Commun. Adhes. 14: 57-73
  14. Bolon, M.L., Kidder, G.M., Simon, A.M. and Tyml, K. (2007). "Lipopolysaccharide reduces electrical coupling in microvascular endothelial cells by targeting connexin40 in a tyrosine-, ERK1/2-, PKA- and PKC-dependent manner".  J. Cell. Physiol. 211: 159-166.
  15. Kahiri CN, Khalil MW, Tekpetey F, Kidder GM. (2006). "Leydig cell function in mice lacking connexin43". Reproduction. 132:607-616.