Assistant Professor3901 Rainbow Boulevard
3024 Wahl Hall East
Kansas City, Kansas 66160
Phone: (913) 588-7419
Fax: (913) 588-7430
Email: agodwin@kumc.edu
Ph.D., Yale University, 1991; Postdoctoral, University of Utah
Hox genes are evolutionarily conserved transcription factors that are important in determining changes along the major anterior-posterior axis in animals as diverse as flatworms, fruit flies, and man. Targeted mutations in the mouse Hox genes often mimic aspects of human birth defects. Little is understood about how these genes carry out this process, especially which genes are regulated by these transcription factors. Hence, increased understanding of the basic biology of Hox genes may eventually aid understanding of the underlying causes of some birth defects. The Godwin laboratory is pursuing detailed examination of the interacting partners and the genes controlled by Hoxc13, a model of some human ectodermal dysplasias. Pups born to female Hoxc12 mutant mice die within a few days after birth due to uterine conditions. We are using these mice as a model to examine the role of Hox genes in uterine control of fetal development.
Godwin A R, Capecchi MR (1998) Hoxc13 mutant mice lack external hair. Genes & Dev 12, 11-20.
Godwin AR, Stadler HS, Nakamura K, Capecchi MR (1998) Detection of targeted GFP-HOX gene fusions during mouse embryogenesis. Proc Natl Acad Sci USA 95,13042-13047.
Godwin AR, Capecchi MR (1999) Hair defects in Hoxc13 mutants. J Invest Dermatol Symp Proc 4, 244 -247.
Thummel, R., Li, L., Tanase, C., Sarras, M. P., Jr., and A. R. Godwin (2004) Differences in Expression Pattern and Function between Zebrafish Hoxc13 Orthologs: Recruitment of Hoxc13b into an Early Embryonic Role. Dev Biol. 274(2), 318-33
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