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Endocrinology, doi:10.1210/en.2008-0584
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Endocrinology Vol. 149, No. 12 6176-6186
Copyright © 2008 by The Endocrine Society

Testis Development, Fertility, and Survival in Ethanolamine Kinase 2-Deficient Mice

Sonja E. Gustin1, Patrick S. Western1, Peter J. McClive, Vincent R. Harley, Peter A. Koopman and Andrew H. Sinclair

Murdoch Children’s Research Institute and Department of Pediatrics (S.E.G., P.S.W., P.J.M., A.H.S.), University of Melbourne, Royal Children’s Hospital, Melbourne, Victoria 3052, Australia; Prince Henry’s Institute for Medical Research (V.R.H.), Monash University, Clayton, Victoria 3800, Australia; and Institute for Molecular Bioscience (P.A.K.), The University of Queensland, Brisbane, Queensland 4072, Australia

Address all correspondence and requests for reprints to: Andrew Sinclair, Murdoch Children’s Research Institute, Royal Children’s Hospital, Melbourne, Victoria 3052, Australia. E-mail: andrew.sinclair{at}mcri.edu.au.

Ethanolamine kinase 2 (Eki2) was previously isolated from a differential expression screen designed to identify candidate genes involved in testis development and differentiation. In mouse, Eki2 is specifically up-regulated in Sertoli cells of the developing testis at the time of sex determination. Based on this expression profile, Eki2 was considered a good candidate testis-determining gene. To investigate a possible role of Eki2 in testis development, we have generated a mouse with targeted disruption of the Eki2 gene by using an EGFP replacement strategy. No abnormalities were detected in the Eki2-deficient mice with regard to embryonic and adult testis morphology, differentiation, function, or fertility. Furthermore, no significant differences were observed in litter sizes, pup mortality rates, or distribution of the sexes among the offspring. Ethanolamine kinases are involved in the biosynthesis of phosphatidylethanolamine, a major membrane phospholipid. Expression analysis indicates that the absence of an apparent phenotype in the Eki2-deficient mice may be due to compensation by Eki2-family members or the activation of an alternative pathway to generate phosphatidylethanolamine. Expression of EGFP in this mouse model enabled the isolation of gonad cell populations, providing a useful resource from which to obtain relatively pure early steroidogenic cells for further studies.




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[Abstract] [Full Text] [PDF]




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