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

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Endocrinology 2008 Dec;149(12):6176-86. Epub 2008 Aug

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

Gustin, SE;Harley, VR;Koopman, PA;McClive, PJ;Sinclair, AH.;Western, PS

Murdoch Children's Research Institute, University of Melbourne, Royal Children's Hospital, Melbourne, Victoria 3052, Australia.

Service type: Knockout mice


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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