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Biology of Reproduction 65, 829-838 (2001)
© 2001 Society for the Study of Reproduction, Inc.

Regular Article

Failure of Spermatogenesis in Mice Lacking Connexin431

Wendi A. Roscoea,b,c,d, Kevin J. Barra,b,c,d, Abdul Amir Mhawia,b,c,d, David K. Pomerantza,b, and Gerald M. Kidder2,a,b,c,d

a Departments of Physiology, b Obstetrics and Gynaecology, c Paediatrics, The University of Western Ontario, London, Ontario, Canada N6A 5C1 d Child Health Research Institute, London, Ontario, Canada N6C 2V5

ABSTRACT

Connexin43 (Cx43), a gap junction protein encoded by the Gja1 gene, is expressed in several cell types of the testis. Cx43 gap junctions couple Sertoli cells with each other, Leydig cells with each other, and spermatogonia/spermatocytes with Sertoli cells. To investigate the role of this communication pathway in spermatogenesis, we studied postnatal testis development in mice lacking Cx43. Because such mice die shortly after birth, it was necessary to graft testes from null mutant fetuses under the kidney capsules of adult males for up to 3 wk. Grafted wild-type testes were used as controls. In our initial experiments with wild-type testes, histological examination indicated that the development of grafted testes kept pace with that of nongrafted testes in terms of the onset of meiosis, but this development required the presence of the host gonads. When excised grafts were stimulated in vitro with cAMP or LH, there was no significant difference in androgen production between null mutant and wild-type testes, indicating that the absence of Cx43 had not compromised steroidogenesis. Previous research has shown that Cx43 null mutant neonates have a germ cell deficiency that arises during fetal life, and our analysis of grafted testes demonstrated that this deficiency persists postnatally, giving rise to a "Sertoli cell only" phenotype. These results indicate that intercellular communication via Cx43 channels is required for postnatal expansion of the male germ line.

FOOTNOTES

First decision: 16 February 2001.

1 This work was supported by grants from the Natural Sciences and Engineering Research Council of Canada (to G.M.K.) and the Medical Research Council of Canada (to D.K.P.).

2 Correspondence: Gerald M. Kidder, Department of Physiology, The University of Western Ontario, London, ON, Canada N6A 5C1. FAX: 519 661 3827; gerald.kidder{at}med.uwo.ca




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