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Human Molecular Genetics Advance Access published online on August 4, 2004
Human Molecular Genetics, doi:10.1093/hmg/ddh240
© 2004 by Oxford University Press
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Article

The AZFa gene DBY (DDX3Y) is widely transcribed but the protein is limited to the male germ cells by translation control

H. J. Ditton 1, J. Zimmer 1, C. Kamp 1, E. Rajpert-De Meyts 2, P. H. Vogt 3*

1 Section of Molecular Genetics & Infertility, Department of Gynecological Endocrinology & Reproductive Medicine, University of Heidelberg, Heidelberg, Germany
2 Department of Growth & Reproduction, Copenhagen University Hospital (Rigshospitalet) Section GR-5064, Copenhagen, Denmark
3 Section of Molecular Genetics & Infertility, Department of Gynecological Endocrinology & Reproductive Medicine, University of Heidelberg, Voßstrasse 9, D-69115, Heidelberg, Germany

* To whom correspondence should be addressed. E-mail: peter_vogt{at}med.uni-heidelberg.de.


  Abstract

We explored the function of the human DEAD BOX Y RNA helicase DBY (DDX3Y) gene located in the AZFa region on the human Y chomosome (Yq11.21). Deletion of this Y interval is known as a major cause for the occurrence of a severe testicular pathology, the Sertoli-cell-only (SCO) syndrome. DBY has a structural homologue on the short arm of the X chromosome DBX (DDX3X) (Xp11.4). We found widespread transcription of both genes in each tissue analysed although predominantly in testis tissue. However, translation of DBY was detected only in the male germ line, while DBX protein was expressed in all tissues analysed. In testis tissue sections, DBY protein was found predominantly in spermatogonia, whereas DBX protein was expressed after meiosis in spermatids. We conclude that although both RNA helicases are structurally very similar, they have diverged functionally to fulfil different roles in the RNA metabolism of human spermatogenesis, and that deletion of the DBY gene is the most likely cause of the severe testicular pathology observed in men with AZFa deletions.


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