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Human Molecular Genetics Advance Access originally published online on February 27, 2007
Human Molecular Genetics 2007 16(7):763-773; doi:10.1093/hmg/ddm012
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© The Author 2007. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Success and failure in human spermatogenesis as revealed by teratozoospermic RNAs

Adrian E. Platts1, David J. Dix3, Hector E. Chemes4, Kary E. Thompson3, Robert Goodrich1, John C. Rockett3, Vanesa Y. Rawe5, Silvina Quintana4, Michael P. Diamond1, Lillian F. Strader3 and Stephen A. Krawetz1,2,6,*

1 Department of Obstetrics and Gynecology, 2 Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, USA, 3 Office of Research and Development, U.S. Environmental Protection Agency, USA, 4 Centro de Investigaciones Endocrinologicas, Argentina, 5 Centro de Estudios en Ginecología y Reproducción, Argentina and 6 Institute for Scientific Computing, Wayne State University

* To whom correspondence should be addressed at: Charlotte B. Failing Professor of Fetal Therapy and Diagnosis, 253 C.S. Mott Center, 275 East Hancoc, Detroit, MI 48201, USA. Tel: +1 3135776770; Fax: +1 31357-8554; Email: steve{at}compbio.med.wayne.edu

Received December 29, 2006; Revised January 26, 2006; Accepted February 2, 2007

We are coming to appreciate that at fertilization human spermatozoa deliver the paternal genome alongside a suite of structures, proteins and RNAs. Although the role of some of the structures and proteins as requisite elements for early human development has been established, the function of the sperm-delivered RNAs remains a point for discussion. The presence of RNAs in transcriptionally quiescent spermatozoa can only be derived from transcription that precedes late spermiogenesis. A cross-platform microarray strategy was used to assess the profile of human spermatozoal transcripts from fertile males who had fathered at least one child compared to teratozoospermic individuals. Unsupervised clustering of the data followed by pathway and ontological analysis revealed the transcriptional perturbation common to the affected individuals. Transcripts encoding components of various cellular remodeling pathways, such as the ubiquitin–proteosome pathway, were severely disrupted. The origin of the perturbation could be traced as far back as the pachytene stage of spermatogenesis. It is anticipated that this diagnostic strategy will prove valuable for understanding male factor infertility.


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