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Hum. Reprod. Advance Access originally published online on February 22, 2006
Human Reproduction 2006 21(5):1194-1203; doi:10.1093/humrep/dei479
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© The Author 2006. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

An azoospermic man with a double-strand DNA break-processing deficiency in the spermatocyte nuclei: Case report

R.B. Sciurano1, M.I. Rahn1, M.I. Pigozzi1, S. Brugo Olmedo2 and Alberto J. Solari1,3

1 Facultad de Medicina, Centro de Investigaciones en Reproducción (CIR) and 2 CEGYR, Viamonte, Buenos Aires, Argentina

3 To whom correspondence should be addressed at: Facultad de Medicina, CIR, Paraguay 2155, 11219 Buenos Aires, Argentina. E-mail: ajsolari{at}mail.retina.ar

BACKGROUND: The mechanisms of meiotic arrest in human spermatogenesis are poorly known. METHODS AND RESULTS: A testicular biopsy from an azoospermic male showed complete spermatogenesis arrest at the spermatocyte stage, asynapsis, lack of formation of the XY body, partial reversion to a mitotic-like division and cell degeneration both at the prophase and at the abnormal cell divisions. Synaptonemal complex analysis showed minor segments of synapsis and mainly single axes. Fluorescent immunolocalization of meiotic proteins showed normal SYCP3, scarcity of SYCP1, null MLH1 foci, about 10 patches of {gamma}-H2AX, abnormal presence of BRCA1 among autosomal axes, absence of RAD51 in early and advanced spermatocytes and permanence of {gamma}-H2AX labelling up to the abnormal spermatocyte divisions that are the most advanced stage reached. There are at least six dominions of evenly packed chromatin resembling that of the normal XY body, but no true XY body. CONCLUSIONS: The protein phenotype and the fine structure of the nuclei are compatible with a deficiency of the processing of double-strand DNA breaks in the zygotene-like spermatocytes, but the features of this defect do not agree with Spo11, Sycp1, Atm and Dmc1 null mutations, which give absence of XY body, synapsis disturbances and spermatocyte apoptosis in mice.

Key words: asynapsis/azoospermia/double-strand DNA breaks/meiotic arrest/SPO11


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