An azoospermic man with a double-strand DNA break-processing deficiency in the spermatocyte nuclei: Case report
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...
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| Published in | Human reproduction (Oxford) Vol. 21; no. 5; pp. 1194 - 1203 |
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| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford
Oxford University Press
01.05.2006
Oxford Publishing Limited (England) |
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| Abstract | 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 γ-H2AX, abnormal presence of BRCA1 among autosomal axes, absence of RAD51 in early and advanced spermatocytes and permanence of γ-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. |
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| AbstractList | BACKGROUNDThe mechanisms of meiotic arrest in human spermatogenesis are poorly known. METHODS AND RESULTSA 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. CONCLUSIONSThe 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. 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 γ-H2AX, abnormal presence of BRCA1 among autosomal axes, absence of RAD51 in early and advanced spermatocytes and permanence of γ-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. The mechanisms of meiotic arrest in human spermatogenesis are poorly known. 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. 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. 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. |
| Author | Rahn, M.I. Solari, Alberto J. Sciurano, R.B. Pigozzi, M.I. Olmedo, S. Brugo |
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| Cites_doi | 10.1016/S1097-2765(00)00098-8 10.1038/5075 10.1093/humupd/7.2.191 10.1073/pnas.91.14.6559 10.1016/S0092-8674(02)00615-3 10.1016/S0140-6736(03)14845-3 10.1038/ng1484 10.1242/dev.00410 10.1101/gad.13.5.523 10.1016/j.fertnstert.2003.05.021 10.1016/S0091-679X(08)60881-X 10.32604/biocell.2003.27.329 10.1007/BF00368145 10.1016/S0959-437X(02)00282-4 10.1093/humrep/deh335 10.1016/j.cub.2004.11.032 10.1016/S0074-7696(08)60928-6 10.1016/S1534-5807(03)00093-5 10.1093/humrep/14.suppl_1.82 10.1101/gad.10.19.2411 10.1016/S0092-8674(00)81312-4 10.1128/MCB.25.16.7203-7215.2005 10.1093/humrep/11.suppl_4.1 10.1242/jcs.02466 10.1016/S1097-2765(00)80070-2 10.1016/j.yexcr.2004.03.008 10.1073/pnas.93.13.6236 10.1016/S1097-2765(00)80069-6 10.1016/S0968-0004(00)01742-4 10.1016/S1097-2765(00)00097-6 10.1007/BF01953855 10.1016/S1097-2765(00)80404-9 10.1016/S0070-2153(01)52008-6 10.1126/science.1069398 10.1007/s00412-005-0334-8 10.1038/85830 |
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| Copyright | 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 2006 2006 INIST-CNRS Copyright Oxford University Press(England) May 2006 |
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| Keywords | asynapsis double-strand DNA breaks meiotic arrest azoospermia SPO11 Human Deficiency Break Male Germinal cell Case study Vertebrata Azoospermia Double stranded DNA Mammalia Spermatocyte Male sterility Male genital diseases |
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| Snippet | BACKGROUND: The mechanisms of meiotic arrest in human spermatogenesis are poorly known. METHODS AND RESULTS: A testicular biopsy from an azoospermic male... The mechanisms of meiotic arrest in human spermatogenesis are poorly known. A testicular biopsy from an azoospermic male showed complete spermatogenesis arrest... BACKGROUNDThe mechanisms of meiotic arrest in human spermatogenesis are poorly known. METHODS AND RESULTSA testicular biopsy from an azoospermic male showed... |
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| SubjectTerms | Adaptor Proteins, Signal Transducing Adenosine Triphosphatases - genetics Adult asynapsis Ataxia Telangiectasia Mutated Proteins azoospermia Biological and medical sciences BRCA1 Protein - analysis Carrier Proteins Cell Cycle Proteins - analysis Cell Cycle Proteins - genetics Cell Nucleus - chemistry Cell Nucleus - metabolism Cell Nucleus - ultrastructure Chromosome Pairing - genetics DNA - metabolism DNA Damage - genetics DNA Repair DNA-Binding Proteins - analysis DNA-Binding Proteins - genetics double-strand DNA breaks Endodeoxyribonucleases Esterases - genetics Gynecology. Andrology. Obstetrics Histones - analysis Humans Male Medical sciences Meiosis - genetics meiotic arrest Mutation MutL Protein Homolog 1 Nuclear Proteins - analysis Nuclear Proteins - genetics Oligospermia - genetics Oligospermia - metabolism Protein-Serine-Threonine Kinases - analysis Rad51 Recombinase - analysis Spermatocytes - chemistry Spermatocytes - metabolism Spermatocytes - ultrastructure Spermatogenesis - genetics SPO11 Synaptonemal Complex - chemistry Synaptonemal Complex - genetics Synaptonemal Complex - metabolism Testis - pathology Tumor Suppressor Proteins - analysis |
| Title | An azoospermic man with a double-strand DNA break-processing deficiency in the spermatocyte nuclei: Case report |
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