BACKGROUND: High-throughput studies provide a wide spectrum of genes for use as predictive markers during testicular sperm extraction (TESE) in combination with ICSI. In this work, we used the specimens from testicular biopsies of men with non-obstructive azoospermia who underwent TESE to investigate the expression of spermatogenesis-related genes MND1, SPATA22, GAPDHS and ACR. METHODS: Testicular biopsy specimens were subdivided into three groups: hypospermatogenesis (HS); maturation arrest (MA); and Sertoli cell-only syndrome (SCO). The levels of expression of the spermatogenesis-related genes MND1, SPATA22, GAPDHS and ACR in the testes were compared among these three groups using the reverse transcription polymerase chain reaction (RT-PCR) technique. RESULTS: Analysis of the expression of spermatogenic genes in human testes with abnormal spermatogenesis showed different expression patterns in patients from different groups. Fertilization rate for studied set of patients was 66% and pregnancy rate 29%. For HS group fertilization rate was 72% and pregnancy rate 32%, while for MA group fertilization and pregnancy rates were 54% and 26%, respectively. Fertilization rates in relation to the studied genes were uniformly around 70%, pregnancy rates for ACR and GAPDHS genes were surprisingly low at 6% and 8% correspondingly. CONCLUSIONS: Analysis of the expression of genes involved in spermatogenesis can be a fast additional test for the level of spermatogenesis in testicular samples.

• MeSH
• Acrosin genetics   MeSH
• Azoospermia genetics   pathology   MeSH
• Biopsy MeSH
• Adult MeSH
• Fertilization MeSH
• Glyceraldehyde-3-Phosphate Dehydrogenases genetics   MeSH
• Sperm Injections, Intracytoplasmic MeSH
• Middle Aged MeSH
• Humans MeSH
• Testicular Diseases genetics   pathology   MeSH
• Sperm Retrieval MeSH
• Oligospermia genetics   pathology   MeSH
• Reverse Transcriptase Polymerase Chain Reaction MeSH
• Cell Cycle Proteins genetics   MeSH
• Sertoli Cell-Only Syndrome genetics   pathology   MeSH
• Spermatogenesis genetics   MeSH
• Gene Expression Profiling MeSH
• Pregnancy MeSH
• Testis metabolism   pathology   MeSH
• Pregnancy Rate MeSH
• Check Tag
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Pregnancy MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Acrosin MeSH
• Glyceraldehyde-3-Phosphate Dehydrogenases MeSH
• MND1 protein, human MeSH Browser
• Cell Cycle Proteins MeSH
• SPATA22 protein, human MeSH Browser

Theory predicts that sexually antagonistic mutations will be over- or under-represented on the X and Z chromosomes, depending on their average dominance coefficients. However, as little is known about the dominance coefficients for new mutations, the effect of sexually antagonistic selection is difficult to predict. To elucidate the role of sexually antagonistic selection in the evolution of Z chromosome gene content in chicken, we analyzed publicly available microarray data from several somatic tissues as well as somatic and germ cells of the ovary. We found that the Z chromosome is enriched for genes showing preferential expression in ovarian somatic cells, but not for genes with preferential expression in primary oocytes or non-sex-specific somatic tissues. Our results suggest that sexual antagonism leads to a higher abundance of female-benefit alleles on the Z chromosome. No bias toward Z-linkage for oocyte-enriched genes can be explained by lower intensity of sexually antagonistic selection in ovarian germ cells compared to ovarian somatic cells. An alternative explanation would be that meiotic Z chromosome inactivation hinders accumulation of oocyte-expressed genes on the Z chromosome. Our results are consistent with findings in mammals and indicate that recessive rather than dominant sexually antagonistic mutations shape the gene content of the X and Z chromosomes.

• MeSH
• Databases, Genetic MeSH
• Granulosa Cells metabolism   MeSH
• Dosage Compensation, Genetic genetics   MeSH
• Chickens genetics   MeSH
• Linear Models MeSH
• Meiosis MeSH
• Mutation MeSH
• Oogenesis MeSH
• Organ Specificity MeSH
• Ovary cytology   metabolism   physiology   MeSH
• Sex Chromosomes genetics   metabolism   MeSH
• Chi-Square Distribution MeSH
• Oligonucleotide Array Sequence Analysis MeSH
• Selection, Genetic MeSH
• Gene Expression Profiling MeSH
• Gene Expression Regulation, Developmental * MeSH
• Animals MeSH
• Check Tag
• Female MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH

Several lines of evidence suggest that the X chromosome of various animal species has an unusual complement of genes with sex-biased or sex-specific expression. However, the study of the X chromosome gene content in different organisms provided conflicting results. The most striking contrast concerns the male-biased genes, which were reported to be almost depleted from the X chromosome in Drosophila but overrepresented on the X chromosome in mammals. To elucidate the reason for these discrepancies, we analysed the gene content of the Z chromosome in chicken. Our analysis of the publicly available expressed sequence tags (EST) data and genome draft sequence revealed a significant underrepresentation of ovary-specific genes on the chicken Z chromosome. For the brain-expressed genes, we found a significant enrichment of male-biased genes but an indication of underrepresentation of female-biased genes on the Z chromosome. This is the first report on the nonrandom gene content in a homogametic sex chromosome of a species with heterogametic female individuals. Further comparison of gene contents of the independently evolved X and Z sex chromosomes may offer new insight into the evolutionary processes leading to the nonrandom genomic distribution of sex-biased and sex-specific genes.

• MeSH
• Expressed Sequence Tags MeSH
• Genetic Linkage MeSH
• Dosage Compensation, Genetic MeSH
• Chickens genetics   MeSH
• Chromosome Mapping MeSH
• Sex Chromosomes genetics   MeSH
• Sex Factors MeSH
• Gene Expression Profiling MeSH
• Animals MeSH
• Check Tag
• Male MeSH
• Female MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH