In the past 10 years, more than 100 different genetically engineered mice have been developed with an abnormality in spermatogenesis. More than half of these male infertility animal models have been reported in the past three years alone. Spermatogenic defects in these models vary considerably, ranging from the inappropriate migration of primordial germ cells to the inability of mature spermatozoa to bind the zona pellucida. Many of these genetically engineered mice have been reviewed previously [1-4]. Rather than discussing all of the genes that have been connected with male infertility, the purpose of this review will be highlighting the genes that seem to have the greatest potential for being clinically relevant, based on a main phenotype of male infertility in the knockout mouse model.

Our laboratory is actively evaluating infertility candidate genes in infertile humans. Because of our interests it is important to identify genes for which the gene structure, including exons, introns, and their boundaries can be established. Therefore, each time a candidate murine gene was identified, a literature search was conducted and the NCBI databases searched to determine if a human homologue had been reported or published. In several cases there was no information currently available on the nucleotide or amino acid sequence in humans. If an amino acid sequence was available, it was used to conduct a translated BLAST search of the HTGS (high throughput genomic sequences) database of the human genome. If the structure of the gene in humans could be derived from the BLAST analysis or a published account it was included in this review. If the structure could not be determined, it was excluded.

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