Abstract
The TSPY gene, which encodes the testis-specific protein, Y-encoded, was first discovered and characterized in humans, but orthologous genes were subsequently identified on the Y chromosome of many other placental mammals. TSPY is expressed in the testis and to a much lesser extent in the prostate gland, and it is assumed that TSPY serves function in spermatogonial proliferation and/or differentiation. It is further supposed that TSPY is involved in male infertility and exerts oncogenic effects in gonadal and prostate tumor formation. As a member of the TSPY/SET/NAP protein family, TSPY is able to bind cyclin B types, and stimulates the cyclin B1-CDK1 kinase activity, thereby accelerating the G2/M phase transition of the cell cycle of target cells. Because the laboratory mouse carries only a nonfunctional Y-chromosomal Tspy-ps pseudogene, a knockout mouse model for functional research analyses is not a feasible approach. In the last decade, three classical transgenic mouse models have been developed to contribute to our understanding of TSPY regulation, expression and function. The different transgenic mouse approaches and their relevance for studying TSPY regulation, expression and function are discussed in this review.
Highlights
The human TSPY cluster on the human Y chromosome is unique because it represents the largest and most homogenous protein-coding tandem array in the human genome [1]
The functions of human TSPY genes are still unknown, but multiple in vivo and in vitro studies point to a role of TSPY in cell cycle regulation of fetal and spermatogenic germ cells
The multiplicity and sequence diversity of human TSPY gene copies make the analyses of regulation, expression and function extremely difficult
Summary
The human TSPY cluster on the human Y chromosome is unique because it represents the largest and most homogenous protein-coding tandem array in the human genome [1]. While many MSY genes degenerate during evolution due to accumulation of deleterious mutations as a consequence of their suppressed recombination with their X-homologs [4], others avoid degeneration by being present in multiple, nearly identical copies, thereby having the chance to compensate the effects of null alleles via unequal sister chromatid exchange or Y-Y gene conversion [1,5] This strategy is applied to the TSPY gene, being organized in multiple copies and functionally conserved in primates and cattle [6,7,8,9]. What diverse function(s) TSPY may fulfill in spermatogonial proliferation, differentiation and male meiosis within the testis, and whether it has a physiological function in the prostate, is currently unknown It was shown in stably transfected human HeLa and mouse. Tspy-ps in species of the subgenus Mus, including the laboratory mouse [11,12,35], has enabled the generation of different transgenic mouse models for studying human TSPY regulation, expression and function in vivo
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