Abstract
The mammalian Y chromosome carries a factor that initiates male sexual development by directing the fetal gonads to form testes. Wachtel and his colleagues1 proposed that this testis-determining function of the Y is mediated by the male-specific cell-surface antigen H–Y, originally defined by skin grafting2. This attractive hypothesis, which has been widely accepted, was based on the assumption that serological tests using antisera raised against male cells were recognizing H–Y antigen. Although disputed3, this assumption is supported by some recent studies4–6. However, mice have been described7 which develop testes but lack the cell-surface H–Y antigen as defined by T-cell-mediated transplantation tests. Thus, although it remains possible that a serologically detected male-specific antigen is responsible for testis determination, it seems that H–Y, as originally defined, is not. We show here that H–Y-negative male mice, in losing the genetic information that encodes H–Y, have also lost genetic information required for spermatogenesis. This result identifies a gene on the mouse Y,distinct from the testis-determining gene, which is necessary for spermatogenesis, and raises the intriguing possibility that the product of this ‘spermatogenesis gene’ is H–Y antigen.
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Burgoyne, P., Levy, E. & McLaren, A. Spermatogenic failure in male mice lacking H–Y antigen. Nature 320, 170–172 (1986). https://doi.org/10.1038/320170a0
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DOI: https://doi.org/10.1038/320170a0
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