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RBMY evolved on the Y chromosome from a ubiquitously transcribed X-Y identical gene

Nature Genetics volume 22, pages 224–226 (1999)Cite this article

The X and Y chromosomes are believed to have evolved from an autosomal pair1. Most of the ancestral autosomal genes have been lost from the non-recombining segment of the mammalian Y chromosome (NRY), although some functional X-homologous genes remain2,3,4 (X-NRY genes). The NRY also contains genes with no obvious X homologue. These genes are present in multiple copies on the NRY and are likely to act as male fertility factors, as they are transcribed specifically in testis2. Two of these genes, DAZ (for deleted in azoospermia) and RBMY, are candidate human azoospermia factor (AZF) genes5,6 and encode, respectively, homologues of the RNA-binding proteins DAZL (encoded by DAZL) and HNRNPG (encoded by HNRPG), whose genes have been mapped to autosomes7,8. DAZ arose during primate evolution by transposition of DAZL directly into NRY (Refs 7,9), and this is the accepted model for the origin of all such NRY genes2,10,11,12. In contrast to DAZ, however, RBMY has been on the Y chromosome since before the divergence of eutherian and metatherian mammals more than 130 million years ago10. The only other genes to have been conserved as long on the NRY are X-NRY genes4. We therefore investigated the possibility that RBMY is a diverged X-NRY gene.

Previous mapping of EIF2S3 (encoding EIF-2γ) has shown that localization of a gene to the X chromosome may be masked by the presence of closely related retroposons13. To investigate whether this might be the case for the HNRPG-homologous gene, we derived primers for human14 (oMJ506/508) and mouse11 (oMJ506/522) from HNRPG sequences corresponding to exons 2 and 3 of RBMY (ref. 12). Two types of fragments were amplified from human and mouse genomic DNAs. One, which corresponded in size and sequence to the cDNA (165 bp), was obtained with mouse and human primers in their respective species. A larger fragment was obtained using human primers in both mouse (350 bp) and human (370 bp), and sequencing revealed two blocks of homology to the cDNA sequence, interrupted by a putative 195-bp intron in the same position as the corresponding RBMY intron. We conclude that the larger fragments represent the human and mouse HNRPG-homologous structural genes and that based on the absence of intronic sequence, the previously published mouse Hnrpg gene is a retroposon.

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Figure 1: The HNRPG-homologous structural gene maps to the X chromosome in mouse and human.
Figure 2: Two widely transcribed splice variants are expressed from Rbmx.

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Acknowledgements

We thank N. Levy and J. Belouque for sequencing; P. Avner for DNA from the clone 8, 6/6 and CAK cell lines; N. Affara for DNA from the MOG cell line and comments on the manuscript; and M.A. Mitchell for proofreading the manuscript. This work was supported in part by a grant from the Groupement de recherches et d'études sur les génomes. S.M. was supported by a study grant from the Association pour la recherche sur le cancer and N.S. was supported by a studentship from the Ministère de l'éducation nationale, de l'enseignement supérieur et de la recherche.

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  1. INSERM U.491, Faculté de médecine, 27 bd. Jean Moulin, Marseille, 13385 Cedex 05, France

    Sophie Mazeyrat, Noëmie Saut, Marie-Geneviève Mattei & Michael J. Mitchell

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  1. Sophie Mazeyrat
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Correspondence to Michael J. Mitchell.

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Mazeyrat, S., Saut, N., Mattei, MG. et al. RBMY evolved on the Y chromosome from a ubiquitously transcribed X-Y identical gene. Nat Genet 22, 224–226 (1999). https://doi.org/10.1038/10282

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