Polymorphisms exist at many genetic loci. At some loci, however, polymorphism is so high that tens and even hundreds of different alleles coexist in the population. Two such highly polymorphic systems are the immunoglobulin genes and the vertebrate major histocompatibility loci. The origin and maintenance of highly polymorphic loci remain open to debate but it seems likely that special mechanisms contribute to their variability and that their polymorphism serves important biological roles. The high degree of polymorphism at the H–2 class I major histocompatibility locus of the mouse has been documented by both tissue transplantation and serological methods1. More recently, molecular cloning and DNA sequencing of some of the class I genes has shown that most of the sequence variability is concentrated in the first two domains and is often found in clustered regions within them2–4. In addition, several groups have suggested that gene conversion events among the many class I genes may contribute to H–2 polymorphism5,6; such events would have to occur during meiosis to produce heritable alterations. The strongest evidence for gene conversion comes from sequence analysis of mutant class I H–2 alleles where concerted changes at adjoining sites in DNA imply gene conversion by distant but closely related loci5,6. We report here an analysis of these mutants indicating that the chromosomes containing loci that have experienced gene conversion originated from females. These data suggest a striking preference for mammalian meiotic gene conversion events during female rather than male gametogenesis.
Subscribe to Journal
Get full journal access for 1 year
only $3.90 per issue
All prices are NET prices.
VAT will be added later in the checkout.
Rent or Buy article
Get time limited or full article access on ReadCube.
All prices are NET prices.
Klein, J. & Figueroa, F. Immun. Rev. 60, 23–58 (1981).
Moore, K. W., Sher, B. T., Sun, Y. H., Eakle, K. A. & Hood, L. Science 215, 679–682 (1981).
Evans, G. A., Margulies, D. H., Camerini-Otero, R. D., Ozato, K. & Seidman, J. G. Proc. natn. Acad. Sci. U.S.A. 79, 1994–1998 (1982).
Kvist, S., Roverts, L. & Dobberstein, B. EMBO J. 2, 245–254 (1983).
Weiss, E. et al. Nature 301, 671–674 (1983).
Schulze, D. H., Pease, L. R., Wallace, R. B. & Nathenson, S. G. Proc. natn. Acad. Sci. U.S.A. 80, 2007–2011 (1983).
Kohn, H. I. et al. Immunogenetics 7, 279–294 (1978).
Nairn, R., Yamaga, K. & Nathenson, S. G. A. Rev. Genet. 14, 241–277 (1980).
Bailey, D. W. & Kohn, H. I. Genet. Res. 6, 330–340 (1965).
Melvold, R. W. & Kohn, H. I. Mutat. Res. 27, 415–418 (1975).
Egorov, I. K. & Blandova, Z. K. Genet. Res. 19, 133–143 (1972).
Klein, J. in Biology of the Mouse Histocompatibility-2 Complex, 215–217 (Springer, New York, 1975).
Egel, R. Nature 290, 191–192 (1981).
About this article
Cite this article
Loh, D., Baltimore, D. Sexual preference of apparent gene conversion events in MHC genes of mice. Nature 309, 639–640 (1984). https://doi.org/10.1038/309639a0
Extensive genetic polymorphism of four plasma α-protease inhibitors in pigs and evidence for tight linkage between the structural loci of these inhibitors
Animal Genetics (2009)
Annual Review of Genetics (2005)
Timing and Effects of Template Number for Gene Conversion of Major Histocompatibility Complex Genes in the Mouse
The Journal of Immunology (2002)
Comparative genomic analysis of the MHC: the evolution of class I duplication blocks, diversity and complexity from shark to man
Immunological Reviews (2002)