International Mammalian Genome Society

The 15th International Mouse Genome Conference (2001)


Dr. Fernando Pardo-Manuel de Villena
The University of North Carolina at Chapel Hill
Dept of Genetics CB # 7264
102 Mason Farm Road
Chapel Hill 27599-7264

Co-Authors: Carmen Sapienza
Institutions: Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine

Speciation is often accompanied by changes in chromosomal number or form even though such changes significantly reduce the fertility of hybrid intermediates. We have addressed this evolutionary paradox by expanding the principle that nonrandom segregation of chromosomes takes place whenever human or mouse females are heterozygous carriers of Robertsonian translocations. Our analysis of 1,170 mammalian karyotypes provides strong evidence that karyotypic evolution is driven by nonrandom segregation during female meiosis. The pertinent variable in this form of meiotic drive is the presence of differing numbers of centromeres on paired homologues. This situation is encountered in all heterozygous carriers of Robertsonian translocations. Whenever paired chromosomes have different numbers of centromeres, the inherent asymmetry of female meiosis and the polarity of the meiotic spindle dictates that the partner with the greater number of centromeres will attach preferentially to the pole that is most efficient at capturing centromeres. This mechanism explains how chromosomal variants become fixed in populations, as well as why closely related species often appear to have evolved by directional adjustment of the karyotype towards or away from a particular chromosome form. If differences in the ability of particular DNA sequences to function as centromeres are also considered, nonrandom segregation is likely to affect karyotype evolution across a very broad phylogenetic range.

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