Abstract
Little agreement exists regarding the biological factors able to promote karyotype diversification; the main efforts, however, to explain the fixation and spreading of rearranged chromosomes are based on population genetics theories. Considering the karyotype structure in relation to genome structuring and functioning we found a close relationship between the rate of karyotypic diversification and the degree of homology of the telomeric DNA sequences in a given genome. We suggest for Robertsonian (Rb) chromosome formation and fixation a molecular mechanism triggered by intrinsic genomic traits: this is able to explain the differential rate at which Rb chromosomes arise in different karyotypes, why the house mouse karyotypic diversification occurs so fast and the presence of so many Rb populations that differ in terms of number and arm-composition of Rb chromosomes.
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