MICROSATELLITES, TRANSPOSABLE ELEMENTS AND THE X-CHROMOSOME

Variability at microsatellite (MS) loci is generally perceived as resu lting from an interaction between mutation and genetic drift and, to a lesser extent, selection and recombination. Less investigated has bee n the reason for MS accumulation in genomes. We present here a simple model that could account for the variation in density of MS loci, assu ming that they are created either through replication slippage or in a ssociation with transposable elements. Microsatellites then evolve und er the forces cited above. We use this framework to revisit two result s obtained from high-density genomic maps of the human and mouse genom es built with thousands of CA repeats: MS loci are (1) less variable a nd (2) less dense on the X chromosome than on autosomes. The first res ult is most likely explained by differential mutation on the X chromos ome and the autosomes. The second result may be explained by different ial mutation, provided the distributions of MS loci are still not at e quilibrium. Selection, acting either directly on large allele size or indirectly on the transposable elements associated with MS, may explai n the same result. The framework developed here is a first step toward more rigorous models, calling for additional data.