Molecular Biology and Evolution, Vol 15, 28-34, Copyright © 1998 by Society for Molecular Biology and Evolution
P Jarne, P David and F Viard
Variability at microsatellite (MS) loci is generally perceived as resulting
from an interaction between mutation and genetic drift and, to a lesser
extent, selection and recombination. Less investigated has been the reason
for MS accumulation in genomes. We present here a simple model that could
account for the variation in density of MS loci, assuming that they are
created either through replication slippage or in association with
transposable elements. Microsatellites then evolve under the forces cited
above. We use this framework to revisit two results obtained from
high-density genomic maps of the human and mouse genomes built with
thousands of CA repeats: MS loci are (1) less variable and (2) less dense
on the X chromosome than on autosomes. The first result is most likely
explained by differential mutation on the X chromosome and the autosomes.
The second result may be explained by differential mutation, provided the
distributions of MS loci are still not at equilibrium. Selection, acting
either directly on large allele size or indirectly on the transposable
elements associated with MS, may explain the same result. The framework
developed here is a first step toward more rigorous models, calling for
additional data.
ORIGINAL ARTICLE
Microsatellites, transposable elements and the X chromosome
Institut des Sciences de l'Evolution, Universite Montpellier II, France. jarne@isem.univ-montp2.fr
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