Cell, Volume 103, Issue 5, 711-721, 22 November 2000
Evolutionary Implications of the Frequent Horizontal Transfer of Mismatch Repair Genes
Erick Denamur1, Guillaume Lecointre2, Pierre Darlu4, Olivier Tenaillon3, Cécile Acquaviva1, Chalom Sayada5, Ivana Sunjevaric6, Rodney Rothstein3, 6, Jacques Elion1, François Taddei3, Miroslav Radman3, 1, *, 
and Ivan Matic3
1 INSERM U 458, Hôpital Robert Debré, 48 boulevard Sérurier, 75935 Paris Cedex 19, France
2 Service de Systématique Moléculaire (GDR CNRS 1005), Muséum National d\'Histoire Naturelle, 43 rue Cuvier, 75231 Paris Cedex 05, France
3 INSERM E9916, Faculté de Médecine Necker-Enfants Malades, Université Paris V, 156 rue Vaugirard, 75730 Paris Cedex 15, France
4 INSERM U 155, 80 rue du Général Leclerc, 94276 Kremlin-Bicêtre, France
5 ACTGene Recherche et Développements, Allée Christophe Colomb, Génopole, 91035 Evry Cedex, France
6 Department of Genetics and Development, Columbia University, College of Physicians and Surgeons, New York, New York 10032, USA
Correspondence: Miroslav Radman, (phone)+33 1 40 61 53 20, (fax)+33 1 40 61 53 20-
Abstract
- Mutation and subsequent recombination events create genetic diversity, which is subjected to natural selection. Bacterial mismatch repair (MMR) deficient mutants, exhibiting high mutation and homeologous recombination rates, are frequently found in natural populations. Therefore, we have explored the possibility that MMR deficiency emerging in nature has left some “imprint” in the sequence of bacterial genomes. Comparative molecular phylogeny of MMR genes from natural Escherichia coli isolates shows that, compared to housekeeping genes, individual functional MMR genes exhibit high sequence mosaicism derived from diverse phylogenetic lineages. This apparent horizontal gene transfer correlates with hyperrecombination phenotype of MMR-deficient mutators. The sequence mosaicism of MMR genes may be a hallmark of a mechanism of adaptive evolution that involves modulation of mutation and recombination rates by recurrent losses and reacquisitions of MMR gene functions.
