Mutation, Recombination, and Incipient Speciation of Bacteria in the Laboratory

Mutations in the DNA mismatch repair system increase mutation and recombination. They may thereby promote the genetic divergence that underlies speciation, after which the reacquisition of a functional repair system may sustain that divergence by creating a barrier to recombination. We tested severa...

Full description

Saved in:
Bibliographic Details
Published inProceedings of the National Academy of Sciences - PNAS Vol. 96; no. 13; pp. 7348 - 7351
Main Authors Vulić, Marin, Lenski, Richard E., Radman, Miroslav
Format Journal Article
LanguageEnglish
Published United States National Academy of Sciences of the United States of America 22.06.1999
National Acad Sciences
National Academy of Sciences
The National Academy of Sciences
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Mutations in the DNA mismatch repair system increase mutation and recombination. They may thereby promote the genetic divergence that underlies speciation, after which the reacquisition of a functional repair system may sustain that divergence by creating a barrier to recombination. We tested several lines of Escherichia coli, derived from a common ancestor and evolved for 20,000 generations, for their recombination ability. Some lines, but not others, had become mismatch repair-defective mutators during experimental evolution, providing different opportunities for DNA sequence divergence. We knocked out the repair system in lines that had retained this function, and we restored function to those lines that had become defective. We then estimated recombination rates in various crosses between these repair-deficient and -proficient strains. The effect of the mismatch repair system on recombination was greatest in those lines that had evolved nonfunctional repair, indicating they had undergone more sequence divergence and, consequently, were more sensitive to the recombination-inhibiting effect of a functional repair system. These results demonstrate the establishment of an incipient genetic barrier between formerly identical lines, and they support a model in which the mismatch repair system can influence speciation dynamics through its simultaneous effects on mutation and recombination.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
To whom reprint requests should be addressed at present address: Department of Microbiology and Molecular Genetics, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115. e-mail: mvulic@hms.harvard.edu.
Present address: Faculté de Médicine Necker–Enfants Malades INSERM E9916, Université de Paris-V, 156 rue de Vaugirard, 75730 Paris Cedex 15, France.
Edited by John Maynard Smith, University of Sussex, Brighton, United Kingdom, and approved May 4, 1999
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.96.13.7348