Skip to main content
padlock icon - secure page this page is secure

Free Content An Arabidopsis MLH1 mutant exhibits reproductive defects and reveals a dual role for this gene in mitotic recombination

Download Article:

You have access to the full text article on a website external to Ingenta Connect.

Please click here to view this article on Wiley Online Library.

You may be required to register and activate access on Wiley Online Library before you can obtain the full text. If you have any queries please visit Wiley Online Library


The eukaryotic DNA mismatch repair (MMR) system contributes to maintaining genome integrity and DNA sequence fidelity in at least two important ways: by correcting errors arising during DNA replication, and also by preventing recombination events between divergent sequences. This study aimed to investigate the role of one key MMR gene in recombination. We obtained a mutant line in which the AtMLH1 gene has been disrupted by the insertion of a T-DNA within the coding region. Transcript analysis indicated that no full-length transcript was produced in mutant plants. The loss of a functional AtMLH1 gene led to a significant reduction in fertility in both homozygotes and heterozygotes, and we observed a strong bias against transmission of the mutant allele. To investigate the role of AtMLH1 in mitotic recombination, the mutant was crossed to a series of recombination reporter lines. A strong decrease (72%) in the frequency of homologous recombination was observed in the mutant. However, the decline in recombination due to homeology was less severe in the Atmlh1 mutant than in a wild-type control. These data demonstrate a dual role for AtMLH1 in recombination: it is both required for recombination and acts to limit recombination between diverged sequences.
No References
No Citations
No Supplementary Data
No Article Media
No Metrics

Keywords: DNA mismatch repair; anti-recombination activity; homeologous recombination; homologous recombination; mitotic recombination; segregation bias

Document Type: Research Article

Publication date: August 1, 2007

  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content
Cookie Policy
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more