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This Article Full Text Full Text (PDF) All Versions of this Article: mic.0.026401-0v1 155/7/2320    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Google Scholar Articles by Handa, N. Articles by Kobayashi, I. PubMed PubMed Citation Articles by Handa, N. Articles by Kobayashi, I. Agricola Articles by Handa, N. Articles by Kobayashi, I.

Contribution of RecFOR machinery of homologous recombination to cell survival after loss of a restriction–modification gene complex

Asao Ichige^1,2,

¹ Laboratory of Social Genome Sciences, Department of Medical Genome Sciences, Graduate School of Frontier Sciences, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan
² Institute of Medical Science, University of Tokyo, Shirokanedai, Tokyo 108-8639, Japan
³ Graduate Program in Biophysics and Biochemistry, Graduate School of Science, University of Tokyo, Japan

Loss of a type II restriction–modification (RM) gene complex, such as EcoRI, from a bacterial cell leads to death of its descendent cells through attack by residual restriction enzymes on undermethylated target sites of newly synthesized chromosomes. Through such post-segregational host killing, these gene complexes impose their maintenance on their host cells. This finding led to the rediscovery of type II RM systems as selfish mobile elements. The host prokaryote cells were found to cope with such attacks through a variety of means. The RecBCD pathway of homologous recombination in Escherichia coli repairs the lethal lesions on the chromosome, whilst it destroys restricted non-self DNA. recBCD homologues, however, appear very limited in distribution among bacterial genomes, whereas homologues of the RecFOR proteins, responsible for another pathway, are widespread in eubacteria, just like the RM systems. In the present work, therefore, we examined the possible contribution of the RecFOR pathway to cell survival after loss of an RM gene complex. A recF mutation reduced survival in an otherwise rec-positive background and, more severely, in a recBC sbcBC background. We also found that its effect is prominent in the presence of specific non-null mutant forms of the RecBCD enzyme: the resistance to killing seen with recC1002, recC1004, recC2145 and recB2154 is severely reduced to the level of a null recBC allele when combined with a recF, recO or recR mutant allele. Such resistance was also dependent on RecJ and RecQ functions. UV resistance of these non-null recBCD mutants is also reduced by recF, recJ or recQ mutation. These results demonstrate that the RecFOR pathway of recombination can contribute greatly to resistance to RM-mediated host killing, depending on the genetic background.

Correspondence
Ichizo Kobayashi
ikobaya{at}ims.u-tokyo.ac.jp

Present address: Noda Institute for Scientific Research, 399 Noda, Noda-shi, Chiba prefecture, 278-0037 Japan.