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

¹ University of Tokyo;
² Noda Institute for Scientific Research

ABSTRACT

Loss of a type II restriction-modification gene complex, such as EcoRI, from a bacterial cell leads to death of its descendant cells through attack by residual restriction enzyme molecules on under-methylated target sites of newly synthesized chromosomes. Through such post-segregational host killing, these gene complexes force their maintenance on their host cells. This finding led to re-discovery of type II restriction-modification systems as selfish mobile elements. The host prokaryote cells were found to cope with such attacks through a variety of means. RecBCD pathway of homologous recombination in Escherichia coli repairs the lethal lesions on the chromosome while it destroys restricted non-self DNA. The recBCD homologs, however, appears very limited in distribution among bacterial genomes, while homologs of RecFOR proteins responsible for another pathway are widespread in eubacteria, just as the restriction-modification systems are. In the present work, therefore, we examined possible contribution of RecFOR pathway in cell survival after loss of a restriction-modification gene complex. A recF mutation reduced the survival in 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 RecBCD enzyme: the resistance to killing seen with recC1002, recC1004, recC2145 and recB2154 is much 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 decreased by recF, recJ or recQ mutation. These results demonstrate that RecFOR pathway of recombination can greatly contribute to resistance to restriction-modification-mediated host killing depending on genetic backgrounds.

³ E-mail: ikobaya{at}ims.u-tokyo.ac.jp