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Journal of Bacteriology, November 2002, p. 6100-6108, Vol. 184, No. 22
0021-9193/02/$04.00+0     DOI: 10.1128/JB.184.22.6100-6108.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

A DNA Methyltransferase Can Protect the Genome from Postdisturbance Attack by a Restriction-Modification Gene Complex

Noriko Takahashi, Yasuhiro Naito, Naofumi Handa, and Ichizo Kobayashi*

Division of Molecular Biology, Department of Basic Medical Sciences, Institute of Medical Science, University of Tokyo, Shirokanedai, Tokyo 108-8639, Japan

Received 8 February 2002/ Accepted 19 August 2002

In prokaryotic genomes, some DNA methyltransferases form a restriction-modification gene complex, but some others are present by themselves. Dcm gene product, one of these orphan methyltransferases found in Escherichia coli and related bacteria, methylates DNA to generate 5'-CmCWGG just as some of its eukaryotic homologues do. Vsr mismatch repair function of an adjacent gene prevents C-to-T mutagenesis enhanced by this methylation but promotes other types of mutation and likely has affected genome evolution. The reason for the existence of the dcm-vsr gene pair has been unclear. Earlier we found that several restriction-modification gene complexes behave selfishly in that their loss from a cell leads to cell killing through restriction attack on the genome. There is also increasing evidence for their potential mobility. EcoRII restriction-modification gene complex recognizes the same sequence as Dcm, and its methyltransferase is phylogenetically related to Dcm. In the present work, we found that stabilization of maintenance of a plasmid by linkage of EcoRII gene complex, likely through postsegregational cell killing, is diminished by dcm function. Disturbance of EcoRII restriction-modification gene complex led to extensive chromosome degradation and severe loss of cell viability. This cell killing was partially suppressed by chromosomal dcm and completely abolished by dcm expressed from a plasmid. Dcm, therefore, can play the role of a "molecular vaccine" by defending the genome against parasitism by a restriction-modification gene complex.

* Corresponding author. Mailing address: Division of Molecular Biology, Department of Basic Medical Sciences, Institute of Medical Science, University of Tokyo, Shirokanedai, Tokyo 108-8639, Japan. Phone: 81-3-5449-5326. Fax: 81-3-5449-5422. E-mail: ikobaya{at}ims.u-tokyo.ac.jp.

Journal of Bacteriology, November 2002, p. 6100-6108, Vol. 184, No. 22
0021-9193/02/$04.00+0     DOI: 10.1128/JB.184.22.6100-6108.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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