The restriction systems McrA and McrB of Escherichia coli K-12 are known to attack DNA containing modified cytosine. In strains lacking both activities, however, we observed that DNA methylated at CG dinucleotides (as is mammalian DNA) was still significantly restricted. We show that this substantial barrier to the acceptance of 5-methylcytosine-containing DNA is attributable to a hitherto unknown activity of the Mrr restriction system. Strikingly, the multiple systems used by this gut inhabitant to determine the fate of invading DNA will all limit genetic exchange with its mammalian host(s), reinforcing the idea that one role of DNA methylation is to serve as a "molecular passport" (E.

Restriction-modification systems can protect bacteria against viral infection.

To understand the role of restriction in regulating gene flow in bacterial populations, we would like to understand the regulation of restriction enzyme activity. Several antirestriction (restriction alleviation) systems are known that reduce the activity of type I restriction enzymes like EcoKI in vivo. Most of these do not act on type II or type Ill enzymes, but little information is available for the unclassified modificationdependent systems, of which there are three in E. coli K-12. Of particular interest are two physiological controls on type I enzymes: EcoKI restriction is reduced 2 to 3 orders of magnitude following DNA damage, and a similar effect is seen constitutively in Dam-cells. We used the behavior of EcoKI as a control for testing the response to UV treatment of the three endogenous modification-dependent restriction systems of K-12, McrA, McrBC, and Mrr. Two of these were also tested for response to Dam status. We find that all four resident restriction systems show reduced activity following UV treatment, but not in a unified fashion; each response was genetically and physiologically distinct. Possible mechanisms are discussed.

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