The DNA adenine methyltransferase of Escherichia coli methylates adenines at GATC sequences. The mutant deficient in this methylase has no apparent deficiency in the cell division process in spite of the absence of both synchrony in initiations of chromosomal DNA replication and sequestration of replication origin (oriC) at hemimethylated state. However, the dam mutant cannot resume cell division after hyperosmotic shock differing from the wild-type strain. This inhibition is not provoked by induction of the cell division inhibitor, SfiA protein. Although the FtsZ protein is present in the dam mutant in a reduced amount compared to wild-type, the quantitative difference of this protein is not the main reason of division arrest provoked by hyperosmotic shock. This observation supports the idea of oriC-membrane interaction playing a role both in chromosome partitioning and cell division as predicted by replicon theory.