The DNA adenine methyltransferase of Escherichia coli methylates adeni
nes at GATC sequences. The mutant deficient in this methylase has no a
pparent deficiency in the cell division process in spite of the absenc
e of both synchrony in initiations of chromosomal DNA replication and
sequestration of replication origin (oriC) at hemimethylated state. Ho
wever, the dam mutant cannot resume cell division after hyperosmotic s
hock differing from the wild-type strain. This inhibition is not provo
ked by induction of the cell division inhibitor, SfiA protein. Althoug
h the FtsZ protein is present in the dam mutant in a reduced amount co
mpared to wild-type, the quantitative difference of this protein is no
t the main reason of division arrest provoked by hyperosmotic shock. T
his observation supports the Idea of oriC-membrane interaction playing
a role both in chromosome partitioning and cell division as predicted
by replicon theory.