When DNA replication is interrupted in bacteria. a specific inhibitor
(SfiA), a component of the SOS system, is synthesised which transientl
y blocks cell division. This is the prototype, dispensable, cell cycle
checkpoint, essential for maximal survival under a particular stress.
In contrast. no process specifically signalling the termination of ch
romosomal replication to activate the subsequent division event. which
might be termed an essential checkpoint. has yet been demonstrated. I
n E coli. a specific mechanism is apparently required to reactivate re
plication forks blocked by damage. but its molecular basis is unclear.
induction of the stringent response. mediated by RclA via the level o
f ppGpp. presumably to optimise macromolecular synthesis according to
the availability of nutrients. activates a control system which inhibi
ts DNA replication in both E coli and B subtilis. In E toll. this bloc
ks new rounds of initiation Lit oriC. although the mechanism is not cl
ear. Conversely, initiation is not blocked in B subtilis. but replicat
ion is blocked apparently at a number of distinct sites 100-200 kb dow
nstream and either side of oriC. This nutrient-dependent replicating c
heckpoint specifically requires RTP, the chromosomal terminator protei
n, and new evidence indicates that specific RTP binding sites ma be in
volved in this post-initiation control mechanism. A similar post-initi
ation control mechanism appears to block replication reversibly after
premature initiation in B subtilis. indicating that this system may ha
ve a dual function, limiting replication in starvation conditions anti
as a mechanism to compensate for premature initiations.