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. Author manuscript; available in PMC: 2013 Mar 21.
Published in final edited form as: Curr Biol. 2001 Nov 27;11(23):R979–R982. doi: 10.1016/s0960-9822(01)00579-6

Figure 2. Inhibition of late origin firing by the intra-S phase checkpoint could depend either directly or indirectly on Rad53.

Figure 2

In either case, replication complexes (pink ovals) that are slowed or stalled due to DNA damage generate a signal that activates Rad53 (indicated by a star), which then stabilises stalled replication forks. (a) Activated Rad53 also acts to inhibit late origin firing. (b) Activated Rad53 stabilises stalled forks against breakdown, and these stabilised forks generate a separate (Rad53-independent) signal that inhibits late origins. In either case, collapsed forks are proposed to be unable to activate Rad53, so that the fork collapse that occurs in a rad53 mutant would remove the late origin inhibition, leading to late origin activation as observed.