Fig. 8: Model for the effect of H3K4 methylation in relieving transcription-replication conflicts.

a Upon HU-stress, the S-phase checkpoint kinase Rad53 is activated to stabilize replication fork integrity; meanwhile, transcription-deposited H3K4 methylation acts as a series of speed bumps to decelerate fork progression, relieving transcription-replication conflicts to reduce DNA damage at highly transcribed regions. b Conversely, without H3K4 methylation, rapid fork movement aggravates transcription-replication conflicts (red explosion drawing) and leads to error-prone replication and genome instability.