Working model of the mechanism of tachpyridine-induced G₂ arrest. Tachpyridine activates ATR (and possibly ATM), which phosphorylates p53 on serine 15, followed by phosphorylation of CHK1 and CHK2. The CHK kinases then signal G₂ arrest through phosphorylation of key substrates important for G₂ to M progression. Signaling events not required for G₂ arrest are indicated by gray dashed lines.