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. 2004 Jul;24(14):6215–6230. doi: 10.1128/MCB.24.14.6215-6230.2004

FIG. 9.

FIG. 9.

Genetic interactions of histone H2A-AQE mutations with mutations in DNA damage checkpoint genes. (A to D) Survival of cells carrying various combinations of mutations in H2A (hta1-S129A and hta2-S128A, indicated as hta1 hta2), checkpoint (rad3Δ, crb2Δ, and chk1Δ), and DNA repair (rqh1Δ) genes after exposure to the indicated dose of IR. Strains used were rad3Δ (TMN2947), rad3Δ hta1 hta2 (TMN3299), rad3Δ crb2Δ (TMN3300), crb2Δ (TMN2941), crb2Δ hta1 hta2 (TMN3297), chk1Δ (TMN2943), chk1Δ hta1 hta2 (TMN3298), crb2Δ chk1Δ (TMN3305), crb2Δ chk1Δ hta1 hta2 (TMN3308), rqh1Δ (TMN3301), rqh1Δ hta1 hta2 (TMN3302), crb2Δ rqh1Δ (TMN3303), crb2Δ rqh1Δ hta1 hta2 (TMN3307), chk1Δ rqh1Δ (TMN3304), chk1Δ rqh1Δ hta1 hta2 (TMN3422), and crb2Δ chk1Δ rqh1Δ (TMN3306). Error bars indicate standard deviations from at least three experiments. (E) Model depicting the γ-H2A-dependent modulation of Crb2 functions involving Chk1 and Rqh1, based on genetic interactions of IR sensitivity. (F) Model for the mammalian γ-H2AX-dependent DNA damage response. A speculative negative role of the γ-H2AX in DNA repair is indicated as a gray inhibitory sign covered with question marks.