Figure 5
From: A cell cycle-independent mode of the Rad9-Dpb11 interaction is induced by DNA damage
Lack of damage-induced Rad9 S/TP phosphorylation does not directly affect checkpoint signalling or DNA end resection. (A,B) The rad9-AA mutant – in contrast to the rad9Δ mutant – does not induce hyper-resection in G1-arrested cells. A site-specific DSB was induced at the MAT locus using galactose-induced HO in G1-arrested cells. DNA end resection is shown by ChIP against RPA at 0, 2, 4 and 6 h after HO induction within 0–80 kb distance to the DSB. (A) Resection was measured in WT, rad9Δ, yku70Δ and rad9Δ yku70Δ strains. FACS profiles in Fig. S5A. (B) as (A), but with WT, rad9-AA, yku70Δ and rad9-AA yku70Δ strains. FACS profiles in Fig. S5B. (C) The rad9-AA mutant does not induce apparent defects in checkpoint activation in G1 even in the background of the ddc1-T602A mutation. Hyperphosphorylation of Rad53 induced by different concentrations of phleomycin added to the growth medium is used as measure of checkpoint activation. FACS profiles in Fig. S5C.
