Fig. 4

Sister loci acceleration and coalescence in telophase depends on Rad9 but is independent of Rad52. a Sister telomeres need the DNA damage checkpoint (Rad9 branch) to move to the same cell body and coalesce after DSBs in telophase. FM916 (rad9Δ) was treated like in Fig. 2a. Relative position of cXIIr sister telomeres was categorised as depicted on the left (one representative experiment ± CI95); categories 1, 2 and 3 as defined in Fig. 3a. b The increase in inter sister telomere movement also depends on Rad9. Kinetograms of 2-min movies from 10 randomly selected cells in the previous experiment. The MIM is also displayed within the charts (mean ± s.d., n = 10 cells). Note that the acceleration in interloci movement after phleomycin addition is only one-third of that observed in DDC-proficient cells (compare with Fig. 3c). c Sister telomeres coalescence is independent of a functional HR. FM889 (rad52Δ) was treated like in Fig. 2a. Relative position of cXIIr sister telomeres was categorised as depicted on the left (one representative experiment ± CI95); categories 1, 2 and 3 as defined in Fig. 3a. d Rad52 restrains inter sister telomere movement in telophase. Kinetograms of 2-min movies from 10 randomly selected cells in the previous experiment. The MIM is also displayed within the charts (mean ± s.d., n = 10 cells). Note how MIM is already doubled in the mock treatment when compared with the wild type (Fig. 3c). e Formation of de novo chromatin bridges is independent of Rad52. Samples from the previous experiments were taken and the nuclear mass stained with Hoechst. Nuclear morphology was categorised as followed: 1, binuclear; 2, thin bridge; 3, gross/bulgy bridge (±CI95). f HR repairs DSBs in telophase. Clonogenic survival of strains FM588 (WT) and FM889 (rad52Δ) arrested in G₁, G₂ or telophase before treated with phleomycin (mean ± s.e.m., n = 3 independent experiments). Survival is normalised to a parallel mock-treated culture (reference for 100% survival). Source data are provided as a Source Data file