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Fig. S1. Crt1-repressed transcriptional responses impede survival of replication stress. (A) Deletion of CRT1, but not SML1, bypasses HU lethality of the ccr4Δ dun1Δ strain. The indicated ccr4Δ dun1Δ (MT3772), ccr4Δ dun1Δ crt1Δ (MT3773), ccr4Δ dun1Δ sml1Δ (MT3774) and wild-type (BY4741) strains were tested for HU sensitivity by serial dilution and spotting on indicated concentrations of HU. Plates were incubated for 3 days. (B) Deletion of CRT1 bypasses severe HU lethality of the chk1Δ dun1Δ strain. The indicated ccr4Δ dun1Δ (MT3772), ccr4Δ dun1Δ crt1Δ (MT3773), chk1Δ dun1Δ (MT3788) and chk1Δ dun1Δ crt1Δ (MT3870) strains were streaked on rich media (XY) or media containing 20 mM HU (XY + 20 mM HU) and incubated for 3 days. (C) Overexpression of RNR1 is not sufficient to bypass HU lethality of the ccr4Δ dun1Δ strain. A ccr4Δ dun1Δ (MT3800) strain was transformed with one of pGAP (pBAD054 TRP1, empty vector), pGAP-RNR1 (pBAD070 TRP1, RNR1) or pGAP-RNR3 (pBAD079 TRP1, RNR3). A ccr4Δ dun1Δ crt1Δ (MT3773) strain is shown for comparison. Strains were serially diluted, spotted on media lacking tryptophan (-trp) and containing indicated concentrations of HU and incubated for 3 days.
Fig. S2. The replication-stress-response network. The nodes of the network were defined by genome-wide profiles of HU sensitivity (see Fig. 1B and Table 1) and related genetic analyses from this study. Green lines, chemical (HU)-genetic interactions and CCR4-related genetic interactions (this study) or synthetic lethal genetic interactions (Tong et al., 2001); blue lines, protein interactions detected in large-scale yeast two-hybrid studies (Ito et al., 2001; Uetz et al., 2000); pink lines, protein interactions detected by mass spectrometry (Gavin et al., 2002; Ho et al., 2002). Network was created using Osprey Network Visualization software (Breitkreutz et al., 2003). Node colour is based on default Osprey settings for GO annotation.
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