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. 2020 May 29;16(5):e1008816. doi: 10.1371/journal.pgen.1008816

Fig 4. Under conditions of telomere instability, MUS81 is required for growth and viability in the presence of replication fork-stalling agents.

Fig 4

(A) Western blot using antibodies against the DNA damage repair kinase Rad53. Treatment of cells with 0.002% methyl methanesulfonate (MMS) was used as a positive control to activate the DNA damage response resulting in Rad53 phosphorylation as observed by a molecular weight shift. (B) Growth and viability of freshly derived haploid spores (~35 generations) was assessed using chronic exposure to increasing concentrations of methyl methanesulfonate (MMS) and hydroxyurea (HU). Average relative viability are plotted with one standard of error (n = 6). The strains were generated by sporulation of WDHY2961. (C) Growth and viability of various endonuclease mutants was assessed in the presence and absence of functional telomere capping protein Cdc13. Cells were chronically exposed to low doses of replication fork stalling agents, 0.005% methyl methanesulfonate (MMS), 10 mM hydroxyurea (HU) or no additions as control. Cells were incubated at permissive (24°C) and semi-permissive (27°C) temperatures for two to four days. Catalytic mutant, mus81-D414,415A, is represented as mus81-dd. Strains used are as follows: Wild type (W303-RAD5, MAT α), mus81-dd (WDHY2835), mus81Δ (WDHY1858), yen1Δ (WDHY2755), rad1Δ (WDHY3106), slx1Δ (WDHY3148), cdc13-1 (WDHY3086), cdc13-1 mus81-dd (WDHY3052), cdc13-1 mus81Δ (WDHY3058), cdc13-1 yen1Δ (WDHY3056), cdc13-1 rad1Δ (WDHY3054), and cdc13-1 slx1Δ (WDHY3112).