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. Author manuscript; available in PMC: 2014 Sep 1.
Published in final edited form as: DNA Repair (Amst). 2013 Jul 6;12(9):751–760. doi: 10.1016/j.dnarep.2013.06.003

FIG. 4.

FIG. 4

Ddc2-Rad53 fusion protein does not rescue sgs1Δ exo1Δ double mutants from DDR defect. (A) Viability assay for G1 cells expressing Ddc2-Rad53. Cells transformed with Ddc2-Rad53 or empty vector (pRS316) were arrested in αF then mock-treated or exposed to DNA damaging agents (IR or UV). Ten-fold serial dilutions were spotted on solid media and then exposed to irradiation. All plates were incubated at 30°C for 2 days. (B) IR-induced activation of RNR3 promoter transcription in G1 cells expressing Ddc2-Rad53. Overnight cultures were diluted and then arrested in G1 using αF. Cells were Mock treated or exposed to 300 Gy IR. 45 mins after irradiation, protein samples were extracted and β-galactosidase activity measured by spectroscopy. A measurement of the β-galactosidase activity is shown. Error bars represent standard deviation from three independent experiments (*, P<0.05).