Hegde V, McFarlane R J, Taylor E M, Price C
Department of Molecular Biology and Biotechnology, University of Sheffield, U.K.
Mol Gen Genet. 1996 Jun 24;251(4):483-92. doi: 10.1007/BF02172377.
We have recently demonstrated that Schizosaccharomyces pombe cells treated with the nucleoside analogue 5-azacytidine (5-azaC) require previously characterised G2 checkpoint mechanisms for survival. Here we present a survey of known DNA repair mutations which defines those genes required for survival in the presence of 5-azaC. Using a combination of single-mutant and epistasis analyses we find that the excision, mismatch and recombinational repair pathways are all required in some degree for the repair of 5-azaC-mediated DNA damage. There are distinct differences in the epistatic interactions of several of the repair mutations with respect to 5-azaC-mediated DNA damage relative to UV-mediated DNA damage.