UC Davis

Strains of Arabidopsis thaliana that lack a DNA glycosylase to recognize and remove 7,8-dihydro-8-oxoguanine from their DNA are expected to be compromised in their ability to deal with this highly mutagenic base, which is formed in the presence of reactive oxygen species (ROS). We have identified two strains, one containing a Ds insertion in an exon of the gene that codes for oxoguanine glycosylase and one containing a T-DNA insertion in the gene that codes for formamidopyrimidine glycosylase (both EC 3.2.2.23), and have crossed them to produce the double mutant. The homozygous mutant strains showed no phenotypic difference from the wild type in growth, development or reproductive potential under either normal conditions or conditions known to induce the formation of ROS. The lack of phenotype may be ascribed to the redundant nature of the base excision repair pathway in Arabidopsis. Longer multigenerational studies may be needed to determine the quantitative selective advantage of individual DNA glycosylase genes.