Repair of simple DNA methylation damage has not been fully understood. Yeast cells have been shown to deal with methylation damage by distinct repair mechanisms. However, the pathways resulting in complete repair of damage and restoration of correct DNA content is not yet clear. ngs1-1, a new mutant sensitive to methyl methanesulfonate (MMS) was isolated in 1986. It was shown not to be allelic to known DNA repair genes at the time. We cloned the NGS1 gene by functional complementation of MMS sensitivity and showed that it is allelic to MRE11, a gene involved in meiotic recombination and repair. Gap repair technique was used to localize the mutation in ngs1-1 mutant. Two mutations were found of which one is a nonsense mutation. The second mutation, though a missense, also confers MMS sensitivity. We are now studying the interaction of these alleles in vivo in terms of MMS sensitivity and cell growth rate. We also cloned the human homologue of the yeast NGS1 gene. Our human sequence is, in most regions, identical to the reported human MRE11. The major difference is that our human clone contains an additional 84 base pairs in the coding region. The human NGS1 does not complement the yeast ngs1*delta* mutant due to sequence or species specific protein-protein interactions. We are now studying the reasons for this lack of complementation.