DNA repair deficiency

DNA repair deficiency Arne Klungland1, Hans Krokan2 and Erling Seeberg1 1Department of Molecular Biology, Institute of Medical Microbiology, Uni6ersity of Oslo, The National Hospital, 0027 Oslo, Norway 2UNIGEN Center for Molecular Biology, The Norwegian University of Science and Technology, Trondheim, Norway. Isolation and characterisation of mutant organisms have been crucial for the analysis of molecular cellular processes and for the study of the normal function of specific genes. The ease of producing bacterial (E. coli), yeast (S. cereviciae and S. pombe) and fruit fly (D. melanogaster) mutants are the most important reason for these organisms developing into essential models for molecular biology. Today, the combined efforts of producing defined mutants and studying them by microarray and proteomic tools has taken these studies from “functional genetics” to “functional genomics”. We here describe two specific protocols for addressing functional genomics by studying DNA repair deficiency – connecting the activities of Arne Klungland and Erling Seeberg at The National Hospital/University of Oslo with that of Hans Krokan at UNIGEN, the Norwegian University of Science and Technology, Trondheim. Specific aim 1 Targeting mutator proteins to the nuclear and mitochondria genome. Specific aim 2 Depleting cellular repair capacity for methylated ssDNA and RNA.