A unified model explaining the preferential repair of active over inactive genes and of the transcribed over the nontranscribed strand

Abstract

DNA lesions are removed more efficiently and at higher rates from active than from inactive genes and from the transcribed compared with the nontranscribed strand. A unifying model is presented explaining the heterogeneity in DNA repair activities through the genome in terms of chromatin structure, nuclear matrix anchorage, transcription factor binding, protein phosphorylation mechanisms, and the linkage of repair mechanisms to other nuclear functions including transcription and replication. Transcription factors, preferentially assembled into complexes on the regulatory regions of active but not of inactive genes are proposed to contribute to repair differences.