Dual involvement of TFIIH in DNA repair and transcription

The catrier of genetic information, deoxyribonucleic acid (DNA), appears at the macromolecular level as an extremely stable molecule as it is faithfully duplicated and transmitted from mother to daughter cells. At the molecular level, however, DNA is subject to continuous attack, even under physiological conditions and temperatme (1). Such endogenous damage is mainly due to reactivity of the base moiety and not of the sugat'-phosphate backbone. The main lesions introduced are due to hydrolysis, e.g. of the N-glycosidic bond resulting in abasic sites, oxidation reactions, and non-enzymatic alkylation. In contrast to these modifications, DNA damage can also be induced by environmental factors, such as chemicals that are reactive with base groups, or physical agents, sllch as UV or ionizing radiation. Both spontaneous and induced DNA damage can interfere directly with DNA metabolism and result in abnormal cell behavior, cell death, or induction of permanent alterations of the genetic material.