Nucleotide excision repair. II: From yeast to mammals.
An intricate network of repair systems safeguards the integrity of genetic material, by eliminating DNA lesions induced by numerous environmental and endogenous genotoxic agents. Nucleotide excision repair (NER) is one of the most versatile DNA repair systems. Deficiencies in this process give rise to the classical human DNA repair disorders xeroderma pigmentosum (XP) and Cockayne's syndrome (CS), and to a recently recognized disease called PIBIDS, a photosensitive form of the brittle hair disorder trichothiodystrophy. This is the second of a two-part review on NER. Part I (in the previous issue of TIG) concentrated on the main characteristics of the NER pathway of E. coli and yeast. Part II compares the mammalian and yeast systems, and attempts to integrate current knowledge on the eukaryotic pathway to suggest an outline for the reaction mechanism.
Hoeijmakers
J H
JH
Department of Cell Biology and Genetics, Erasmus University, Rotterdam, The Netherlands.
D000818:Animals; D003057:Cockayne Syndrome / Q000235:genetics; D006224:Cricetinae; D004260:DNA Repair / Q000235:genetics*; D005800:Genes, Fungal; D006801:Humans; D008322:Mammals / Q000235:genetics*; D010787:Photosensitivity Disorders / Q000235:genetics; D012441:Saccharomyces cerevisiae / Q000235:genetics*; D014983:Xeroderma Pigmentosum / Q000235:genetics