Repair of UV-damaged DNA by mammalian cells and Saccharomyces cerevisiae

Curr Opin Genet Dev. 1994 Apr;4(2):212-20. doi: 10.1016/s0959-437x(05)80047-4.

Abstract

Cells use many strategies to repair genomic damage caused by environmental agents and arising from the natural instability of the polynucleotide structure. Nucleotide excision repair is the most versatile DNA repair pathway and is the main defense of mammalian cells against UV-induced DNA damage. Defects in proteins involved in this pathway can lead to inherited disorders (such as xeroderma pigmentosum, Cockayne's syndrome and trichothiodystrophy) that are associated with hypersensitivity to sunlight. Most of the proteins and genes involved in these syndromes have now been identified. Study of UV-sensitive yeast RAD mutants has greatly aided this process and has revealed strong conservation of the components of nucleotide excision repair in eukaryotes. It has recently become clear that some of the proteins involved in the DNA repair process have dual functions and also participate in basal transcription and DNA replication.

Publication types

  • Review

MeSH terms

  • Animals
  • DNA Damage*
  • DNA Helicases / metabolism
  • DNA Repair Enzymes
  • DNA Repair*
  • DNA-Binding Proteins*
  • Endonucleases*
  • Fungal Proteins / metabolism
  • Humans
  • Mammals
  • Proteins / metabolism
  • Saccharomyces cerevisiae / genetics*
  • Saccharomyces cerevisiae / radiation effects
  • Saccharomyces cerevisiae Proteins
  • Transcription, Genetic
  • Ultraviolet Rays*

Substances

  • DNA-Binding Proteins
  • Fungal Proteins
  • Proteins
  • Saccharomyces cerevisiae Proteins
  • ERCC1 protein, human
  • Endonucleases
  • RAD1 protein, S cerevisiae
  • DNA Helicases
  • DNA Repair Enzymes