原核生物DNA的修复机制
原核生物DNA的修复机制
DNADAMAGEDNA is constantly subjected to injuries inflictedby external agents such as UV light or cigarettesmoke, by intracellular by-products of metabolismsuch as reactive oxygen species, or by spontaneousdecay. DNA lesions interfere with replication andwith transcription and if left in DNA can causemutation, malfunction, and cell death. Thesedeleterious effects are usually prevented by DNArepair mechanisms, which remove the damagednucleotide and restore the original DNA sequence
DNA DAMAGE ⚫ DNA is constantly subjected to injuries inflicted by external agents such as UV light or cigarette smoke, by intracellular by-products of metabolism such as reactive oxygen species, or by spontaneous decay. DNA lesions interfere with replication and with transcription and if left in DNA can cause mutation, malfunction, and cell death. These deleterious effects are usually prevented by DNA repair mechanisms, which remove the damaged nucleotide and restore the original DNA sequence
DNAREPAIRMECHISMMismatch repair MMRNERNucleotide excission repairGGRGlobalrepairgenomicTCRTranscription coupledrepairBERBase excission repairRecombinational repairDBSDoublestrand break repairSOS translesionreplicationerror-freeerror-phoneO-methylguonine-DNA methyltransferaesMGMT
DNA REPAIR MECHISM ⚫ Mismatch repair MMR ⚫ Nucleotide excission repair NER ⚫ Global genomic repair GGR ⚫ Transcription coupled repair TCR ⚫ Base excission repair BER ⚫ Recombinational repair ⚫ Doublestrand break repair DBS ⚫ SOS translesion replication error-free errorphone ⚫ O6 -methyl guonine-DNA methyltransferaes MGMT
DNA Damage Control by NovelDNA Polymerases: TranslesionReplication and MutagenesisPublished,JBCPapers inPress,May22,2001DOI10.1074/jbc.R100019200Zvi LivnehFrom the Department of Biological ChemistryWeizmannInstituteof Science,Rehovot76100.Israel
Roles of DNA polymerases V and I in SOS-inducederror-prone and error-free repair inEscherichia coliPhuong Pham*, Savithri Rangarajan*,Roger Woodgate,and MyroF.Goodman