1. mismatch repair
    • Mut S scans dna (looks for sites of methylation)
    • identifies mutation
    • atp opens up mut s
    • mut h make a nick
    • mut l binds
    • exonuclease removes dna
    • dna polymerase corrects
  2. DAM methylation
    • tags the parent strand
    • methylation directs mut h to bind to the daughter strand only
  3. mismatch repair directionality
    goes from 5' to 3'
  4. types of DNA damage
    • deamination: the removal of an amine group (NH3) from the addition of a water
    • depurination: removal of a purine from the addition of water
    • alkylation: the transfer of an alkyl group from one molecule to another
    • oxidation: the addition of oxygen to a compound with a loss of electrons
    • UV damage (thymine dimers): Ultraviolet light induces the formation of covalent linkages by reactions localized on the C=C double bonds
    • base analogs: a purine or pyrimidine base that differs slightly in structure from the normal nitrogenous bases
    • intercalating agents: inclusion of a molecule between two molecules
  5. the ames test
    assay to assess the mutagenic potential of chemical compounds. faster reversion means higher mutagenic potential
  6. photo reactivation
    DNA repair enzymes that repair damage caused by exposure to ultraviolet light. they break certain types of pyrimidine dimers that arise when a pair of thymine or cytosinebases on the same strand of DNA become covalently linked
  7. removal of alkylation
    methyltransferase remvoes a methyl group from a molecule and transfers it onto its tail
  8. base exicion pathway
    • damaged base
    • Removal of the incorrect base by an appropriate DNA N-glycosylase to create an AP siteap endonuclease creastes a nick
    • Nicking of the damaged DNA strand by AP endonuclease upstream of the AP site, thus creating a 3'-OH terminus adjacent to the AP site
    • Extension of the 3'-OH terminus by a DNA polymerase, accompanied by excision of the AP site
  9. OxoG:A repair
    incorporation of adenine across from 8 oxoguanine (right) during DNA replication causes a G:C base pair to be mutated to T:A.
  10. nucleotide excision pathway
    • recognition of a DNA lesion
    • separation of the double helix at the DNA lesion site
    • single strand incision at both sides of the lesion
    • excision of the lesion-containing single stranded DNA fragment
    • DNA repair synthesis to replace the gap
    • ligation of the remaining single stranded nick
  11. transcription coupled dna repair
  12. non homolgous end joining
  13. translesion dna synthesis
    Once the lesion is generated in the DNA, the replication machine stall, now either the lesion is repaired or bypass by specialized polymerases. Proliferating cell nuclear antigen (PCNA) plays instrumental role in translesion synthesis (TLS) by providing the platform to TLS polymerases for efficient bypass of the lesions. In normal scenario DNA is replicated by polymerase delta bound to PCNA and other accessory proteins. At the site of lesion, replication is stalled and PCNA is ubiquitinated by RAD6/RAD18 proteins dependant manner and polymerase delta is replaced by pol h.
  14. homologous recombination
  15. single strand breaks
  16. holiday junction formation
  17. branch migration
  18. dna processing by Rec BCD
  19. Rec A protein
  20. Ruv AB complex in recombination
  21. Ruv C
  22. homologous recombination in eukaryotes
  23. co localization of Rad51 and Dmc1
  24. Mating type switching
Card Set
lectures 4-6