MBIO

• 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

• tags the parent strand
• methylation directs mut h to bind to the daughter strand only

goes from 5' to 3'

• 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

assay to assess the mutagenic potential of chemical compounds. faster reversion means higher mutagenic potential

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

methyltransferase remvoes a methyl group from a molecule and transfers it onto its tail

• 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

incorporation of adenine across from 8 oxoguanine (right) during DNA replication causes a G:C base pair to be mutated to T:A.

• 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

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.