Slide 1Slide 2Slide 3Slide 4Slide 5Slide 6Slide 7Slide 8Slide 9Slide 10Slide 11Slide 12Slide 13Slide 14Slide 15Slide 16Slide 17Slide 18Slide 19Slide 20Slide 21Slide 22Slide 23Slide 24Slide 25Slide 26Slide 27Fig. 14-1Chapter 14: Mutation & repairFig. 14-2Dose-dependent induction of mutation by X-raysFig. 14-3Fig. 14-4Consequences of mutations on RNA and proteinFig. 14-5Normal keto tautomersStandard base pairingFig. 14-5 & 6Normal keto tautomersStandard base pairingRare tautomersAlternative base pairingFig. 14-7 & 8Some analogs increase tautomeric shiftsFig. 14-9Alkylated bases have altered pairing possibilitiesFig. 14-10Classic frameshift mutagensFig. 14-10Classic frameshift mutagensFig. 14-12UV-induced pyrimidine crosslinksFig. 14-13 & 14Potent carcinogenSynthesized by fungus grown on peanutsFig. 14-18Spontaneous mutations by deaminationFig. 14-19Producing mutation “hotspots” at 5-methyl cytosine sitesFig. 14-21Spontaneous mutation byreplication of repeated nucleotide motifs(frameshift mutations)Fig. 14-22Resulting in clustered occurrence of frameshiftsDNA repair systems• Direct repair of lesion• General excision repair• Specific excision repair• ds-DNA end-joining• Post-replication repairFig. 14-25General types of nucleotide repairFig. 14-26Photo-activated thymine dimer repairFig. 14-27Depurination-activatedexcision repair(AP site repair)Fig. 14-28Nucleotide excision repairFig. 14-32Repair of double-strand breaks: nonhomologous end-joining (non-dividing cells)Error-prone repairFig. 14-33Repair of double-strand breaks: homologous recombination (dividing cells)Error-free repairFig.
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