CHAPTER 15 Mutation Repair and Recombination Copyright 2008

CHAPTER 15 Mutation, Repair, and Recombination Copyright 2008 © W H Freeman and Company

CHAPTER OUTLINE 15. 1 The phenotypic consequences of DNA mutations 15. 2 The molecular basis of spontaneous mutations 15. 3 The molecular basis of induced mutations 15. 6 Cancer: an important phenotypic consequence of mutation

Consequences of point mutations within genes Figure 15 -2

Consequences of point mutations within genes Figure 15 -2 part 1

Consequences of point mutations within genes Figure 15 -2 part 2

Consequences of point mutations within genes Figure 15 -2 part 3

Unnumbered figure pg 515

Point mutations can alter m. RNA splicing Figure 15 -3

Consequences of point mutations on gene products Figure 15 -4

“Fluctuation test” hypotheses Figure 15 -5

Replica plating Figure 15 -6

Replica plating demonstrates the presence of mutants before selection Figure 15 -7

Bases may take on rare tautomeric forms prone to mismatch Figure 15 -8 a

Bases may take on rare tautomeric forms prone to mismatch Figure 15 -8 b

Tautomeric shifts in DNA bases may cause mutations Figure 15 -9

Indel mutations result in frameshifts Figure 15 -10

Unnumbered figure pg 522

Unnumbered figure pg 523

Oxygen radicals can damage DNA Figure 15 -11

Trinucleotide repeats in the FMR-1 gene hinder transcription Figure 15 -12

Slipped mispairing causes repeat expansion Figure 15 -13

Alternative pairings for 5 -bromouracil (5 -BU) Figure 15 -14

Alternative pairings for 2 -aminopurine Figure 15 -15

Unnumbered figure pg 527

Alkylation-induced specific mispairings Figure 15 -16

Intercalating agents Figure 15 -17

Intercalating agents Figure 15 -17 a

Intercalating agents Figure 15 -17 b

UV-light-generated photoproducts Figure 15 -18

Aflatoxin B 1 forms a bulky addition product Figure 15 -19

The Ames test reveals mutagenic compounds Figure 15 -20

Ames test of aflatoxin B 1 mutagenicity Figure 15 -21

Normal cells and cells transformed by an oncogene Figure 15 -35

The ras oncogene is continuously active Figure 15 -36

The ras oncogene is continuously active Figure 15 -36 a

The ras oncogene is continuously active Figure 15 -36 b

Table 15 -1