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Chapter 16

BISC300 Chapter 16: BISC 300 - Study Guide Chapter 16

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Department
Biological Sciences
Course
BISC300
Professor
Cooper Carlton
Semester
Spring

Description
16 Mechanisms of Genetic Variation CHAPTER OVERVIEW This chapter begins with a discussion of mutation and genetic variation and includes molecular mechanisms of mutation and repair. A general discussion of bacterial recombination, plasmids, and transposable elements follows, with examination of the acquisition of genetic information by conjugation, transformation, and transduction. LEARNING OBJECTIVES After studying Dr. Cooper’s Power Point with animations and the links provided here, you should be able to: • Discuss the two causes of mutations and what are the “effects of mutations” (see Table 16.2) - Including point mutations, transition mutations, transversion mutations, etc. - Auxotroph vs prototroph (Figure 16.6 and 16.7) - Describe replica plating and explain how it used to identify mutant phenotypes (or auxotrophs) - How are spontaneous and induced mutations used in the Ames Test to identify potential carcinogens? • Distinguish horizontal gene transfer (HGT) from vertical gene transfer (VGT) - Compare and contrast conjugation, transformation, and transduction (generalized and specialized transduction) and lytic and lysogenic cycles (of transduction) - Who was Fred Griffith and what was his experiment in 1928? http://www.ncbi.nlm.nih.gov/books/NBK22104/ - How did Oswald Avery, Colin McLeod, and Maclyn McCarty improve Dr. Griffith’s experiment? http://www.dnaftb.org/17/animation.html - Described the Hershey Chase experiment https://www.youtube.com/watch?v=X1cd68YkVdM - Who was Bernard Davis and what did his experiment prove? - Mechanisms of Antibiotic-Resistance (Figure 16.31) CHAPTER OUTLINE I. Mutations: Their Chemical Basis and Effects A. Mutation overview 1. A mutation is a stable, heritable change in the genomic nucleotide sequence; this can be a single base change (point mutation), changes of several bases, or larger insertions, deletions, inversions, duplications, and translocations 2. Mutations can arise in two ways: a. Spontaneous mutations arise occasionally in the absence of any added agent b. Induced mutations are the result of exposure to a mutagen (physical or chemical agent) B. Spontaneous mutations 1. Arise occasionally in all cells without exposure to external agents; they are often the result of errors in replication or lesions to the DNA 2. Errors in replication can be due to tautomeric shifts, which cause base substitutions a. Transition mutation—substitution of one purine for another, or of one pyrimidine for another b. Transversion mutation—substitution of a purine for a pyrimidine or vice versa 1 3. Lesions in the structure of DNA; the loss of a nitrogenous base creating an apurinic or apyrimidinic site can cause spontaneous mutations C. Induced mutations 1. Mutations can be induced by agents that damage DNA, alter its chemistry, or interfere with its functioning 2. Base analogs are structurally similar to normal nitrogenous bases and can be incorporated into DNA during replication, but exhibit base-pairing properties different from the bases they replace D. Effects of mutations 1. Forward mutation—a conversion from the most prevalent gene form (wild type) to a mutant form 2. Reversion mutation—a second mutation event that makes the mutant appear to be a wild type again a. Back mutation (true reversion)—conversion of the mutant nucleotide sequence back to the wild-type sequence b. Suppressor mutation—a reestablishment of the wild-type phenotype by a second mutation that overcomes the effect of the first mutation; can be in the same gene or a different gene, but does not restore the original sequence 3. Point mutations affect only one base pair and are more common than large deletions or insertions a. Silent mutations are alterations of the base sequence that do not alter the amino acid sequence of the protein because of code degeneracy b. Missense mutations are alterations of the base sequence that result in the incorporation of a different amino acid in the protein; at the level of protein function, the effect may range from complete loss of activity to no change in activity c. Nonsense mutations are alterations that produce a translation termination codon; this results in premature termination of protein synthesis; location of the mutation within the protein will determine the extent of change in function d. Frameshift mutations are insertions or deletions of one or two base pairs that thereby alter the reading frame of the codons e. Conditional mutations are expressed only under certain environmental conditions f. Biochemical mutations result in changes in the metabolic capabilities of a cell; auxotrophs cannot grow on minimal media because they have lost a biosynthetic capability and require supplements; prototrophs are wild-type organisms that can grow on minimal media g. Resistance mutations result in acquired resistance to some pathogen, chemical, or antibiotic 4. Mutations can also occur in regulatory sequences and in tRNA and rRNA genes; all can give observable phenotypes II. Detection and Isolation of Mutants A. Mutant detection 1. Visual observation of changes in colony characteristics 2. Auxotrophic mutants can be detected by replica plating on media with and without the growth factor required; mutants are those growing with the factor but not without it B. Mutant selection is achieved by finding the environmental condition under which the mutant will grow but the wild type will not (useful for isolating auxotrophic revertants, resistance mutants, and substrate utilization mutations) C. Mutagens and carcinogens 1. Many cancer-causing agents (carcinogens) are also mutagens, therefore tests for mutagenicity can be used as a screen for carcinogenic potential 2. The Ames test is a widely used mutagenicity test; it detects an increase in reversion of special strains of Salmonella typhimurium from histidine auxotrophy to prototrophy after exposure to a potential carcinogen 2 III. C
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