| Preface |
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| Introduction |
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1 | (30) |
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1 | (10) |
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Muller's classification of mutants |
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2 | (7) |
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Modern mutant terminology |
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9 | (1) |
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10 | (1) |
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Dominance and recessivity |
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11 | (3) |
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Dominance and recessivity at the level of the cell |
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12 | (1) |
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Difficulties in applying the terms ``dominant'' and ``recessive'' to sex-linked mutants |
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13 | (1) |
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The genetic utility of dominant and recessive mutants |
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14 | (17) |
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14 | (1) |
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Gallery of model organisms |
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15 | (1) |
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Our favorite organism: Drosophila melanogaster |
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15 | (3) |
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Our second favorite organism: Saccharomyces cerevisiae |
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18 | (1) |
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Our third favorite organism: Caenorhabditis elegans |
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19 | (2) |
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Our new favorite organism: zebrafish |
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21 | (2) |
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23 | (2) |
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25 | (2) |
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27 | (1) |
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28 | (3) |
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31 | (24) |
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Why look for new mutants? |
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32 | (6) |
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Reason 1: To identify genes required for a specific biological process |
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32 | (3) |
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Reason 2: To isolate more mutations in a specific gene of interest |
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35 | (3) |
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Reason 3: To obtain mutations tools for structure--function analysis |
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38 | (1) |
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Reason 4: To isolate mutations in a gene so far identified only by molecular approaches |
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38 | (1) |
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Mutagenesis and mutational mechanisms |
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38 | (8) |
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Method 1: Ionizing radiation (usually X-rays and gamma-rays) |
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39 | (1) |
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Method 2: Chemical mutagens |
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40 | (2) |
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Method 3: Transposons as mutagens |
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42 | (2) |
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Method 4: Targeted gene disruption (a variant on transposon mutagenesis) |
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44 | (2) |
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What phenotype should you screen (or select) for? |
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46 | (1) |
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47 | (8) |
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47 | (1) |
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47 | (1) |
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Keeping too many, keeping too few |
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48 | (1) |
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How many mutants is enough? |
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48 | (2) |
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50 | |
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A screen for embryonic lethal mutations in Drosophila |
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33 | (1) |
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34 | (2) |
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A screen for sex-linked lethal mutations in Drosophila |
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36 | (9) |
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Making phenocopies by RNAi and co-suppression |
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45 | (6) |
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Reviews of mutant isolation schemes and techniques in various organisms |
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51 | (4) |
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55 | (27) |
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The essence of the complementation test |
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55 | (3) |
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Rules for using the complementation test |
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58 | (2) |
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How might the complementation test lie to you? |
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60 | (1) |
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Second-site non-complementation (SSNC) (non-allelic non-complementation) |
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61 | (18) |
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Type 1 SSNC (poisonous interactions): the interaction is allele-specific at both loci |
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62 | (8) |
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Type 2 SSNC (sequestration): the interaction is allele-specific at one locus |
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70 | (6) |
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Type 3 SSNC (combined haplo-insufficiency): the interaction is allele-independent at both loci |
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76 | (1) |
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77 | (2) |
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An extension of second-site non-complementation: dominant enhancers |
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79 | (3) |
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A successful screen for dominant enhancers |
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79 | (2) |
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81 | |
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A more rigorous definition of the complementation test |
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56 | (1) |
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An example of using the complementation test in yeast |
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57 | (1) |
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Transformation rescue is a variant of the complementation test |
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58 | (1) |
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One method for determining whether or not a dominant mutation is an allele of a given gene, or how to make dominants into recessives by pseudo-reversion |
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59 | (3) |
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Pairing-dependent complementation: transvection |
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62 | (5) |
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Synthetic lethality and genetic buffering |
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67 | (15) |
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82 | (25) |
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A basic definition of genetic suppression |
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82 | (1) |
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Intragenic suppression (pseudo-reversion) |
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83 | (5) |
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Intragenic revertants can mediate translational suppression |
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84 | (2) |
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Intragenic suppression as a result of compensatory mutants |
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86 | (2) |
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88 | (1) |
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Transcriptional suppression |
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88 | (2) |
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Suppression at the level of gene expression |
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88 | (1) |
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Suppression of transposon insertion mutants by altering the control of mRNA processing |
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89 | (1) |
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Suppression of nonsense mutants by messenger stabilization in C. elegans |
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89 | (1) |
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Translational suppression |
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90 | (3) |
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Simplicity: tRNA suppressors in E. coli |
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90 | (2) |
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The numerical and functional redundancy of tRNA genes allowing suppressor mutations to be viable |
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92 | (1) |
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Suppression of a frameshift mutation using a mutant tRNA gene |
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93 | (1) |
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Suppressing a nonsense codon using unaltered tRNAs |
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93 | (1) |
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Suppression by post-translational modification |
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93 | (1) |
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Extragenic suppression as a result of protein-protein interaction |
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94 | (6) |
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Searching for suppressors that act by protein-protein interaction in eukaryotes |
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95 | (5) |
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Extragenic suppression as a result of ``lock-and-key'' conformational suppression |
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100 | (1) |
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Suppression without physical interaction |
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100 | (5) |
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101 | (1) |
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``Push me, pull you'' bypass selection by counterbalancing of opposite activities |
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102 | (1) |
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Extra-copy suppression as a form of bypass suppression |
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103 | (2) |
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Suppression of dominant mutations |
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105 | (1) |
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Designing your own screen for suppressor mutations |
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105 | (2) |
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106 | |
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Intragenic suppression of antimorphic mutations that produce a poisonous protein |
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87 | (15) |
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Bypass suppression of a telomere defect in the yeast S. pombe |
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102 | (5) |
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Determining when and where genes function |
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107 | (20) |
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Epistasis: ordering gene function in pathways |
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107 | (11) |
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Ordering gene function in a biosynthetic pathway |
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108 | (1) |
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The use of epistasis in non-biosynthetic pathways: determining if two genes act in the same or different pathways |
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109 | (2) |
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The real value of epistasis analysis is in the dissection of regulatory hierarchies |
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111 | (7) |
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How might an epistasis experiment mislead you? |
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118 | (1) |
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Mosaic analysis: where does a given gene act? |
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118 | (9) |
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Tissure transplantation studies |
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119 | (1) |
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Loss of the unstable ring X chromosome |
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120 | (3) |
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123 | (1) |
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Genetically controllable mitotic recombination: the FLP-FRT system |
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124 | (2) |
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126 | (1) |
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Genetic fine-structure analysis |
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127 | (24) |
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Intragenic mapping (then) |
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127 | (7) |
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The first efforts towards finding structure within a gene |
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127 | (2) |
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The unit of recombination and mutation is the base pair |
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129 | (5) |
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134 | (1) |
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Intragenic complementation meets intragenic recombination: the basis of fine-structure analysis |
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135 | (3) |
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The formal analysis of intragenic complementation |
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136 | (2) |
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An example of fine-structure analysis for a eukaryotic gene encoding a multifunctional protein |
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138 | (1) |
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A genetic and functional dissection of the HIS4 gene in yeast |
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138 | (1) |
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Fine-structure analysis of genes with complex regulatory elements in eukaryotes |
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139 | (3) |
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Genetic and functional dissection of the cut gene in Drosophila |
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139 | (3) |
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Pairing-dependent intragenic complementation |
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142 | (9) |
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Genetic and functional dissection of the yellow gene in Drosophila |
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142 | (1) |
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The influence of the zeste gene on pairing-dependent complementation at the white locus in Drosophila |
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143 | (2) |
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Genetic and functional dissection of BX-C in Drosophila |
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145 | (1) |
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146 | (1) |
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Genetic and functional dissection of the rudimentary gene in Drosophila |
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147 | (4) |
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151 | (49) |
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An introduction to meiosis |
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151 | (9) |
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A cytological description of meiosis |
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158 | (2) |
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A more detailed description of meiotic prophase |
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160 | (1) |
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Crossingover and chiasmata: recombination involves the physical interchange of genetic material and ensures homolog separation |
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160 | (2) |
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The classical analysis of recombination |
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162 | (5) |
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Measuring the frequency of recombination |
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167 | (26) |
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The curious relationship between the frequency of recombination and chiasma frequency (and why it matters) |
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167 | (1) |
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Map lengths and recombination frequency |
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168 | (3) |
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Determining the fraction of bivalents with zero, one, two, or more exchanges (tetrad analysis) |
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171 | (11) |
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Statistical estimation of recombination frequencies (LOD scores) |
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182 | (10) |
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The actual distribution of exchange events |
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192 | (1) |
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Practicalities of mapping |
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193 | (1) |
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The mechanism of recombination |
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193 | (7) |
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193 | (2) |
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195 | (3) |
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The currently accepted mechanism of recombination: the DSBR model |
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198 | (1) |
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199 | |
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The molecular biology of synapsis |
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155 | (1) |
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Do specific chromosomal sites mediate pairing? |
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156 | (7) |
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Crossingover in compound X chromosomes |
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163 | (3) |
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Does any sister chromatid exchange occur during meiosis? |
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166 | (11) |
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Using tetrad analysis to determine linkage |
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177 | (1) |
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Mapping centromeres in fungi with unordered tetrads |
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177 | (23) |
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Meiotic chromosome segregation |
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200 | (19) |
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Types and consequences of failed segregation |
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201 | (1) |
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The origin of spontaneous nondisjunction |
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202 | (2) |
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204 | (9) |
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The isolation and analysis of the S. cerevisiae centromere |
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204 | (3) |
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The isolation and analysis of the Drosophila centromere |
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207 | (6) |
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213 | (6) |
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How chiasmata ensure segregation |
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213 | (1) |
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214 | (4) |
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218 | |
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Identifying genes that encode centromere-binding proteins in yeast |
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206 | (6) |
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The concept of the epigenetic centromere in Drosophila and humans |
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212 | (5) |
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Achiasmate heterologous segregation in Drosophila females |
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217 | (2) |
| Epilogue |
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219 | (1) |
| References |
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220 | (16) |
| Partial author index |
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236 | (2) |
| Subject index |
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238 | |
Other versions by this Author
