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Muscle disorders

Keams-Sayre syndrome, 3:53, 3:53 mitochondrial diseases, 3:54 roundworms to study, 4:63 spinal muscular atrophy, 3:124 See also Muscular dystrophy Muscles actin proteins, 2:29 cell shape, 1:109 gene therapy, 2:78 healthy tissue, 3:84 MyoD protein, 2:65 myoglobin proteins, 2:29 Muscular dystrophy (MD), 3:83-87 Becker (BMD), 3:84 characteristics, 3:83 drug therapies, 3:87 Emery-Dreifuss, 3:125 gene therapy, 2:75, 2:77-78,

2:80, 2:81, 3:86-87 limb-girdle (LGMD), 3:86 prenatal genetic testing, 3:186 Muscular dystrophy, Duchenne (DMD)

causative gene, 3:84-85, 3:100 characteristics, 3:84, 3:85 gene therapy, 2:73 genetic testing, 2:168, 3:85, 3:184 inheritance patterns, 1:213, 2:191-192, 2:202, 2:203, 3:78, 3:83-84 mutation rates, 3:100 Muscular dystrophy, myotonic causative gene, 3:86 characteristics, 3:85-86, 4:150 genetic testing, 3:86 inheritance patterns, 3:85, 4:150 pleiotropic effects, 3:153-154 as triplet repeat disease, 2:42, 3:86, 4:11, 4:150 Mustard gas, as mutagen, 3:90 Mutable genes, 3:21 Mutagenesis, 3:89-93 defined, 4:182

induced, research role, 3:89,

3:90-92, 3:97-98 site-directed, 3:91 in zebrafish, 4:182-183 See also Carcinogenesis Mutagens, 3:87-89

3:87, 3:92 base analogs, 3:87, 3:88, 3:90-91 base-altering, 3:88 defined, 1:19, 3:89 distinguished from carcinogens, 3:87

impact on tumor suppressor genes, 4:152-153 and increased mutation rates,

3:99-100 intercalating agents, 3:88 promutagens, 1:20 See also Carcinogens; Teratogens Mutagens, specific aflatoxins, 1:244-245 asbestos, 3:89

benzo[a]pyrene, 1:244-245,

1:245, 3:89 5-bromo-deoxyuridine, 3:87 dimethylsulfate, 1:242 ethidium bromide, 3:88 fTee radicals, 3:88, 3:89 industrial toxins, 1:77, 1:119, 1:123, 1:210, 1:214, 1:239, 1:242

light and high-energy particles, 3:88

mustard gas, 3:90 nitrite preservatives, 3:88 smoke, 1:77, 1:92, 1:98, 1:100, 1:179-180, 1:242, 3:88, 3:89 transposons, 3:91, 3:97 See also Radiation, ionizing; Radiation, ultraviolet Mutation analysis as gene discovery tool, 2:59 pedigrees as tools, 3:140 Mutation fixation, 1:241-242, 1:241 Mutation rates, 3:98-101 amino acids, 3:94 breast cancer genes, 1:91-92 deamination errors, 1:241 DNA repair gene, 1:242 Duchenne muscular dystrophy,

3:100 eggs vs. sperm, 2:192 factors that influence, 3:99-100 hemophilia, 2:143 HIV, 2:155, 2:157 human genome, 3:99, 3:177 Huntington's disease, 3:100 hydrolysis errors, 1:240 mammals, 1:240, 3:101 measuring, 3:80, 3:99 molecular clocks, 3:63, 3:67,

3:98, 3:100-101 point mutations, 2:27 reduced by antioxidants, 3:89, 3:100 Mutations, 3:93-98

alkylation errors, 1:240, 1:242 apoptosis studies, 1:32-33 back, 3:65, 3:100

and cell cycle regulation,

1:107-108 cloning implications, 1:160 and complex traits, 1:177-181 conservative, 2:157 de novo, 1:120

deamination errors, 1:240-242, 1:240

defined, 1:92, 2:21, 3:63, 4:17 distinguished from polymorphisms, 2:126 distinguished from SNPs, 2:118 and divergence from common ancestry, 3:63, 3:65, 3:167-168, 4:178-179 DNA libraries of, 2:122 and DNA repair function, 1:230 enzyme defects, 3:38 exogenous and endogenous, 1:242

in extranuclear genes, 2:194, 2:198

gene expression role, 2:54,

2:65-66 genetic analysis role, 2:43 in germ-line cells, 3:93, 3:99 in Hardy-Weinberg model, 2:134 hydrolysis errors, 1:240, 1:240 impact on protein structure, 1:53 of maize, 3:9-10, 3:9 missense, 2:127, 3:153 in mitochondrial DNA, 3:42,

3:51, 3:53-54 Muller's hypotheses, 3:80-81 neutral, overlapping genes and, 3:136

in noncoding regions, 3:65,

3:82-83, 3:93, 3:99 nonsense, 2:127, 3:153 organism's tolerance of,

2:157-158, 4:67-68 outcrossing and, 1:35 oxidation errors, 1:240, 1:242 phenotype manifestations, 1:35,

1:75, 1:155, 1:156-157 premutations, 2:40-42 in pseudogenes, 2:29-30,

3:209-212 rarity of, 3:90 reverse, 1:19-20 selective advantages, 3:94 silent, 2:127, 2:157, 3:93, 3:96, 3:99

of sperm, 3:99, 4:25 splice junction, 4:101 spontaneous, 1:97, 3:90, 3:100,

4:75, 4:153 transition, 3:95

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