Genetic theory and analysis: finding meaning in a genome
Gespeichert in:
| Beteiligte Personen: | , , |
|---|---|
| Format: | Buch |
| Sprache: | Englisch |
| Veröffentlicht: |
Hoboken, New Jersey
Wiley
[2023]
|
| Ausgabe: | Second edition |
| Schlagwörter: | |
| Links: | http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=034823128&sequence=000001&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA |
| Abstract: | "Since the first edition of this book was published, there have been many advances in genetics and genomics that are captured in this edition--to a point. Many genetics textbooks are geared either toward introductory undergraduate and/or medical students, providing primary information and touching on well-known historical milestones in biology. The spirit of this book has always been to consolidate and discuss key genetic studies from the literature then link those to current ideas in genetics. The goal is to provide a solid foundation to understand how genetic analysis was done in the past and link it to how it is being used today. For example, in the past, an investigator may have done a technically challenging screen to identify genes of interest in a biological pathway, while today, new sequencing technology could be used to identify mutations more easily in genes in that same pathway. Real-world clinical examples highlight the importance and relevance of the topics discussed to human disease. Finally, this edition will also include a glossary to make the content more accessible to undergraduates"-- |
| Beschreibung: | 1. Auflage unter dem Titel: Advanced genetic analysis: finding meaning in a genome (2003) |
| Umfang: | xiv, 284 Seiten Illustrationen, Diagramme |
| ISBN: | 9781118086926 |
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| 520 | 3 | |a "Since the first edition of this book was published, there have been many advances in genetics and genomics that are captured in this edition--to a point. Many genetics textbooks are geared either toward introductory undergraduate and/or medical students, providing primary information and touching on well-known historical milestones in biology. The spirit of this book has always been to consolidate and discuss key genetic studies from the literature then link those to current ideas in genetics. The goal is to provide a solid foundation to understand how genetic analysis was done in the past and link it to how it is being used today. For example, in the past, an investigator may have done a technically challenging screen to identify genes of interest in a biological pathway, while today, new sequencing technology could be used to identify mutations more easily in genes in that same pathway. Real-world clinical examples highlight the importance and relevance of the topics discussed to human disease. Finally, this edition will also include a glossary to make the content more accessible to undergraduates"-- | |
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| adam_text | Contents Preface xi Introduction xiii Mutation 1 Types of Mutations 1 Muller’s Classification of Mutants 2 Nullomorphs 2 Hypomorphs 4 Hypermorphs 5 Antimorphs 6 Neomorphs 8 Modem Mutant Terminology 10 Loss-of-Function Mutants 10 Dominant Mutants 10 Gain-of-Function Mutants 11 Separation-of-Function Mutants 11 DNA-Level Terminology 11 Base-Pair-Substitution Mutants 11 Base-Pair Insertions or Deletions 12 Chromosomal Aberrations 12 1.2 Dominance and Recessivity 13 The Cellular Meaning of Dominance 13 The Cellular Meaning of Recessivity 15 Difficulties in Applying the Terms Dominant and Recessive to Sex-Linked Mutants The Genetic Utility of Dominant and Recessive Mutants 17 1.3 Summary 17 References 17 1 1.1 2 2.1 Mutant Hunts 20 Why Look for New Mutants? 20 Reason 1: To Identify Genes Required for a Specific Biological Process 21 Reason 2: To Isolate more Mutations in a Specific Gene of Interest 31 Reason 3: To Obtain Mutants for a Structure-Function Analysis 32 Reason 4: To Isolate Mutations in a Gene So Far Identified only by Computational Approaches 32 16
vi J Contents Mutagenesis and Mutational Mechanisms 32 Method 1: Ionizing Radiation 33 Method 2: Chemical Mutagens 33 Alkylating Agents 34 Crosslinking Agents 35 Method 3: Transposons 35 Identifying Where Your Transposon Landed 37 Why not Always Screen With TEs? 40 Method 4: Targeted Gene Disruption 40 RNA Interference 40 CRISPR/Cas9 41 TALENs 42 So Which Mutagen Should You Use? 43 2.3 What Phenotype Should You Screen (or Select) for? 44 2.4 Actually Getting Started 45 Your Starting Material 45 Pilot Screen 45 What to Keep? 45 How many Mutants is Enough? 46 Estimating the Number of Genes not Represented by Mutants in Your New Collection 46 2.5 Summary 48 References 48 2.2 3 Complementation 51 3.1 The Essence of the Complementation Test 51 3.2 Rules for Using the Complementation Test 55 The Complementation Test Can be Done Only When Both Mutants are Fully Recessive 55 The Complementation Test Does Not Require that the Two Mutants Have Exactly the Same Phenotype 56 The Phenotype of a Compound Heterozygote Can be More Extreme than that of Either Homozygote 56 3.3 How the Complementation Test Might Lie to You 57 Two Mutations in the Same Gene Complement Each Other 57 A Mutation in One Gene Silences Expression of a Nearby Gene 57 Mutations in Regulatory Elements 59 3.4 Second-Site Noncomplementation (Nonallelic Noncomplementation) 59 Type 1SSNC (Poisonous Interactions): The Interaction is Allele Specific at Both Loci 60 An Example of Type 1 SSNC Involving the Alpha- and Beta-Tubulin Genes in Yeast 60 An Example of Type 1 SSNC Involving the Actin Genes in Yeast 62 Type 2 SSNC
(Sequestration): The Interaction is Allele Specific at One Locus 66 An Example of Type 2 SSNC Involving the Tubulin Genes in Drosophila 66 An Example of Type 2 SSNC in Drosophila that Does Not Involve the Tubulin Genes 69
Contents I vîi An Example of Type 2 SSNC in the Nematode Caenorhabditis elegans 71 Type 3 SSNC (Combined Haploinsufficiency): The Interaction is Allele-Independent at Both Loci 72 An Example of Type 3 SSNC Involving Two Motor Protein Genes in Flics 72 Summary of SSNC in Model Organisms 72 SSNC in Humans (Digenic Inheritance) 73 Pushing the Limits: Third-Site Noncomplementation 74 3.5 An Extension of SSNC: Dominant Enhancers 74 A Successful Screen for Dominant Enhancers 75 3.6 Summary 76 References 77 4 4.1 4.2 4.3 4.4 4.5 4.6 Meiotic Recombination 81 An Introduction to Meiosis 81 A Cytological Description of Meiosis 88 A More Detailed Description of Meiotic Prophase 89 Crossing Over and Chiasmata 92 The Classical Analysis of Recombination 93 Measuring the Frequency of Recombination 96 The Curious Relationship Between the Frequency of Recombination and Chiasma Frequency 97 Map Lengths and Recombination Frequency 97 The Mapping Function 99 Tetrad Analysis 100 Statistical Estimation of Recombination Frequencies 101 Two-Point Linkage Analysis 101 What Constitutes Statistically Significant Evidence for Linkage? 104 An Example of LOD Score Analysis 105 Multipoint Linkage Analysis 105 Local Mapping via Haplotype Analysis 106 The Endgame 108 The Actual Distribution of Exchange Events 109 The Centromere Effect 110 The Effects of Heterozygosity for Aberration Breakpoints on Recombination 110 Practicalities of Mapping 110 The Mechanism of Recombination 111 Gene Conversion 111 Early Models of Recombination 112 The Holliday Model 112 The Meselson-Radding Model 114 The Currently Accepted
Mechanism of Recombination: The Double-Strand Break Repair Model 114 Class I Versus Class II Recombination Events 116 Summary 117 References 118
νϋί I Contents Identifying Homologous Genes 126 Homology 126 Orthologs 127 Paralogs 127 Xenologs 128 5.2 Identifying Sequence Homology 128 Nucleotide-Nucleotide BLAST (blastn) 129 An Example Using blastn 129 Translated Nucleotide-Protein BLAST (blastx) 131 An Example Using blastx 131 Protein-Protein BLAST (blastp) 132 An Example Using blastp 132 Translated BLASTx (tblastx) and Translated BLASTn (tblastn) 133 5.3 How Similar is Similar? 133 5.4 Summary 134 References 134 5 5.1 6 6.1 6.2 6.3 6.4 6.5 6.6 136 Intragenic Suppression 137 Intragenic Suppression of Loss-of-Function Mutations 137 Intragenic Suppression of a Frameshift Mutation by the Addition of a Second, Compensatory Frameshift Mutation 138 Intragenic Suppression of Missense Mutations by the Addition of a Second and Compensatory Missense Mutation 140 Intragenic Suppression of Antimorphic Mutations that Produce a Poisonous Protein 141 Extragenic Suppression 141 Transcriptional Suppression 141 Suppression at the Level of Gene Expression 142 A CRISPR Screen for Suppression of Inhibitor Resistance in Melanoma 142 Suppression of Transposon-Insertion Mutants by Altering the Control of mRNA Processing 143 Suppression of Nonsense Mutants by Messenger Stabilization 143 Translational Suppression 144 tRNA-Mediated Nonsense Suppression 144 The Numerical and Functional Redundancy of tRNA Genes Allows Suppressor Mutations to be Viable 146 tRNA-Mediated Frameshift Suppression 146 Suppression by Post-Translational Modification 147 Conformational Suppression: Suppression as a Result of Protein-Protein Interaction 147 Searching for
Suppressors that Act by Protein-Protein Interaction in Eukaryotes 148 Actin and Fimbrin in Yeast 148 Mediator Proteins and RNA Polymerase II in Yeast 150 “Lock-and-key” Conformational Suppression 152 Suppression of a Flagellar Motor Mutant in E. coli 152 Suppression of a Mutant Transporter Gene in C. elegans 152 Suppression of a Telomerase Mutant in Humans 153 Suppression
Contents J ix Bypass Suppression: Suppression Without Physical Interaction “Push me, Pull You” Bypass Suppression 155 Multicopy Bypass Suppression 156 6.8 Suppression of Dominant Mutations 157 6.9 Designing Your Own Screen for Suppressor Mutations 157 6.10 Summary 158 References 158 6.7 7 7.1 7.2 7.3 7.4 154 163 Ordering Gene Function in Pathways 163 Biosynthetic Pathways 164 Nonbiosynthetic Pathways 165 Dissection of Regulatory Hierarchies 167 Epistasis Analysis Using Mutants with Opposite Effects on the Phenotype 167 Hierarchies for Sex Determination in Drosophila 169 Epistasis Analysis Using Mutants with the Same or Similar Effects on the Final Phenotype 170 Using Opposite-Acting Conditional Mutants to Order Gene Function by Reciprocal Shift Experiments 170 Using a Drug or Agent that Stops the Pathway at a Given Point 170 Exploiting Subtle Phenotypic Differences Exhibited by Mutants that Affect the Same Signal State 172 How Might an Epistasis Experiment Mislead You? 172 Summary 173 References 173 Epistasis Analysis Mosaic Analysis 175 Tissue Transplantation 176 Early Tissue Transplantation in Drosophila 176 Tissue Transplantation in Zebrafish 177 8.2 Mitotic Chromosome Loss 178 Loss of the Unstable Ring-X Chromosome 179 Other Mechanisms of Mitotic Chromosome Loss 179 Mosaics Derived from Sex Chromosome Loss in Humans and Mice (Turner Syndrome) 180 8.3 Mitotic Recombination 181 Gene Knockout Using the FLP/FRT or Cre-Lox Systems 182 8.4 Tissue-Specific Gene Expression 184 Gene Knockdown Using RNAi 184 Tissue-Specific Gene Editing Using CRISPR/Cas9 185 8.5 Summary 187
References 188 8 8.1 Meiotic Chromosome Segregation 191 9.1 Types and Consequences of Failed Segregation 192 9.2 The Origin of Spontaneous Nondisjunction 193 9
XI Contents MI Exceptions 194 Mil Exceptions 194 9.3 The Centromere 195 The Isolation and Analysis of the Saccharomyces cerevisiae Centromere 195 The Isolation and Analysis of the Drosophila Centromere 198 The Concept of the Epigenetic Centromere in Drosophila and Humans 200 Holocentric Chromosomes 201 9.4 Chromosome Segregation Mechanisms 202 Chiasmate Chromosome Segregation 202 Segregation Without Chiasmata (Achiasmate Chromosome Segregation) 203 Achiasmate Segregation in Drosophila Males 203 Achiasmate Segregation in D. melanogaster Females 204 Achiasmate Segregation in S. cerevisiae 205 Achiasmate Segregation in 5. pombe 207 Achiasmate Segregation in Silkworm Females 207 9.5 Meiotic Drive 207 Meiotic Drive Via Spore Killing 207 An Example in Schizosaccharomyces pombe 207 An Example in D. melanogaster 208 Meiotic Drive Via Directed Segregation 208 9.6 Summary 210 References 210 Appendix A: Model Organisms 215 Appendix B: Genetic Fine-Structure Analysis Appendix C: Tetrad Analysis 250 Glossary 262 Index 275 228
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| indexdate | 2024-12-20T20:13:14Z |
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| isbn | 9781118086926 |
| language | English |
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| physical | xiv, 284 Seiten Illustrationen, Diagramme |
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| spellingShingle | Miller, Danny E. Miller, Angela L. Hawley, R. Scott Genetic theory and analysis finding meaning in a genome Genanalyse (DE-588)4200230-8 gnd |
| subject_GND | (DE-588)4200230-8 |
| title | Genetic theory and analysis finding meaning in a genome |
| title_alt | Advanced genetic analysis |
| title_auth | Genetic theory and analysis finding meaning in a genome |
| title_exact_search | Genetic theory and analysis finding meaning in a genome |
| title_full | Genetic theory and analysis finding meaning in a genome Danny E. Miller, Angela L. Miller, R. Scott Hawley |
| title_fullStr | Genetic theory and analysis finding meaning in a genome Danny E. Miller, Angela L. Miller, R. Scott Hawley |
| title_full_unstemmed | Genetic theory and analysis finding meaning in a genome Danny E. Miller, Angela L. Miller, R. Scott Hawley |
| title_short | Genetic theory and analysis |
| title_sort | genetic theory and analysis finding meaning in a genome |
| title_sub | finding meaning in a genome |
| topic | Genanalyse (DE-588)4200230-8 gnd |
| topic_facet | Genanalyse |
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| Signatur: |
1002 BIO 180 2024 B 815(2) Lageplan |
|---|---|
| Exemplar 1 | Ausleihbar Am Standort |