{"product_id":"genetic-theory-and-analysis-isbn-9781118086926","title":"Genetic Theory and Analysis","description":"\u003cb\u003eGENETIC THEORY AND ANALYSIS\u003c\/b\u003e \u003cp\u003e\u003cb\u003eUnderstand and apply what drives change of characteristic genetic traits and heredity\u003c\/b\u003e \u003c\/p\u003e\u003cp\u003eGenetics is the study of how traits are passed from parents to their offspring and how the variation in those traits affects the development and health of the organism. Investigating how these traits affect the organism involves a diverse set of approaches and tools, including genetic screens, DNA and RNA sequencing, mapping, and methods to understand the structure and function of proteins. Thus, there is a need for a textbook that provides a broad overview of these methods.  \u003c\/p\u003e\u003cp\u003e\u003ci\u003eGenetic Theory and Analysis\u003c\/i\u003e meets this need by describing key approaches and methods in genetic analysis through a historical lens. Focusing on the five basic principles underlying the field—mutation, complementation, recombination, segregation, and regulation—it identifies the full suite of tests and methodologies available to the geneticist in an age of flourishing genetic and genomic research. This second edition of the text has been updated to reflect recent advances and increase accessibility to advanced undergraduate students. \u003c\/p\u003e\u003cp\u003e\u003ci\u003eGenetic Theory and Analysis, 2nd edition\u003c\/i\u003e readers will also find: \u003c\/p\u003e\u003cul\u003e\n\u003cli\u003eDetailed treatment of subjects including mutagenesis, meiosis, complementation, suppression, and more\u003c\/li\u003e \u003cli\u003eUpdated discussion of epistasis, mosaic analysis, RNAi, genome sequencing, and more\u003c\/li\u003e \u003cli\u003eAppendices discussing model organisms, genetic fine-structure analysis, and tetrad analysis\u003c\/li\u003e\n\u003c\/ul\u003e \u003cp\u003e\u003ci\u003eGenetic Theory and Analysis\u003c\/i\u003e is ideal for both graduate students and advanced undergraduates undertaking courses in genetics, genetic engineering, and computational biology. \u003c\/p\u003e\u003cp\u003ePreface xi\u003c\/p\u003e \u003cp\u003eIntroduction xiii\u003c\/p\u003e \u003cp\u003e\u003cb\u003e1 Mutation 1\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003e1.1 Types of Mutations 1\u003c\/p\u003e \u003cp\u003eMuller’s Classification of Mutants 2\u003c\/p\u003e \u003cp\u003eNullomorphs 2\u003c\/p\u003e \u003cp\u003eHypomorphs 4\u003c\/p\u003e \u003cp\u003eHypermorphs 5\u003c\/p\u003e \u003cp\u003eAntimorphs 6\u003c\/p\u003e \u003cp\u003eNeomorphs 8\u003c\/p\u003e \u003cp\u003eModern Mutant Terminology 10\u003c\/p\u003e \u003cp\u003eLoss-of-Function Mutants 10\u003c\/p\u003e \u003cp\u003eDominant Mutants 10\u003c\/p\u003e \u003cp\u003eGain-of-Function Mutants 11\u003c\/p\u003e \u003cp\u003eSeparation-of-Function Mutants 11\u003c\/p\u003e \u003cp\u003eDNA-Level Terminology 11\u003c\/p\u003e \u003cp\u003eBase-Pair-Substitution Mutants 11\u003c\/p\u003e \u003cp\u003eBase-Pair Insertions or Deletions 12\u003c\/p\u003e \u003cp\u003eChromosomal Aberrations 12\u003c\/p\u003e \u003cp\u003e1.2 Dominance and Recessivity 13\u003c\/p\u003e \u003cp\u003eThe Cellular Meaning of Dominance 13\u003c\/p\u003e \u003cp\u003eThe Cellular Meaning of Recessivity 15\u003c\/p\u003e \u003cp\u003eDifficulties in Applying the Terms Dominant and Recessive to Sex-Linked Mutants 16\u003c\/p\u003e \u003cp\u003eThe Genetic Utility of Dominant and Recessive Mutants 17\u003c\/p\u003e \u003cp\u003e1.3 Summary 17\u003c\/p\u003e \u003cp\u003e References 17\u003c\/p\u003e \u003cp\u003e\u003cb\u003e2 Mutant Hunts 20\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003e2.1 Why Look for New Mutants? 20\u003c\/p\u003e \u003cp\u003eReason 1: To Identify Genes Required for a Specific Biological Process 21\u003c\/p\u003e \u003cp\u003eReason 2: To Isolate more Mutations in a Specific Gene of Interest 31\u003c\/p\u003e \u003cp\u003eReason 3: To Obtain Mutants for a Structure-Function Analysis 32\u003c\/p\u003e \u003cp\u003eReason 4: To Isolate Mutations in a Gene So Far Identified only by Computational Approaches 32\u003c\/p\u003e \u003cp\u003e2.2 Mutagenesis and Mutational Mechanisms 32\u003c\/p\u003e \u003cp\u003eMethod 1: Ionizing Radiation 33\u003c\/p\u003e \u003cp\u003eMethod 2: Chemical Mutagens 33\u003c\/p\u003e \u003cp\u003eAlkylating Agents 34\u003c\/p\u003e \u003cp\u003eCrosslinking Agents 35\u003c\/p\u003e \u003cp\u003eMethod 3: Transposons 35\u003c\/p\u003e \u003cp\u003eIdentifying Where Your Transposon Landed 37\u003c\/p\u003e \u003cp\u003eWhy not Always Screen With TEs? 40\u003c\/p\u003e \u003cp\u003eMethod 4: Targeted Gene Disruption 40\u003c\/p\u003e \u003cp\u003eRNA Interference 40\u003c\/p\u003e \u003cp\u003eCRISPR\/Cas9 41\u003c\/p\u003e \u003cp\u003eTALENs 42\u003c\/p\u003e \u003cp\u003eSo Which Mutagen Should You Use? 43\u003c\/p\u003e \u003cp\u003e2.3 What Phenotype Should You Screen (or Select) for? 44\u003c\/p\u003e \u003cp\u003e2.4 Actually Getting Started 45\u003c\/p\u003e \u003cp\u003eYour Starting Material 45\u003c\/p\u003e \u003cp\u003ePilot Screen 45\u003c\/p\u003e \u003cp\u003eWhat to Keep? 45\u003c\/p\u003e \u003cp\u003eHow many Mutants is Enough? 46\u003c\/p\u003e \u003cp\u003eEstimating the Number of Genes not Represented by Mutants in Your New Collection 46\u003c\/p\u003e \u003cp\u003e2.5 Summary 48\u003c\/p\u003e \u003cp\u003e References 48\u003c\/p\u003e \u003cp\u003e\u003cb\u003e3 Complementation 51\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003e3.1 The Essence of the Complementation Test 51\u003c\/p\u003e \u003cp\u003e3.2 Rules for Using the Complementation Test 55\u003c\/p\u003e \u003cp\u003eThe Complementation Test Can be Done Only When Both Mutants are Fully Recessive 55\u003c\/p\u003e \u003cp\u003eThe Complementation Test Does Not Require that the Two Mutants Have Exactly the Same Phenotype 56\u003c\/p\u003e \u003cp\u003eThe Phenotype of a Compound Heterozygote Can be More Extreme than that of Either Homozygote 56\u003c\/p\u003e \u003cp\u003e3.3 How the Complementation Test Might Lie to You 57\u003c\/p\u003e \u003cp\u003eTwo Mutations in the Same Gene Complement Each Other 57\u003c\/p\u003e \u003cp\u003eA Mutation in One Gene Silences Expression of a Nearby Gene 57\u003c\/p\u003e \u003cp\u003eMutations in Regulatory Elements 59\u003c\/p\u003e \u003cp\u003e3.4 Second-Site Noncomplementation (Nonallelic Noncomplementation) 59\u003c\/p\u003e \u003cp\u003eType 1 SSNC (PoisonousInteractions): The Interaction is Allele Specific at Both Loci 60\u003c\/p\u003e \u003cp\u003eAn Example of Type 1 SSNC Involving the Alpha- and Beta-Tubulin Genes in Yeast 60\u003c\/p\u003e \u003cp\u003eAn Example of Type 1 SSNC Involving the Actin Genes in Yeast 62\u003c\/p\u003e \u003cp\u003eType 2 SSNC (Sequestration): The Interaction is Allele Specific at One Locus 66\u003c\/p\u003e \u003cp\u003eAn Example of Type 2 SSNC Involving the Tubulin Genes in Drosophila 66\u003c\/p\u003e \u003cp\u003eAn Example of Type 2 SSNC in Drosophila that Does Not Involve the Tubulin Genes 69\u003c\/p\u003e \u003cp\u003eAn Example of Type 2 SSNC in the Nematode Caenorhabditis elegans 71\u003c\/p\u003e \u003cp\u003eType 3 SSNC (Combined Haploinsufficiency): The Interaction is Allele-Independent at Both Loci 72\u003c\/p\u003e \u003cp\u003eAn Example of Type 3 SSNC Involving Two Motor Protein Genes in Flies 72\u003c\/p\u003e \u003cp\u003eSummary of SSNC in Model Organisms 72\u003c\/p\u003e \u003cp\u003eSSNC in Humans (Digenic Inheritance) 73\u003c\/p\u003e \u003cp\u003ePushing the Limits: Third-Site Noncomplementation 74\u003c\/p\u003e \u003cp\u003e3.5 An Extension of SSNC: Dominant Enhancers 74\u003c\/p\u003e \u003cp\u003eA Successful Screen for Dominant Enhancers 75\u003c\/p\u003e \u003cp\u003e3.6 Summary 76\u003c\/p\u003e \u003cp\u003e References 77\u003c\/p\u003e \u003cp\u003e\u003cb\u003e4 Meiotic Recombination 81\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003e4.1 An Introduction to Meiosis 81\u003c\/p\u003e \u003cp\u003eA Cytological Description of Meiosis 88\u003c\/p\u003e \u003cp\u003eA More Detailed Description of Meiotic Prophase 89\u003c\/p\u003e \u003cp\u003e4.2 Crossing Over and Chiasmata 92\u003c\/p\u003e \u003cp\u003e4.3 The Classical Analysis of Recombination 93\u003c\/p\u003e \u003cp\u003e4.4 Measuring the Frequency of Recombination 96\u003c\/p\u003e \u003cp\u003eThe Curious Relationship Between the Frequency of Recombination and Chiasma Frequency 97\u003c\/p\u003e \u003cp\u003eMap Lengths and Recombination Frequency 97\u003c\/p\u003e \u003cp\u003eThe Mapping Function 99\u003c\/p\u003e \u003cp\u003eTetrad Analysis 100\u003c\/p\u003e \u003cp\u003eStatistical Estimation of Recombination Frequencies 101\u003c\/p\u003e \u003cp\u003eTwo-Point Linkage Analysis 101\u003c\/p\u003e \u003cp\u003eWhat Constitutes Statistically Significant Evidence for Linkage? 104\u003c\/p\u003e \u003cp\u003eAn Example of LOD Score Analysis 105\u003c\/p\u003e \u003cp\u003eMultipoint Linkage Analysis 105\u003c\/p\u003e \u003cp\u003eLocal Mapping via Haplotype Analysis 106\u003c\/p\u003e \u003cp\u003eThe Endgame 108\u003c\/p\u003e \u003cp\u003eThe Actual Distribution of Exchange Events 109\u003c\/p\u003e \u003cp\u003eThe Centromere Effect 110\u003c\/p\u003e \u003cp\u003eThe Effects of Heterozygosity for Aberration Breakpoints on Recombination 110\u003c\/p\u003e \u003cp\u003ePracticalities of Mapping 110\u003c\/p\u003e \u003cp\u003e4.5 The Mechanism of Recombination 111\u003c\/p\u003e \u003cp\u003eGene Conversion 111\u003c\/p\u003e \u003cp\u003eEarly Models of Recombination 112\u003c\/p\u003e \u003cp\u003eThe Holliday Model 112\u003c\/p\u003e \u003cp\u003eThe Meselson–Radding Model 114\u003c\/p\u003e \u003cp\u003eThe Currently Accepted Mechanism of Recombination: The Double-Strand Break Repair Model 114\u003c\/p\u003e \u003cp\u003eClass I Versus Class II Recombination Events 116\u003c\/p\u003e \u003cp\u003e4.6 Summary 117\u003c\/p\u003e \u003cp\u003eReferences 118\u003c\/p\u003e \u003cp\u003e\u003cb\u003e5 Identifying Homologous Genes 126\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003e5.1 Homology 126\u003c\/p\u003e \u003cp\u003eOrthologs 127\u003c\/p\u003e \u003cp\u003eParalogs 127\u003c\/p\u003e \u003cp\u003eXenologs 128\u003c\/p\u003e \u003cp\u003e5.2 Identifying Sequence Homology 128\u003c\/p\u003e \u003cp\u003eNucleotide–Nucleotide BLAST (blastn) 129\u003c\/p\u003e \u003cp\u003eAn Example Using blastn 129\u003c\/p\u003e \u003cp\u003eTranslated Nucleotide–Protein BLAST (blastx) 131\u003c\/p\u003e \u003cp\u003eAn Example Using blastx 131\u003c\/p\u003e \u003cp\u003eProtein–Protein BLAST (blastp) 132\u003c\/p\u003e \u003cp\u003eAn Example Using blastp 132\u003c\/p\u003e \u003cp\u003eTranslated BLASTx (tblastx) and Translated BLASTn (tblastn) 133\u003c\/p\u003e \u003cp\u003e5.3 How Similar is Similar? 133\u003c\/p\u003e \u003cp\u003e5.4 Summary 134\u003c\/p\u003e \u003cp\u003e References 134\u003c\/p\u003e \u003cp\u003e\u003cb\u003e6 Suppression 136\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003e6.1 Intragenic Suppression 137\u003c\/p\u003e \u003cp\u003eIntragenic Suppression of Loss-of-Function Mutations 137\u003c\/p\u003e \u003cp\u003eIntragenic Suppression of a Frameshift Mutation by the Addition of a Second, Compensatory Frameshift Mutation 138\u003c\/p\u003e \u003cp\u003eIntragenic Suppression of Missense Mutations by the Addition of a Second and Compensatory Missense Mutation 140\u003c\/p\u003e \u003cp\u003eIntragenic Suppression of Antimorphic Mutations that Produce a Poisonous Protein 141\u003c\/p\u003e \u003cp\u003e6.2 Extragenic Suppression 141\u003c\/p\u003e \u003cp\u003e6.3 Transcriptional Suppression 141\u003c\/p\u003e \u003cp\u003eSuppression at the Level of Gene Expression 142\u003c\/p\u003e \u003cp\u003eA CRISPR Screen for Suppression of Inhibitor Resistance in Melanoma 142\u003c\/p\u003e \u003cp\u003eSuppression of Transposon-Insertion Mutants by Altering the Control of mRNA Processing 143\u003c\/p\u003e \u003cp\u003eSuppression of Nonsense Mutants by Messenger Stabilization 143\u003c\/p\u003e \u003cp\u003e6.4 Translational Suppression 144\u003c\/p\u003e \u003cp\u003etRNA-Mediated Nonsense Suppression 144\u003c\/p\u003e \u003cp\u003eThe Numerical and Functional Redundancy of tRNA Genes Allows Suppressor Mutations to be Viable 146\u003c\/p\u003e \u003cp\u003etRNA-Mediated Frameshift Suppression 146\u003c\/p\u003e \u003cp\u003e6.5 Suppression by Post-Translational Modification 147\u003c\/p\u003e \u003cp\u003e6.6 Conformational Suppression: Suppression as a Result of Protein–Protein Interaction 147\u003c\/p\u003e \u003cp\u003eSearching for Suppressors that Act by Protein–Protein Interaction in Eukaryotes 148\u003c\/p\u003e \u003cp\u003eActin and Fimbrin in Yeast 148\u003c\/p\u003e \u003cp\u003eMediator Proteins and RNA Polymerase II in Yeast 150\u003c\/p\u003e \u003cp\u003e“Lock-and-key” Conformational Suppression 152\u003c\/p\u003e \u003cp\u003eSuppression of a Flagellar Motor Mutant in \u003ci\u003eE. coli\u003c\/i\u003e 152\u003c\/p\u003e \u003cp\u003eSuppression of a Mutant Transporter Gene in \u003ci\u003eC. elegans\u003c\/i\u003e 152\u003c\/p\u003e \u003cp\u003eSuppression of a Telomerase Mutant in Humans 153\u003c\/p\u003e \u003cp\u003e6.7 Bypass Suppression: Suppression Without Physical Interaction 154\u003c\/p\u003e \u003cp\u003e“Push me, Pull You” Bypass Suppression 155\u003c\/p\u003e \u003cp\u003eMulticopy Bypass Suppression 156\u003c\/p\u003e \u003cp\u003e6.8 Suppression of Dominant Mutations 157\u003c\/p\u003e \u003cp\u003e6.9 Designing Your Own Screen for Suppressor Mutations 157\u003c\/p\u003e \u003cp\u003e6.10 Summary 158\u003c\/p\u003e \u003cp\u003e References 158\u003c\/p\u003e \u003cp\u003e\u003cb\u003e7 Epistasis Analysis 163\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003e7.1 Ordering Gene Function in Pathways 163\u003c\/p\u003e \u003cp\u003eBiosynthetic Pathways 164\u003c\/p\u003e \u003cp\u003eNonbiosynthetic Pathways 165\u003c\/p\u003e \u003cp\u003e7.2 Dissection of Regulatory Hierarchies 167\u003c\/p\u003e \u003cp\u003eEpistasis Analysis Using Mutants with Opposite Effects on the Phenotype 167\u003c\/p\u003e \u003cp\u003eHierarchies for Sex Determination in Drosophila 169\u003c\/p\u003e \u003cp\u003eEpistasis Analysis Using Mutants with the Same or Similar Effects on the Final Phenotype 170\u003c\/p\u003e \u003cp\u003eUsing Opposite-Acting Conditional Mutants to Order Gene Function by Reciprocal Shift Experiments 170\u003c\/p\u003e \u003cp\u003eUsing a Drug or Agent that Stops the Pathway at a Given Point 170\u003c\/p\u003e \u003cp\u003eExploiting Subtle Phenotypic Differences Exhibited by Mutants that Affect the Same Signal State 172\u003c\/p\u003e \u003cp\u003e7.3 How Might an Epistasis Experiment Mislead You? 172\u003c\/p\u003e \u003cp\u003e7.4 Summary 173\u003c\/p\u003e \u003cp\u003e References 173\u003c\/p\u003e \u003cp\u003e\u003cb\u003e8 Mosaic Analysis 175\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003e8.1 Tissue Transplantation 176\u003c\/p\u003e \u003cp\u003eEarly Tissue Transplantation in Drosophila 176\u003c\/p\u003e \u003cp\u003eTissue Transplantation in Zebrafish 177\u003c\/p\u003e \u003cp\u003e8.2 Mitotic Chromosome Loss 178\u003c\/p\u003e \u003cp\u003eLoss of the Unstable Ring-X Chromosome 179\u003c\/p\u003e \u003cp\u003eOther Mechanisms of Mitotic Chromosome Loss 179\u003c\/p\u003e \u003cp\u003eMosaics Derived from Sex Chromosome Loss in Humans and Mice (Turner Syndrome) 180\u003c\/p\u003e \u003cp\u003e8.3 Mitotic Recombination 181\u003c\/p\u003e \u003cp\u003eGene Knockout Using the FLP\/FRT or Cre-Lox Systems 182\u003c\/p\u003e \u003cp\u003e8.4 Tissue-Specific Gene Expression 184\u003c\/p\u003e \u003cp\u003eGene Knockdown Using RNAi 184\u003c\/p\u003e \u003cp\u003eTissue-Specific Gene Editing Using CRISPR\/Cas9 185\u003c\/p\u003e \u003cp\u003e8.5 Summary 187\u003c\/p\u003e \u003cp\u003eReferences 188\u003c\/p\u003e \u003cp\u003e\u003cb\u003e9 Meiotic Chromosome Segregation 191\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003e9.1 Types and Consequences of Failed Segregation 192\u003c\/p\u003e \u003cp\u003e9.2 The Origin of Spontaneous Nondisjunction 193\u003c\/p\u003e \u003cp\u003eMI Exceptions 194\u003c\/p\u003e \u003cp\u003eMII Exceptions 194\u003c\/p\u003e \u003cp\u003e9.3 The Centromere 195\u003c\/p\u003e \u003cp\u003eThe Isolation and Analysis of the Saccharomyces cerevisiae Centromere 195\u003c\/p\u003e \u003cp\u003eThe Isolation and Analysis of the Drosophila Centromere 198\u003c\/p\u003e \u003cp\u003eThe Concept of the Epigenetic Centromere in Drosophila and Humans 200\u003c\/p\u003e \u003cp\u003eHolocentric Chromosomes 201\u003c\/p\u003e \u003cp\u003e9.4 Chromosome Segregation Mechanisms 202\u003c\/p\u003e \u003cp\u003eChiasmate Chromosome Segregation 202\u003c\/p\u003e \u003cp\u003eSegregation Without Chiasmata (Achiasmate Chromosome Segregation) 203\u003c\/p\u003e \u003cp\u003eAchiasmate Segregation in Drosophila Males 203\u003c\/p\u003e \u003cp\u003eAchiasmate Segregation in D. melanogaster Females 204\u003c\/p\u003e \u003cp\u003eAchiasmate Segregation in S. cerevisiae 205\u003c\/p\u003e \u003cp\u003eAchiasmate Segregation in S. pombe 207\u003c\/p\u003e \u003cp\u003eAchiasmate Segregation in Silkworm Females 207\u003c\/p\u003e \u003cp\u003e9.5 Meiotic Drive 207\u003c\/p\u003e \u003cp\u003eMeiotic Drive Via Spore Killing 207\u003c\/p\u003e \u003cp\u003eAn Example in Schizosaccharomyces pombe 207\u003c\/p\u003e \u003cp\u003eAn Example in D. melanogaster 208\u003c\/p\u003e \u003cp\u003eMeiotic Drive Via Directed Segregation 208\u003c\/p\u003e \u003cp\u003e9.6 Summary 210\u003c\/p\u003e \u003cp\u003eReferences 210\u003c\/p\u003e \u003cp\u003eAppendix A: Model Organisms 215\u003c\/p\u003e \u003cp\u003eAppendix B: Genetic Fine-Structure Analysis 228\u003c\/p\u003e \u003cp\u003eAppendix C: Tetrad Analysis 250\u003c\/p\u003e \u003cp\u003eGlossary 262\u003c\/p\u003e \u003cp\u003eIndex 275\u003c\/p\u003e  \u003cp\u003e\u003cb\u003eDanny E. Miller, MD, PhD\u003c\/b\u003e is an Assistant Professor in the Department of Pediatrics, Division of Genetic Medicine and Laboratory Medicine \u0026amp; Pathology at the University of Washington in Seattle, WA, USA. He is the recipient of the 2017 Larry Sandler Memorial Award, the 2018 Lawrence E. Lamb Prize for Medical Research, and a 2022 National Institutes of Health Director’s Early Independence Award. Dr Miller is a leader in the field of long-read sequencing technology and the use of new technology to evaluate individuals with unsolved genetic disorders. \u003c\/p\u003e\u003cp\u003e\u003cb\u003eAngela L. Miller\u003c\/b\u003e is a Research Coordinator at the University of Washington in Seattle, WA, USA, with a background in journalism, visual communications, and molecular biology. She has published several peer-reviewed papers and has won multiple national awards for her work as a journal art director.  \u003c\/p\u003e\u003cp\u003e\u003cb\u003eR. Scott Hawley, PhD\u003c\/b\u003e is an Investigator at the Stowers Institute for Medical Research, Kansas City, MO, USA. He is a member of the National Academy of Sciences and former President of the Genetics Society of America, with faculty positions at the University of Kansas Medical Center and the University of Missouri-Kansas City. During his distinguished career, Dr. Hawley has mentored hundreds of trainees, received numerous genetics awards, written six textbooks, and published extensively on meiosis.   \u003c\/p\u003e\u003cp\u003e\u003cb\u003eUnderstand and apply what drives change of characteristic genetic traits and heredity\u003c\/b\u003e \u003c\/p\u003e\u003cp\u003eGenetics is the study of how traits are passed from parents to their offspring and how the variation in those traits affects the development and health of the organism. Investigating how these traits affect the organism involves a diverse set of approaches and tools, including genetic screens, DNA and RNA sequencing, mapping, and methods to understand the structure and function of proteins. Thus, there is a need for a textbook that provides a broad overview of these methods.  \u003c\/p\u003e\u003cp\u003e\u003ci\u003eGenetic Theory and Analysis\u003c\/i\u003e meets this need by describing key approaches and methods in genetic analysis through a historical lens. Focusing on the five basic principles underlying the field—mutation, complementation, recombination, segregation, and regulation—it identifies the full suite of tests and methodologies available to the geneticist in an age of flourishing genetic and genomic research. This second edition of the text has been updated to reflect recent advances and increase accessibility to advanced undergraduate students. \u003c\/p\u003e\u003cp\u003e\u003ci\u003eGenetic Theory and Analysis, 2nd edition\u003c\/i\u003e readers will also find: \u003c\/p\u003e\u003cul\u003e\n\u003cli\u003eDetailed treatment of subjects including mutagenesis, meiosis, complementation, suppression, and more\u003c\/li\u003e \u003cli\u003eUpdated discussion of epistasis, mosaic analysis, RNAi, genome sequencing, and more\u003c\/li\u003e \u003cli\u003eAppendices discussing model organisms, genetic fine-structure analysis, and tetrad analysis\u003c\/li\u003e\n\u003c\/ul\u003e \u003cp\u003e\u003ci\u003eGenetic Theory and Analysis\u003c\/i\u003e is ideal for both graduate students and advanced undergraduates undertaking courses in genetics, genetic engineering, and computational biology.\u003c\/p\u003e","brand":"Wiley","offers":[{"title":"Default Title","offer_id":47989278671077,"sku":"NP9781118086926","price":79.0,"currency_code":"USD","in_stock":false}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/1842\/7735\/files\/9781118086926.jpg?v=1761783491","url":"https:\/\/k12savings.com\/es\/products\/genetic-theory-and-analysis-isbn-9781118086926","provider":"K12savings","version":"1.0","type":"link"}