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    Lewin's genes XII / Jocelyn E. Krebs, University of Alaska, Anchorage, Elliott S. Goldstein, Arizona State University, Stephen T. Kilpatrick, University of Pittsburgh at Johnstown.

    • Title:Lewin's genes XII / Jocelyn E. Krebs, University of Alaska, Anchorage, Elliott S. Goldstein, Arizona State University, Stephen T. Kilpatrick, University of Pittsburgh at Johnstown.
    •    
    • Variant Title:Genes XII
      Lewin's genes 12
      Lewin's genes twelve
    • Author/Creator:Krebs, Jocelyn E., author.
    • Other Contributors/Collections:Goldstein, Elliott S., author.
      Kilpatrick, Stephen T., author.
    • Published/Created:Burlington, MA : Jones & Bartlett Learning, [2018]
      ©2018
    • Holdings

       
    • Library of Congress Subjects:Genetics.
      Genes.
    • Medical Subjects: Genetic Phenomena.
    • Description:xxv, 837 pages : illustrations (chiefly color) ; 29 cm
    • Summary:Long considered the quintessential molecular biology textbook, for decades Lewin's Genes has provided the most modern presentation to this transformative and dynamic science. Now in its twelfth edition, this classic text continues to lead with new information and cutting-edge developments, covering gene structure, sequencing, organization, and expression. Leading scientists provide revisions and updates in their respective areas of study offering readers current research and relevant information on the rapidly changing subjects in molecular biology. No other text offers a broader understanding of this exciting and vital science or does so with higher quality art and illustrations. Lewin's Genes XII continues to be the clear choice for molecular biology and genetics.
    • Notes:Includes index.
      Includes bibliographical references and index.
    • ISBN:9781284104493
      1284104494
    • Contents:Machine generated contents note: pt. I Genes and Chromosomes
      ch. 1 Genes Are DNA and Encode RNAs and Polypeptides / Esther Siegfried
      1.1. Introduction
      1.2. DNA Is the Genetic Material of Bacteria and Viruses
      1.3. DNA Is the Genetic Material of Eukaryotic Cells
      1.4. Polynucleotide Chains Have Nitrogenous Bases Linked to a Sugar-Phosphate Backbone
      1.5. Supercoiling Affects the Structure of DNA
      1.6. DNA Is a Double Helix
      1.7. DNA Replication Is Semiconservative
      1.8. Polymerases Act on Separated DNA Strands at the Replication Fork
      1.9. Genetic Information Can Be Provided by DNA or RNA
      1.10. Nucleic Acids Hybridize by Base Pairing
      1.11. Mutations Change the Sequence of DNA
      1.12. Mutations Can Affect Single Base Pairs or Longer Sequences
      1.13. Effects of Mutations Can Be Reversed
      1.14. Mutations Are Concentrated at Hotspots
      1.15. Many Hotspots Result from Modified Bases
      1.16. Some Hereditary Agents Are Extremely Small
      1.17. Most Genes Encode Polypeptides
      1.18. Mutations in the Same Gene Cannot Complement
      1.19. Mutations May Cause Loss of Function or Gain of Function
      1.20. Locus Can Have Many Different Mutant Alleles
      1.21. Locus Can Have More Than One Wild-Type Allele
      1.22. Recombination Occurs by Physical Exchange of DNA
      1.23. Genetic Code Is Triplet
      1.24. Every Coding Sequence Has Three Possible Reading Frames
      1.25. Bacterial Genes Are Colinear with Their Products
      1.26. Several Processes Are Required to Express the Product of a Gene
      1.27. Proteins Are trans-Acting but Sites on DNA Are c/'s-Acting
      ch. 2 Methods in Molecular Biology and Genetic Engineering
      2.1. Introduction
      2.2. Nucleases
      2.3. Cloning
      2.4. Cloning Vectors Can Be Specialized for Different Purposes
      2.5. Nucleic Acid Detection
      2.6. DNA Separation Techniques
      2.7. DNA Sequencing
      2.8. PCR and RT-PCR
      2.9. Blotting Methods
      2.10. DNA Microarrays
      2.11. Chromatin Immunoprecipitation
      2.12. Gene Knockouts, Transgenics, and Genome Editing
      ch. 3 Interrupted Gene
      3.1. Introduction
      3.2. Interrupted Gene Has Exons and Introns
      3.3. Exon and Intron Base Compositions Differ
      3.4. Organization of Interrupted Genes Can Be Conserved
      3.5. Exon Sequences Under Negative Selection Are Conserved but Introns Vary
      3.6. Exon Sequences Under Positive Selection Vary but Introns Are Conserved
      3.7. Genes Show a Wide Distribution of Sizes Due Primarily to Intron Size and Number Variation
      3.8. Some DNA Sequences Encode More Than One Polypeptide
      3.9. Some Exons Correspond to Protein Functional Domains
      3.10. Members of a Gene Family Have a Common Organization
      3.11. There Are Many Forms of Information in DNA
      3.12. Content of the Genome
      4.1. Introduction
      4.2. Genome Mapping Reveals That Individual Genomes Show Extensive Variation
      4.3. SNPs Can Be Associated with Genetic Disorders
      4.4. Eukaryotic Genomes Contain Nonrepetitive and Repetitive DNA Sequences
      4.5. Eukaryotic Protein-Coding Genes Can Be Identified by the Conservation of Exons and of Genome Organization
      4.6. Some Eukaryotic Organelles Have DNA
      4.7. Organelle Genomes Are Circular DNAs That Encode Organelle Proteins
      4.8. Chloroplast Genome Encodes Many Proteins and RNAs
      4.9. Mitochondria and Chloroplasts Evolved by Endosymbiosis
      ch. 5 Genome Sequences and Evolution
      5.1. Introduction
      5.2. Prokaryotic Gene Numbers Range Over an Order of Magnitude
      5.3. Total Gene Number Is Known for Several Eukaryotes
      5.4. How Many Different Types of Genes Are There?
      5.5. Human Genome Has Fewer Genes Than Originally Expected
      5.6. How Are Genes and Other Sequences Distributed in the Genome?
      5.7. Y Chromosome Has Several Male-Specific Genes
      5.8. How Many Genes Are Essential?
      5.9. About 10,000 Genes Are Expressed at Widely Differing Levels in a Eukaryotic Cell
      5.10. Expressed Gene Number Can Be Measured En Masse
      5.11. DNA Sequences Evolve by Mutation and a Sorting Mechanism
      5.12. Selection Can Be Detected by Measuring Sequence Variation
      5.13. Constant Rate of Sequence Divergence Is a Molecular Clock
      5.14. Rate of Neutral Substitution Can Be Measured from Divergence of Repeated Sequences
      5.15. How Did Interrupted Genes Evolve?
      5.16. Why Are Some Genomes So Large?
      5.17. Morphological Complexity Evolves by Adding New Gene Functions
      5.18. Gene Duplication Contributes to Genome Evolution
      5.19. Globin Clusters Arise by Duplication and Divergence
      8.20. Pseudogenes Have Lost Their Original Functions
      5.21. Genome Duplication Has Played a Role in Plant and Vertebrate Evolution
      5.22. What is the Role of Transposable Elements in Genome Evolution
      5.23. There Can Be Biases in Mutation, Gene Conversion, and Codon Usage
      ch. 6 Clusters and Repeats
      6.1. Introduction
      6.2. Unequal Crossing-Over Rearranges Gene Clusters
      6.3. Genes for rRNA Form Tandem Repeats Including an Invariant Transcription Unit
      6.4. Crossover Fixation Could Maintain Identical Repeats
      6.5. Satellite DNAs Often Lie in Heterochromatin
      6.6. Arthropod Satellites Have Very Short Identical Repeats
      6.7. Mammalian Satellites Consist of Hierarchical Repeats
      6.8. Minisatellites Are Useful for DNA Profiling
      6.9. Chromosomes / Hank W. Bass
      7.1. Introduction
      7.2. Viral Genomes Are Packaged into Their Coats
      7.3. Bacterial Genome Is a Nucleoid with Dynamic Structural Properties
      7.4. Bacterial Genome Is Supercoiled and Has Four Macrodomains
      7.5. Eukaryotic DNA Has Loops and Domains Attached to a Scaffold
      7.6. Specific Sequences Attach DNA to an Interphase Matrix
      7.7. Chromatin Is Divided into Euchromatin and Heterochromatin
      7.8. Chromosomes Have Banding Patterns
      7.9. Lampbrush Chromosomes Are Extended
      7.10. Polytene Chromosomes Form Bands
      7.11. Polytene Chromosomes Expand at Sites of Gene Expression
      7.12. Eukaryotic Chromosome Is a Segregation Device
      7.13. Regional Centromeres Contain a Centromeric Histone H3 Variant and Repetitive DNA
      7.14. Point Centromeres in S, cerevisiae Contain Short, Essential DNA Sequences
      7.15. S. cerevisiae Centromere Binds a Protein Complex
      7.16. Telomeres Have Simple Repeating Sequences
      7.17. Telomeres Seal the Chromosome Ends and Function in Meiotic Chromosome Pairing
      7.18. Telomeres Are Synthesized by a Ribonucleoprotein Enzyme
      7.19. Telomeres Are Essential for Survival
      ch. 8 Chromatin / Craig Peterson
      8.1. Introduction
      8.2. DNA Is Organized in Arrays of Nucleosomes
      8.3. Nucleosome Is the Subunit of All Chromatin
      8.4. Nucleosomes Are Covalently Modified
      8.5. Histone Variants Produce Alternative Nucleosomes
      8.6. DNA Structure Varies on the Nucleosomal Surface
      8.7. Path of Nucleosomes in the Chromatin Fiber
      8.8. Replication of Chromatin Requires Assembly of Nucleosomes
      8.9. Do Nucleosomes Lie at Specific Positions?
      8.10. Nucleosomes Are Displaced and Reassembled During Transcription
      8.11. DNase Sensitivity Detects Changes in Chromatin Structure
      8.12. LCR Can Control a Domain
      8.13. Insulators Define Transcriptionally Independent Domains
      pt. II DNA Replication and Recombination
      ch. 9 Replication Is Connected to the Cell Cycle / Barbara Funnell
      9.1. Introduction
      9.2. Bacterial Replication Is Connected to the Cell Cycle
      9.3. Shape and Spatial Organization of a Bacterium Are Important During Chromosome Segregation and Cell Division
      9.4. Mutations in Division or Segregation Affect Cell Shape
      9.5. FtsZ Is Necessary for Septum Formation
      9.6. Min and noc/slm Genes Regulate the Location of the Septum
      9.7. Partition Involves Separation of the Chromosomes
      9.8. Chromosomal Segregation Might Require Site-Specific Recombination
      9.9. Eukaryotic Growth Factor Signal Transduction Pathway Promotes Entry to S Phase
      9.10. Checkpoint Control for Entry into S Phase: p53, a Guardian of the Checkpoint
      9.11. Checkpoint Control for Entry into S Phase: Rb, a Guardian of the Checkpoint
      ch. 10 Replicon: Initiation of Replication
      10.1. Introduction
      10.2. Origin Usually Initiates Bidirectional Replication
      10.3. Bacterial Genome Is (Usually) a Single Circular Replicon
      10.4. Methylation of the Bacterial Origin Regulates Initiation
      10.5. Initiation: Creating the Replication Forks at the Origin oriC
      10.6. Multiple Mechanisms Exist to Prevent Premature Reinitiation of Replication
      10.7. Archaeal Chromosomes Can Contain Multiple Replicons
      10.8. Each Eukaryotic Chromosome Contains Many Replicons
      10.9. Replication Origins Can Be Isolated in Yeast
      10.10. Licensing Factor Controls Eukaryotic Rereplication
      10.11. Licensing Factor Binds to ORC
      ch. 11 DNA Replication
      11.1. Introduction
      11.2. DNA Polymerases Are the Enzymes That Make DNA
      11.3. DNA Polymerases Have Various Nuclease Activities
      11.4. DNA Polymerases Control the Fidelity of Replication
      11.5. DNA Polymerases Have a Common Structure
      11.6. Two New DNA Strands Have Different Modes of Synthesis
      11.7. Replication Requires a Helicase and a Single-Stranded Binding Protein
      11.8. Priming Is Required to Start DNA Synthesis
      11.9. Coordinating Synthesis of the Lagging and Leading Strands
      11.10. DNA Polymerase Holoenzyme Consists of Subcomplexes
      11.11. Clamp Controls Association of Core Enzyme with DNA
      11.12. Okazaki Fragments Are Linked by Ligase
      Contents note continued: 11.13. Separate Eukaryotic DNA Polymerases Undertake Initiation and Elongation
      11.14. Lesion Bypass Requires Polymerase Replacement
      11.15. Termination of Replication
      ch. 12 Extrachromosomal Replicons
      12.1. Introduction
      12.2. Ends of Linear DNA Are a Problem for Replication
      12.3. Terminal Proteins Enable Initiation at the Ends of Viral DNAs
      12.4. Rolling Circles Produce Multimers of a Replicon
      12.5. Rolling Circles Are Used to Replicate Phage Genomes
      12.6. F Plasmid Is Transferred by Conjugation Between Bacteria
      12.7. Conjugation Transfers Single-Stranded DNA
      12.8. Single-Copy Plasmids Have a Partitioning System
      12.9. Plasmid Incompatibility Is Determined by the Replicon
      12.10. ColE1 Compatibility System Is Controlled by an RNA Regulator
      12.11. How Do Mitochondria Replicate and Segregate?
      12.12. D Loops Maintain Mitochondrial Origins
      12.13. Bacterial Ti Plasmid Causes Crown Gall Disease in Plants
      12.14. T-DNA Carries Genes Required for Infection
      12.15. Transfer of T-DNA Resembles Bacterial Conjugation
      ch. 13 Homologous and Site-Specific Recombination / Samantha Hoot
      13.1. Introduction
      13.2. Homologous Recombination Occurs Between Synapsed Chromosomes in Meiosis
      13.3. Double-Strand Breaks Initiate Recombination
      13.4. Gene Conversion Accounts for Interallelic Recombination
      13.5. Synthesis-Dependent Strand-Annealing Model
      13.6. Single-Strand Annealing Mechanism Functions at Some Double-Strand Breaks
      13.7. Break-Induced Replication Can Repair Double-Strand Breaks
      13.8. Recombining Meiotic Chromosomes Are Connected by the Synaptonemal Complex
      13.9. Synaptonemal Complex Forms After Double-Strand Breaks
      13.10. Pairing and Synaptonemal Complex Formation Are Independent
      13.11. Bacterial RecBCD System Is Stimulated by chi Sequences
      13.12. Strand-Transfer Proteins Catalyze Single-Strand Assimilation
      13.13. Holliday Junctions Must Be Resolved
      13.14. Eukaryotic Genes Involved in Homologous Recombination
      1. End Processing/Presynapsis
      2. Synapsis
      3. DNA Heteroduplex Extension and Branch Migration
      4. Resolution
      13.15. Specialized Recombination Involves Specific Sites
      13.16. Site-Specific Recombination Involves Breakage and Reunion
      13.17. Site-Specific Recombination Resembles Topoisomerase Activity
      13.18. Lambda Recombination Occurs in an Intasome
      13.19. Yeast Can Switch Silent and Active Mating-Type Loci
      13.20. Unidirectional Gene Conversion Is Initiated by the Recipient MAT Locus
      13.21. Antigenic Variation in Trypanosomes Uses Homologous Recombination
      13.22. Recombination Pathways Adapted for Experimental Systems
      ch. 14 Repair Systems
      14.1. Introduction
      14.2. Repair Systems Correct Damage to DNA
      14.3. Excision Repair Systems in E. coli
      14.4. Eukaryotic Nucleotide Excision Repair Pathways
      14.5. Base Excision Repair Systems Require Glycosylases
      14.6. Error-Prone Repair and Translesion Synthesis
      14.7. Controlling the Direction of Mismatch Repair
      14.8. Recombination-Repair Systems in E. coli
      14.9. Recombination Is an Important Mechanism to Recover from Replication Errors
      14.10. Recombination-Repair of Double-Strand Breaks in Eukaryotes
      14.11. Nonhomologous End Joining Also Repairs Double-Strand Breaks
      14.12. DNA Repair in Eukaryotes Occurs in the Context of Chromatin
      14.13. RecA Triggers the SOS System
      ch. 15 Transposable Elements and Retroviruses / Damon Lisch
      15.1. Introduction
      15.2. Insertion Sequences Are Simple Transposition Modules
      15.3. Transposition Occurs by Both Replicative and Nonreplicative Mechanisms
      15.4. Transposons Cause Rearrangement of DNA
      15.5. Replicative Transposition Proceeds Through a Cointegrate
      15.6. Nonreplicative Transposition Proceeds by Breakage and Reunion
      15.7. Transposons Form Superfamilies and Families
      15.8. Role of Transposable Elements in Hybrid Dysgenesis
      15.9. P Elements Are Activated in the Germ line
      15.10. Retrovirus Life Cycle Involves Transposition-Like Events
      15.11. Retroviral Genes Code for Polyproteins
      15.12. Viral DNA Is Generated by Reverse Transcription
      15.13. Viral DNA Integrates into the Chromosome
      15.14. Retroviruses May Transduce Cellular Sequences
      15.15. Retroelements Fall into Three Classes
      15.16. Yeast Ty Elements Resemble Retroviruses
      15.17. Alu Family Has Many Widely Dispersed Members
      15.18. LINEs Use an Endonuclease to Generate a Priming End
      ch. 16 Somatic DNA Recombination and Hypermutation in the Immune System / Paolo Casali
      16.1. Immune System: Innate and Adaptive Immunity
      16.2. Innate Response Utilizes Conserved Recognition Molecules and Signaling Pathways
      16.3. Adaptive Immunity
      16.4. Clonal Selection Amplifies Lymphocytes That Respond to a Given Antigen
      16.5. Ig Genes Are Assembled from Discrete DNA Segments in B Lymphocytes
      16.6. L Chains Are Assembled by a Single Recombination Event
      16.7. H Chains Are Assembled by Two Sequential Recombination Events
      16.8. Recombination Generates Extensive Diversity
      16.9. V(D)J DNA Recombination Relies on RSS and Occurs by Deletion or Inversion
      16.10. Allelic Exclusion Is Triggered by Productive Rearrangements
      16.11. RAG1/RAG2 Catalyze Breakage and Religation of V(D)J Gene Segments
      16.12. B Cell Development in the Bone Marrow: From Common Lymphoid Progenitor to Mature B Cell
      16.13. Class Switch DNA Recombination
      16.14. CSR Involves AID and Elements of the NHEJ Pathway
      16.15. Somatic Hypermutation Generates Additional Diversity and Provides the Substrate for Higher-Affinity Submutants
      16.16. SHM Is Mediated by AID, Ung, Elements of the Mismatch DNA Repair Machinery, and Translesion DNA Synthesis Polymerases
      16.17. Igs Expressed in Avians Are Assembled from Pseudogenes
      16.18. Chromatin Architecture Dynamics of the IgH Locus in V(D) Recombination, CSR, and SHM
      16.19. Epigenetics of V(D)J Recombination, CSR, and SHM
      16.20. B Cell Differentiation Results in Maturation of the Antibody Response and Generation of Long-lived Plasma Cells and Memory B Cells
      16.21. T Cell Receptor Antigen Is Related to the BCR
      16.22. TCR Functions in Conjunction with the MHC
      16.23. MHC Locus Comprises a Cohort of Genes Involved in Immune Recognition
      pt. III Transcription and Posttranscriptional Mechanisms
      ch. 17 Prokaryotic Transcription
      17.1. Introduction
      17.2. Transcription Occurs by Base Pairing in a "Bubble" of Unpaired DNA
      17.3. Transcription Reaction Has Three Stages
      17.4. Bacterial RNA Polymerase Consists of Multiple Subunits
      17.5. RNA Polymerase Holoenzyme Consists of the Core Enzyme and Sigma Factor
      17.6. How Does RNA Polymerase Find Promoter Sequences?
      17.7. Holoenzyme Goes Through Transitions in the Process of Recognizing and Escaping from Promoters
      17.8. Sigma Factor Controls Binding to DNA by Recognizing Specific Sequences in Promoters
      17.9. Promoter Efficiencies Can Be Increased or Decreased by Mutation
      17.10. Multiple Regions in RNA Polymerase Directly Contact Promoter DNA
      17.11. RNA Polymerase
      Promoter and DNA
      Protein Interactions Are the Same for Promoter Recognition and DNA Melting
      17.12. Interactions Between Sigma Factor and Core RNA Polymerase Change During Promoter Escape
      17.13. Model for Enzyme Movement Is Suggested by the Crystal Structure
      17.14. Stalled RNA Polymerase Can Restart
      17.15. Bacterial RNA Polymerase Terminates at Discrete Sites
      17.16. How Does Rho Factor Work?
      17.17. Supercoiling Is an Important Feature of Transcription
      17.18. Phage T7 RNA Polymerase Is a Useful Model System
      17.19. Competition for Sigma Factors Can Regulate Initiation
      17.20. Sigma Factors Can Be Organized into Cascades
      17.21. Sporulation Is Controlled by Sigma Factors
      17.22. Antitermination Can Be a Regulatory Event
      ch. 18 Eukaryotic Transcription
      18.1. Introduction
      18.2. Eukaryotic RNA Polymerases Consist of Many Subunits
      18.3. RNA Polymerase I Has a Bipartite Promoter
      18.4. RNA Polymerase III Uses Downstream and Upstream Promoters
      18.5. Start Point for RNA Polymerase II
      18.6. TBP Is a Universal Factor
      18.7. Basal Apparatus Assembles at the Promoter
      18.8. Initiation Is Followed by Promoter Clearance and Elongation
      18.9. Enhancers Contain Bidirectional Elements That Assist Initiation
      18.10. Enhancers Work by Increasing the Concentration of Activators Near the Promoter
      18.11. Gene Expression Is Associated with Demethylation
      18.12. CpG Islands Are Regulatory Targets
      ch. 19 RNA Splicing and Processing
      19.1. Introduction
      19.2. 5' End of Eukaryotic mRNA Is Capped
      19.3. Nuclear Splice Sites Are Short Sequences
      19.4. Splice Sites Are Read in Pairs
      19.5. Pre-mRNA Splicing Proceeds Through a Lariat
      19.6. snRNAs Are Required for Splicing
      19.7. Commitment of Pre-mRNA to the Splicing Pathway
      19.8. Spliceosome Assembly Pathway
      19.9. Alternative Spliceosome Uses Different snRNPs to Process the Minor Class of Introns
      19.10. Pre-mRNA Splicing Likely Shares the Mechanism with Group II Autocatalytic Introns
      19.11. Splicing Is Temporally and Functionally Coupled with Multiple Steps in Gene Expression
      19.12. Alternative Splicing Is a Rule, Rather Than an Exception, in Multicellular Eukaryotes
      19.13. Splicing Can Be Regulated by Exonic and Intronic Splicing Enhancers and Silencers
      Contents note continued: 19.14. Trans-Splicing Reactions Use Small RNAs
      19.15. 3' Ends of mRNAs Are Generated by Cleavage and Polyadenylation
      19.16. 3' mRNA End Processing Is Critical for Termination of Transcription
      19.17. 3' End Formation of Histone mRNA Requires U7 snRNA
      19.18. tRNA Splicing Involves Cutting and Rejoining in Separate Reactions
      19.19. Unfolded Protein Response Is Related to tRNA Splicing
      19.20. Production of rRNA Requires Cleavage Events and Involves Small RNAs
      ch. 20 mRNA Stability and Localization / Ellen Baker
      20.1. Introduction
      20.2. Messenger RNAs Are Unstable Molecules
      20.3. Eukaryotic mRNAs Exist in the Form of mRNPs from Their Birth to Their Death
      20.4. Prokaryotic mRNA Degradation Involves Multiple Enzymes
      20.5. Most Eukaryotic mRNA Is Degraded via Two Deadenylation-Dependent Pathways
      20.6. Other Degradation Pathways Target Specific mRNAs
      20.7. mRNA-Specific Half-Lives Are Controlled by Sequences or Structures Within the mRNA
      20.8. Newly Synthesized RNAs Are Checked for Defects via a Nuclear Surveillance System
      20.9. Quality Control of mRNA Translation Is Performed by Cytoplasmic Surveillance Systems
      20.10. Translationally Silenced mRNAs Are Sequestered in a Variety of RNA Granules
      20.11. Some Eukaryotic mRNAs Are Localized to Specific Regions of a Cell
      ch. 21 Catalytic RNA / Douglas J. Briant
      21.1. Introduction
      21.2. Group I Introns Undertake Self-Splicing by Transesterification
      21.3. Group I Introns Form a Characteristic Secondary Structure
      21.4. Ribozymes Have Various Catalytic Activities
      21.5. Some Group I Introns Encode Endonucleases That Sponsor Mobility
      21.6. Group II Introns May Encode Multifunction Proteins
      21.7. Some Autosplicing Introns Require Maturases
      21.8. Catalytic Activity of RNase P Is Due to RNA
      21.9. Viroids Have Catalytic Activity
      21.10. RNA Editing Occurs at Individual Bases
      21.11. RNA Editing Can Be Directed by Guide RNAs
      21.12. Protein Splicing Is Autocatalytic
      ch. 22 Translation
      22.1. Introduction
      22.2. Translation Occurs by Initiation, Elongation, and Termination
      22.3. Special Mechanisms Control the Accuracy of Translation
      22.4. Initiation in Bacteria Needs 30S Subunits and Accessory Factors
      22.5. Initiation Involves Base Pairing Between mRNA and rRNA
      22.6. Special Initiator tRNA Starts the Polypeptide Chain
      22.7. Use of fMet-tRNAf Is Controlled by IF-2 and the Ribosome
      22.8. Small Subunits Scan for Initiation Sites on Eukaryotic mRNA
      22.9. Eukaryotes Use a Complex of Many Initiation Factors
      22.10. Elongation Factor Tu Loads Aminoacyl-tRNA into the A Site
      22.11. Polypeptide Chain Is Transferred to Aminoacyl-tRNA
      22.12. Translocation Moves the Ribosome
      22.13. Elongation Factors Bind Alternately to the Ribosome
      22.14. Three Codons Terminate Translation
      22.15. Termination Codons Are Recognized by Protein Factors
      22.16. Ribosomal RNA Is Found Throughout Both Ribosomal Subunits
      22.17. Ribosomes Have Several Active Centers
      22.18. 16S rRNA Plays an Active Role in Translation
      22.19. 23S rRNA Has Peptidyl Transferase Activity
      22.20. Ribosomal Structures Change When the Subunits Come Together
      22.21. Translation Can Be Regulated
      22.22. Cycle of Bacterial Messenger RNA
      ch. 23 Using the Genetic Code
      23.1. Introduction
      23.2. Related Codons Represent Chemically Similar Amino Acids
      23.3. Codon-Anticodon Recognition Involves Wobbling
      23.4. tRNAs Are Processed from Longer Precursors
      23.5. tRNA Contains Modified Bases
      23.6. Modified Bases Affect Anticodon-Codon Pairing
      23.7. Universal Code Has Experienced Sporadic Alterations
      23.8. Novel Amino Acids Can Be Inserted at Certain Stop Codons
      23.9. tRNAs Are Charged with Amino Acids by Aminoacyl-tRNA Synthetases
      23.10. Aminoacyl-tRNA Synthetases Fall into Two Classes
      23.11. Synthetases Use Proofreading to Improve Accuracy
      23.12. Suppressor tRNAs Have Mutated Anticodons That Read New Codons
      23.13. Each Termination Codon Has Nonsense Suppressors
      23.14. Suppressors May Compete with Wild-Type Reading of the Code
      23.15. Ribosome Influences the Accuracy of Translation
      23.16. Frameshifting Occurs at Slippery Sequences
      23.17. Other Recoding Events: Translational Bypassing and the tmRNA Mechanism to Free Stalled Ribosomes
      pt. IV Gene Regulation
      ch. 24 Operon / Lishin Swint-Kruse
      24.1. Introduction
      24.2. Structural Gene Clusters Are Coordinately Controlled
      24.3. lac Operon Is Negative Inducible
      24.4. lac Repressor Is Controlled by a Small-Molecule Inducer
      24.5. c/s-Acting Constitutive Mutations Identify the Operator
      24.6. trans-Acting Mutations Identify the Regulator Gene
      24.7. lac Repressor Is a Tetramer Made of Two Dimers
      24.8. Lac Repressor Binding to the Operator Is Regulated by an Allosteric Change in Conformation
      24.9. lac Repressor Binds to Three Operators and Interacts with RNA Polymerase
      24.10. Operator Competes with Low-Affinity Sites to Bind Repressor
      24.11. lac Operon Has a Second Layer of Control: Catabolite Repression
      24.12. trp Operon Is a Repressible Operon with Three Transcription Units
      24.13. trp Operon Is Also Controlled by Attenuation
      24.14. Attenuation Can Be Controlled by Translation
      24.15. Stringent Control by Stable RNA Transcription
      24.16. r-Protein Synthesis Is Controlled by Autoregulation
      ch. 25 Phage Strategies
      25.1. Introduction
      25.2. Lytic Development Is Divided into Two Periods
      25.3. Lytic Development Is Controlled by a Cascade
      25.4. Two Types of Regulatory Events Control the Lytic Cascade
      25.5. Phage T7 and T4 Genomes Show Functional Clustering
      25.6. Lambda Immediate Early and Delayed Early Genes Are Needed for Both Lysogeny and the Lytic Cycle
      25.7. Lytic Cycle Depends on Antitermination by pN
      25.8. Lysogeny Is Maintained by the Lambda Repressor Protein
      25.9. Lambda Repressor and Its Operators Define the Immunity Region
      25.10. DNA-Binding Form of the Lambda Repressor Is a Dimer
      25.11. Lambda Repressor Uses a Helix-Turn-Helix Motif to Bind DNA
      25.12. Lambda Repressor Dimers Bind Cooperatively to the Operator
      25.13. Lambda Repressor Maintains an Autoregulatory Circuit
      25.14. Cooperative Interactions Increase the Sensitivity of Regulation
      25.15. cII and cIII Genes Are Needed to Establish Lysogeny
      25.16. Poor Promoter Requires cII Protein
      25.17. Lysogeny Requires Several Events
      25.18. Cro Repressor Is Needed for Lytic Infection
      25.19. What Determines the Balance Between Lysogeny and the Lytic Cycle?
      ch. 26 Eukaryotic Transcription Regulation
      26.1. Introduction
      26.2. How Is a Gene Turned On?
      26.3. Mechanism of Action of Activators and Repressors
      26.4. Independent Domains Bind DNA and Activate Transcription
      26.5. Two-Hybrid Assay Detects Protein-Protein Interactions
      26.6. Activators Interact with the Basal Apparatus
      26.7. Many Types of DNA-Binding Domains Have Been Identified
      26.8. Chromatin Remodeling Is an Active Process
      26.9. Nucleosome Organization or Content Can Be Changed at the Promoter
      26.10. Histone Acetylation Is Associated with Transcription Activation
      26.11. Methylation of Histones and DNA Is Connected
      26.12. Promoter Activation Involves Multiple Changes to Chromatin
      26.13. Histone Phosphorylation Affects Chromatin Structure
      26.14. Yeast GAL Genes: A Model for Activation and Repression
      ch. 27 Epigenetics I / Trygve Tollefsbol
      27.1. Introduction
      27.2. Heterochromatin Propagates from a Nucleation Event
      27.3. Heterochromatin Depends on Interactions with Histones
      27.4. Polycomb and Trithorax Are Antagonistic Repressors and Activators
      27.5. CpG Islands Are Subject to Methylation
      27.6. Epigenetic Effects Can Be Inherited
      27.7. Yeast Prions Show Unusual Inheritance
      ch. 28 Epigenetics II / Trygve Tollefsbol
      28.1. Introduction
      28.2. X Chromosomes Undergo Global Changes
      28.3. Chromosome Condensation Is Caused by Condensins
      28.4. DNA Methylation Is Responsible for Imprinting
      28.5. Oppositely Imprinted Genes Can Be Controlled by a Single Center
      28.6. Prions Cause Diseases in Mammals
      ch. 29 Noncoding RNA
      29.1. Introduction
      29.2. Riboswitch Can Alter Its Structure According to Its Environment
      29.3. Noncoding RNAs Can Be Used to Regulate Gene Expression
      ch. 30 Regulatory RNA
      30.1. Introduction
      30.2. Bacteria Contain Regulator RNAs
      30.3. MicroRNAs Are Widespread Regulators in Eukaryotes
      30.4. How Does RNA Interference Work?
      30.5. Heterochromatin Formation Requires MicroRNAs.
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