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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.
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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.
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Variant Title:Genes XII
Lewin's genes 12
Lewin's genes twelve
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Author/Creator:Krebs, Jocelyn E., author.
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Other Contributors/Collections:Goldstein, Elliott S., author.
Kilpatrick, Stephen T., author.
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Published/Created:Burlington, MA : Jones & Bartlett Learning, [2018]
©2018
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Holdings
Holdings Record Display
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Location:WOODWARD LIBRARY stacksWhere is this?
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Call Number: QU500 .K92L 2018
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Number of Items:1
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Status:c.1 On loan - Due on 06-12-2024
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Location:WOODWARD LIBRARY stacksWhere is this?
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Library of Congress Subjects:Genetics.
Genes.
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Medical Subjects: Genetic Phenomena.
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Description:xxv, 837 pages : illustrations (chiefly color) ; 29 cm
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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.
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Notes:Includes index.
Includes bibliographical references and index.
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ISBN:9781284104493
1284104494
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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.