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PART Ⅰ Genes and Chromosomes1

Chapter 1 Genes Are DNA and Encode RNAs and Polypeptides&Edited by Esther Siegfried2

1.1 Introduction3

1.2 DNA Is the Genetic Material of Bacteria and Viruses4

1.3 DNA Is the Genetic Material of Eukaryotic Cells6

1.4 Polynucleotide Chains Have Nitrogenous Bases Linked to a Sugar-Phosphate Backbone6

1.5 Supercoiling Affects the Structure of DNA7

1.6 DNA Is a Double Helix9

1.7 DNA Replication Is Semiconservative11

1.8 Polymerases Act on Separated DNA Strands at the Replication Fork12

1.9 Genetic Information Can Be Provided by DNA or RNA13

1.10 Nucleic Acids Hybridize by Base Pairing15

1.11 Mutations Change the Sequence of DNA16

1.12 Mutations Can Affect Single Base Pairs or Longer Sequences17

1.13 The Effects of Mutations Can Be Reversed18

1.14 Mutations Are Concentrated at Hotspots19

1.15 Many Hotspots Result from Modified Bases19

1.16 Some Hereditary Agents Are Extremely Small20

1.17 Most Genes Encode Polypeptides21

1.18 Mutations in the Same Gene Cannot Complement22

1.19 Mutations May Cause Loss of Function or Gain of Function23

1.20 A Locus Can Have Many Different Mutant Alleles24

1.21 A Locus Can Have More Than One Wild-Type Allele25

1.22 Recombination Occurs by Physical Exchange of DNA25

1.23 The Genetic Code Is Triplet27

1.24 Every Coding Sequence Has Three Possible Reading Frames29

1.25 Bacterial Genes Are Colinear with Their Products29

1.26 Several Processes Are Required to Express the Product of a Gene30

1.27 Proteins Are trans-Acting but Sites on DNAArecis-Acting31

Chapter 2 Methods in Molecular Biology and Genetic Engineering35

2.1Introduction35

2.2 Nucleases36

2.3Cloning38

2.4 Cloning Vectors Can Be Specialized for Different Purposes40

2.5 Nucleic Acid Detection43

2.6 DNA Separation Techniques45

2.7 DNA Sequencing48

2.8 PCR and RT-PCR50

2.9 Blotting Methods55

2.10 DNA Microarrays58

2.11 Chromatin Immunoprecipitation61

2.12 Gene Knockouts，Transgenics，and Genome Editing62

Chapter 3 The Interrupted Gene71

3.1 Introduction71

3.2 An Interrupted Gene Has Exons and Introns72

3.3 Exon and Intron Base Compositions Differ73

3.4 Organization of Interrupted Genes Can Be Conserved73

3.5 Exon Sequences Under Negative Selection Are Conserved but Introns Vary74

3.6 Exon Sequences Under Positive Selection Vary but Introns Are Conserved75

3.7 Genes Show a Wide Distribution of Sizes Due Primarily to Intron Size and Number Variation76

3.8 Some DNA Sequences Encode More Than One Polypeptide78

3.9 Some Exons Correspond to Protein Functional Domains79

3.10 Members of a Gene Family Have a Common Organization81

3.11 There Are Many Forms of Information in DNA82

Chapter 4 The Content of the Genome87

4.1 Introduction87

4.2 Genome Mapping Reveals That Individual Genomes Show Extensive Variation88

4.3 SNPs Can Be Associated with Genetic Disorders89

4.4 Eukaryotic Genomes Contain Nonrepetitive and Repetitive DNA Sequences90

4.5 Eukaryotic Protein-Coding Genes Can Be Identified by the Conservation of Exons and of Genome Organization92

4.6 Some Eukaryotic Organelles Have DNA94

4.7 Organelle Genomes Are Circular DNAs That Encode Organelle Proteins95

4.8 The Chloroplast Genome Encodes Many Proteins and RNAs97

4.9 Mitochondria and Chloroplasts Evolved by Endosymbiosis98

Chapter 5 Genome Sequences and Evolution101

5.1 Introduction102

5.2 Prokaryotic Gene Numbers Range Over an Order of Magnitude103

5.3 Total Gene Number Is Known for Several Eukaryotes104

5.4 How Many Different Types of Genes Are There？106

5.5 The Human Genome Has Fewer Genes Than Originally Expected108

5.6 How Are Genes and Other Sequences Distributed in the Genome？110

5.7 The Y Chromosome Has Several Male-Specific Genes111

5.8 How Many Genes Are Essential？112

5.9 About 10，000 Genes Are Expressed at Widely Differing Levels in a Eukaryotic Cell115

5.10 Expressed Gene Number Can Be Measured En Masse116

5.11 DNA Sequences Evolve by Mutation and a Sorting Mechanism117

5.12 Selection Can Be Detected by Measuring Sequence Variation119

5.13 A Constant Rate of Sequence Divergence Is a Molecular Clock122

5.14 The Rate of Neutral Substitution Can Be Measured from Divergence of Repeated Sequences125

5.15 How Did Interrupted Genes Evolve？126

5.16 Why Are Some Genomes So Large？128

5.17 Morphological Complexity Evolves by Adding New Gene Functions130

5.18 Gene Duplication Contributes to Genome Evolution131

5.19 Globin Clusters Arise by Duplication and Divergence132

5.20 Pseudogenes Have Lost Their Original Functions134

5.21 Genome Duplication Has Played a Role in Plant and Vertebrate Evolution135

5.22 What Is the Role of Transposable Elements in Genome Evolution137

5.23 There Can Be Biases in Mutation，Gene Conversion，and Codon Usage137

Chapter 6 Clusters and Repeats143

6.1 Introduction143

6.2 Unequal Crossing-Over Rearranges Gene Clusters145

6.3 Genes for rRNA Form Tandem Repeats Including an Invariant Transcription Unit147

6.4 Crossover Fixation Could Maintain Identical Repeats150

6.5 Satellite DNAs Often Lie in Heterochromatin152

6.6 Arthropod Satellites Have Very Short Identical Repeats153

6.7 Mammalian Satellites Consist of Hierarchical Repeats154

6.8 Minisatellites Are Useful for DNA Profiling157

Chapter 7 Chromosomes&Edited by Hank W.Bass161

7.1 Introduction162

7.2 Viral Genomes Are Packaged into Their Coats163

7.3 The Bacterial Genome Is a Nucleoid with Dynamic Structural Properties165

7.4 The Bacterial Genome Is Supercoiled and Has Four Macrodomains167

7.5 Eukaryotic DNA Has Loops and Domains Attached to a Scaffold168

7.6 Specific Sequences Attach DNA to an Interphase Matrix169

7.7 Chromatin Is Divided into Euchromatin and Heterochromatin170

7.8 Chromosomes Have Banding Patterns172

7.9 Lampbrush Chromosomes Are Extended173

7.10 Polytene Chromosomes Form Bands174

7.11 Polytene Chromosomes Expand at Sites of Gene Expression175

7.12 The Eukaryotic Chromosome Is a Segregation Device176

7.13 Regional Centromeres Contain a Centromeric Histone H3 Variant and Repetitive DNA177

7.14 Point Centromeres in S.cerevisiae Contain Short，Essential DNA Sequences179

7.15 The S.cerevisiae Centromere Binds a Protein Complex179

7.16 Telomeres Have Simple Repeating Sequences180

7.17 Telomeres Seal the Chromosome Ends and Function in Meiotic Chromosome Pairing181

7.18 Telomeres Are Synthesized by a Ribonucleoprotein Enzyme182

7.19 Telomeres Are Essential for Survival184

Chapter 8 Chromatin&Edited by Craig Peterson189

8.1 Introduction189

8.2 DNA Is Organized in Arrays of Nucleosomes190

8.3 The Nucleosome Is the Subunit of All Chromatin192

8.4 Nucleosomes Are Covalently Modified196

8.5 Histone Variants Produce Alternative Nucleosomes199

8.6 DNA Structure Varies on the Nucleosomal Surface202

8.7 The Path of Nucleosomes in the Chromatin Fiber205

8.8 Replication of Chromatin Requires Assembly of Nucleosomes207

8.9 Do Nucleosomes Lie at Specific Positions？209

8.10 Nucleosomes Are Displaced and Reassembled During Transcription212

8.11 DNase Sensitivity Detects Changes in Chromatin Structure215

8.12 An LCR Can Control a Domain217

8.13 Insulators Define Transcriptionally Independent Domains218

PARTⅡ DNA Replication and Recombination227

Chapter 9 Replication Is Connected to the Cell Cycle&Edited by Barbara Funnell228

9.1 Introduction228

9.2 Bacterial Replication Is Connected to the Cell Cycle230

9.3 The Shape and Spatial Organization of a Bacterium Are Important During Chromosome Segregation and Cell Division231

9.4 Mutations in Division or Segregation Affect Cell Shape232

9.5 FtsZ Is Necessary for Septum Formation233

9.6 min and noc/slm Genes Regulate the Location of the Septum233

9.7 Partition Involves Separation of the Chromosomes234

9.8 Chromosomal Segregation Might Require Site-Specific Recombination235

9.9 The Eukaryotic Growth Factor Signal Transduction Pathway Promotes Entry to S Phase237

9.10 Checkpoint Control for Entry into S Phase：p53，a Guardian of the Checkpoint239

9.11 Checkpoint Control for Entry into S Phase：Rb，a Guardian of the Checkpoint240

Chapter 10 The Replicon：Initiation of Replication245

10.1 Introduction245

10.2 An Origin Usually Initiates Bidirectional Replication246

10.3 The Bacterial Genome Is （Usually） a Single Circular Replicon247

10.4 Methylation of the Bacterial Origin Regulates Initiation248

10.5 Initiation：Creating the Replication Forks at the Origin oriC249

10.6 Multiple Mechanisms Exist to Prevent Premature Reinitiation of Replication251

10.7 Archaeal Chromosomes Can Contain Multiple Replicons252

10.8 Each Eukaryotic Chromosome Contains Many Replicons252

10.9 Replication Origins Can Be Isolated in Yeast253

10.10 Licensing Factor Controls Eukaryotic Rereplication255

10.11 Licensing Factor Binds to ORC256

Chapter 11 DNA Replication261

11.1 Introduction261

11.2 DNA Polymerases Are the Enzymes That Make DNA262

11.3 DNA Polymerases Have Various Nuclease Activities264

11.4 DNA Polymerases Control the Fidelity of Replication264

11.5 DNA Polymerases Have a Common Structure265

11.6 The Two New DNA Strands Have Different Modes of Synthesis266

11.7 Replication Requires a Helicase and a Single-Stranded Binding Protein267

11.8 Priming Is Required to Start DNA Synthesis268

11.9 Coordinating Synthesis of the Lagging and Leading Strands270

11.10 DNA Polymerase Holoenzyme Consists of Subcomplexes270

11.11 The Clamp Controls Association of Core Enzyme with DNA271

11.12 Okazaki Fragments Are Linked by Ligase274

11.13 Separate Eukaryotic DNA Polymerases Undertake Initiation and Elongation276

11.14 Lesion Bypass Requires Polymerase Replacement278

11.15 Termination of Replication279

Chapter 12 Extrachromosomal Replicons283

12.1 Introduction283

12.2 The Ends of Linear DNA Are a Problem for Replication284

12.3 Terminal Proteins Enable Initiation at the Ends of Viral DNAs285

12.4 Rolling Circles Produce Multimers of a Replicon286

12.5 Rolling Circles Are Used to Replicate Phage Genomes287

12.6 The F Plasmid Is Transferred by Conjugation Between Bacteria288

12.7 Conjugation Transfers Single-Stranded DNA290

12.8 Single-Copy Plasmids Have a Partitioning System291

12.9 Plasmid Incompatibility Is Determined by the Replicon293

12.10 The ColE1 Compatibility System Is Controlled by an RNA Regulator293

12.11 How Do Mitochondria Replicate and Segregate？296

12.12 D Loops Maintain Mitochondrial Origins297

12.13 The Bacterial Ti Plasmid Causes Crown Gall Disease in Plants298

12.14 T-DNA Carries Genes Required for Infection299

12.15 Transfer of T- DNA Resembles Bacterial Conjugation301

Chapter 13 Homologous and Site-Specific Recombination&Edited by Hannah L.Klein and Samantha Hoot305

13.1 Introduction306

13.2 Homologous Recombination Occurs Between Synapsed Chromosomes in Meiosis306

13.3 Double-Strand Breaks Initiate Recombination308

13.4 Gene Conversion Accounts for Interallelic Recombination310

13.5 The Synthesis-Dependent Strand-Annealing Model311

13.6 The Single-Strand Annealing Mechanism Functions at Some Double-Strand Breaks312

13.7 Break-Induced Replication Can Repair Double-Strand Breaks313

13.8 Recombining Meiotic Chromosomes Are Connected by the Synaptonemal Complex314

13.9 The Synaptonemal Complex Forms After Double-Strand Breaks315

13.10 Pairing and Synaptonemal Complex Formation Are Independent316

13.11 The Bacterial RecBCD System Is Stimulated by chi Sequences317

13.12 Strand-Transfer Proteins Catalyze Single-Strand Assimilation318

13.13 Holliday Junctions Must Be Resolved321

13.14 Eukaryotic Genes Involved in Homologous Recombination322

1.End Processing/Presynapsis322

2.Synapsis324

3.DNA Heteroduplex Extension and Branch Migration324

4.Resolution324

13.15 Specialized Recombination Involves Specific Sites325

13.16 Site-Specific Recombination Involves Breakage and Reunion326

13.17 Site-Specific Recombination Resembles Topoisomerase Activity327

13.18 Lambda Recombination Occurs in an Intasome328

13.19 Yeast Can Switch Silent and Active Mating-Type Loci329

13.20 Unidirectional Gene Conversion Is Initiated by the Recipient MAT Locus331

13.21 Antigenic Variation in Trypanosomes Uses Homologous Recombination332

13.22 Recombination Pathways Adapted for Experimental Systems332

Chapter 14 Repair Systems339

14.1 Introduction339

14.2 Repair Systems Correct Damage to DNA341

14.3 Excision Repair Systems in E.coli343

14.4 Eukaryotic Nucleotide Excision Repair Pathways344

14.5 Base Excision Repair Systems Require Glycosylases345

14.6 Error-Prone Repair and Translesion Synthesis349

14.7 Controlling the Direction of Mismatch Repair349

14.8 Recombination-Repair Systems in E.coli352

14.9 Recombination Is an Important Mechanism to Recover from Replication Errors353

14.10 Recombination-Repair of Double-Strand Breaks in Eukaryotes354

14.11 Nonhomologous End Joining Also Repairs Double-Strand Breaks356

14.12 DNA Repair in Eukaryotes Occurs in the Context of Chromatin357

14.13 RecA Triggers the SOS System361

Chapter 15 Transposable Elements and Retroviruses&Edited by Damon Lisch367

15.1 Introduction368

15.2 Insertion Sequences Are Simple Transposition Modules369

15.3 Transposition Occurs by Both Replicative and Nonreplicative Mechanisms370

15.4 Transposons Cause Rearrangement of DNA372

15.5 Replicative Transposition Proceeds Through a Cointegrate373

15.6 Nonreplicative Transposition Proceeds by Breakage and Reunion374

15.7 Transposons Form Superfamilies and Families375

15.8 The Role of Transposable Elements in Hybrid Dysgenesis378

15.9 P Elements Are Activated in the Germline379

15.10 The Retrovirus Life Cycle Involves Transposition-Like Events381

15.11 Retroviral Genes Code for Polyproteins381

15.12 Viral DNA Is Generated by Reverse Transcription383

15.13 Viral DNA Integrates into the Chromosome385

15.14 Retroviruses May Transduce Cellular Sequences386

15.15 Retroelements Fall into Three Classes388

15.16 Yeast Ty Elements Resemble Retroviruses389

15.17 The Alu Family Has Many Widely Dispersed Members391

15.18 LINEs Use an Endonuclease to Generate a Priming End392

Chapter 16 Somatic DNA Recombination and Hypermutation in the Immune System&Edited by Paolo Casali397

16.1 The Immune System：Innate and Adaptive Immunity398

16.2 The Innate Response Utilizes Conserved Recognition Molecules and Signaling Pathways399

16.3 Adaptive Immunity401

16.4 Clonal Selection Amplifies Lymphocytes That Respond to a Given Antigen402

16.5 Ig Genes Are Assembled from Discrete DNA Segments in B Lymphocytes404

16.6 L Chains Are Assembled by a Single Recombination Event405

16.7 H Chains Are Assembled by Two Sequential Recombination Events406

16.8 Recombination Generates Extensive Diversity407

16.9 V（D）J DNA Recombination Relies on RSS and Occurs by Deletion or Inversion408

16.10 Allelic Exclusion Is Triggered by Productive Rearrangements410

16.11 RAG1/RAG2 Catalyze Breakage and Religation of V（D）J Gene Segments411

16.12 B Cell Development in the Bone Marrow：From Common Lymphoid Progenitor to Mature B Cell413

16.13 Class Switch DNA Recombination415

16.14 CSR Involves AID and Elements of the NHEJ Pathway416

16.15 Somatic Hypermutation Generates Additional Diversity and Provides the Substrate for Higher-Affinity Submutants418

16.16 SHM Is Mediated by AID，Ung，Elements of the Mismatch DNA Repair Machinery，and Translesion DNA Synthesis Polymerases419

16.17 Igs Expressed in Avians Are Assembled from Pseudogenes420

16.18 Chromatin Architecture Dynamics of the IgH Locus in V（D） J Recombination，CSR，and SHM421

16.19 Epigenetics of V（D）J Recombination，CSR，and SHM423

16.20 B Cell Differentiation Results in Maturation of the Antibody Response and Generation of Long-lived Plasma Cells and Memory B Cells425

16.21 The T Cell Receptor Antigen Is Related to the BCR426

16.22 The TCR Functions in Conjunction with the MHC427

16.23 The MHC Locus Comprises a Cohort of Genes Involved in Immune Recognition428

PARTⅢ Transcription and Posttranscriptional Mechanisms441

Chapter 17 Prokaryotic Transcription442

17.1 Introduction443

17.2 Transcription Occurs by Base Pairing in a “Bubble” of Unpaired DNA444

17.3 The Transcription Reaction Has Three Stages445

17.4 Bacterial RNA Polymerase Consists of Multiple Subunits446

17.5 RNA Polymerase Holoenzyme Consists of the Core Enzyme and Sigma Factor446

17.6 How Does RNA Polymerase Find Promoter Sequences？448

17.7 The Holoenzyme Goes Through Transitions in the Process of Recognizing and Escaping from Promoters448

17.8 Sigma Factor Controls Binding to DNA by Recognizing Specific Sequences in Promoters451

17.9 Promoter Efficiencies Can Be Increased or Decreased by Mutation452

17.10 Multiple Regions in RNA Polymerase Directly Contact Promoter DNA453

17.11 RNA Polymerase-Promoter and DNA-Protein Interactions Are the Same for Promoter Recognition and DNA Melting456

17.12 Interactions Between Sigma Factor and Core RNA Polymerase Change During Promoter Escape458

17.13 A Model for Enzyme Movement Is Suggested by the Crystal Structure459

17.14 A Stalled RNA Polymerase Can Restart461

17.15 Bacterial RNA Polymerase Terminates at Discrete Sites461

17.16 How Does Rho Factor Work？463

17.17 Supercoiling Is an Important Feature of Transcription465

17.18 Phage T7 RNA Polymerase Is a Useful Model System466

17.19 Competition for Sigma Factors Can Regulate Initiation466

17.20 Sigma Factors Can Be Organized into Cascades468

17.21 Sporulation Is Controlled by Sigma Factors469

17.22 Antitermination Can Be a Regulatory Event471

Chapter 18 Eukaryotic Transcription479

18.1 Introduction479

18.2 Eukaryotic RNA Polymerases Consist of Many Subunits481

18.3 RNA Polymerase Ⅰ Has a Bipartite Promoter482

18.4 RNA Polymerase Ⅲ Uses Downstream and Upstream Promoters483

18.5 The Start Point for RNA Polymerase Ⅱ485

18.6 TBP Is a Universal Factor486

18.7 The Basal Apparatus Assembles at the Promoter488

18.8 Initiation Is Followed by Promoter Clearance and Elongation490

18.9 Enhancers Contain Bidirectional Elements That Assist Initiation493

18.10 Enhancers Work by Increasing the Concentration of Activators Near the Promoter494

18.11 Gene Expression Is Associated with Demethylation495

18.12 CpG Islands Are Regulatory Targets496

Chapter 19 RNA Splicing and Processing503

19.1 Introduction503

19.2 The 5’ End of Eukaryotic mRNA Is Capped505

19.3 Nuclear Splice Sites Are Short Sequences506

19.4 Splice Sites Are Read in Pairs507

19.5 Pre-mRNA Splicing Proceeds Through a Lariat508

19.6 snRNAs Are Required for Splicing509

19.7 Commitment of Pre-mRNA to the Splicing Pathway510

19.8 The Spliceosome Assembly Pathway513

19.9 An Alternative Spliceosome Uses Different snRNPs to Process the Minor Class of Introns515

19.10 Pre-mRNA Splicing Likely Shares the Mechanism with Group Ⅱ Autocatalytic Introns516

19.11 Splicing Is Temporally and Functionally Coupled with Multiple Steps in Gene Expression518

19.12 Alternative Splicing Is a Rule，Rather Than an Exception，in Multicellular Eukaryotes519

19.13 Splicing Can Be Regulated by Exonic and Intronic Splicing Enhancers and Silencers522

19.14 trans-Splicing Reactions Use Small RNAs524

19.15 The 3’ Ends of mRNAs Are Generated by Cleavage and Polyadenylation526

19.16 3’ mRNA End Processing Is Critical for Termination of Transcription528

19.17 The 3’ End Formation of Histone mRNA Requires U7 snRNA529

19.18 tRNA Splicing Involves Cutting and Rejoining in Separate Reactions530

19.19 The Unfolded Protein Response Is Related to tRNA Splicing533

19.20 Production of rRNA Requires Cleavage Events and Involves Small RNAs534

Chapter 20 mRNA Stability and Localization&Edited by Ellen Baker543

20.1 Introduction543

20.2 Messenger RNAs Are Unstable Molecules544

20.3 Eukaryotic mRNAs Exist in the Form of mRNPs from Their Birth to Their Death546

20.4 Prokaryotic mRNA Degradation Involves Multiple Enzymes546

20.5 Most Eukaryotic mRNA Is Degraded via Two Deadenylation-Dependent Pathways548

20.6 Other Degradation Pathways Target Specific mRNAs550

20.7 mRNA-Specific Half-Lives Are Controlled by Sequences or Structures Within the mRNA552

20.8 Newly Synthesized RNAs Are Checked for Defects via aNuclear Surveillance System553

20.9 Quality Control of mRNA Translation Is Performed by Cytoplasmic Surveillance Systems555

20.10 Translationally Silenced mRNAs Are Sequestered in a Variety of RNA Granules557

20.11 Some Eukaryotic mRNAs Are Localized to Specific Regions of a Cell558

Chapter 21 Catalytic RNA&Edited by Douglas J.Briant563

21.1 Introduction563

21.2 Group Ⅰ Introns Undertake Self-Splicing by Transesterification564

21.3 Group Ⅰ Introns Form a Characteristic Secondary Structure567

21.4 Ribozymes Have Various Catalytic Activities568

21.5 Some Group Ⅰ Introns Encode Endonucleases That Sponsor Mobility570

21.6 Group Ⅱ Introns May Encode Multifunction Proteins571

21.7 Some Autosplicing Introns Require Maturases572

21.8 The Catalytic Activity of RNase P Is Due to RNA573

21.9 Viroids Have Catalytic Activity573

21.10 RNA Editing Occurs at Individual Bases575

21.11 RNA Editing Can Be Directed by Guide RNAs576

21.12 Protein Splicing Is Autocatalytic578

Chapter 22 Translation583

22.1 Introduction583

22.2 Translation Occurs by Initiation，Elongation，and Termination584

22.3 Special Mechanisms Control the Accuracy of Translation586

22.4 Initiation in Bacteria Needs 30S Subunits and Accessory Factors587

22.5 Initiation Involves Base Pairing Between mRNA and rRNA589

22.6 A Special Initiator tRNA Starts the Polypeptide Chain590

22.7 Use of fMet-tRNAf Is Controlled by IF-2 and the Ribosome591

22.8 Small Subunits Scan for Initiation Sites on Eukaryotic mRNA592

22.9 Eukaryotes Use a Complex of Many Initiation Factors593

22.10 Elongation Factor Tu Loads Aminoacyl-tRNA into the A Site597

22.11 The Polypeptide Chain Is Transferred to Aminoacyl-tRNA598

22.12 Translocation Moves the Ribosome599

22.13 Elongation Factors Bind Alternately to the Ribosome600

22.14 Three Codons Terminate Translation601

22.15 Termination Codons Are Recognized by Protein Factors602

22.16 Ribosomal RNA Is Found Throughout Both Ribosomal Subunits604

22.17 Ribosomes Have Several Active Centers606

22.18 16S rRNA Plays an Active Role in Translation608

22.19 23S rRNA Has Peptidyl Transferase Activity610

22.20 Ribosomal Structures Change When the Subunits Come Together611

22.21 Translation Can Be Regulated612

22.22 The Cycle of Bacterial Messenger RNA613

Chapter 23 Using the Genetic Code621

23.1 Introduction621

23.2 Related Codons Represent Chemically Similar Amino Acids622

23.3 Codon-Anticodon Recognition Involves Wobbling623

23.4 tRNAs Are Processed from Longer Precursors624

23.5 tRNA Contains Modified Bases625

23.6 Modified Bases Affect Anticodon-Codon Pairing627

23.7 The Universal Code Has Experienced Sporadic Alterations628

23.8 Novel Amino Acids Can Be Inserted at Certain Stop Codons630

23.9 tRNAs Are Charged with Amino Acids by Aminoacyl-tRNA Synthetases631

23.10 Aminoacyl-tRNA Synthetases Fall into Two Classes632

23.11 Synthetases Use Proofreading to Improve Accuracy634

23.12 Suppressor tRNAs Have Mutated Anticodons That Read New Codons636

23.13 Each Termination Codon Has Nonsense Suppressors637

23.14 Suppressors May Compete with Wild-Type Reading of the Code638

23.15 The Ribosome Influences the Accuracy of Translation639

23.16 Frameshifting Occurs at Slippery Sequences641

23.17 Other Recoding Events：Translational Bypassing and the tmRNA Mechanism to Free Stalled Ribosomes642

PART Ⅳ Gene Regulation647

Chapter 24 The Operon&Edited by Liskin Swint-Kruse648

24.1 Introduction649

24.2 Structural Gene Clusters Are Coordinately Controlled651

24.3 The lac Operon Is Negative Inducible652

24.4 The lac Repressor Is Controlled by a Small-Molecule Inducer653

24.5 cis-Acting Constitutive Mutations Identify the Operator655

24.6 trans-Acting Mutations Identify the Regulator Gene655

24.7 The lac Repressor Is a Tetramer Made of Two Dimers656

24.8 lac Repressor Binding to the Operator Is Regulated by an Allosteric Change in Conformation658

24.9 The lac Repressor Binds to Three Operators and Interacts with RNA Polymerase660

24.10 The Operator Competes with Low-Affinity Sites to Bind Repressor661

24.11 The lac Operon Has a Second Layer of Control：Catabolite Repression662

24.12 The trp Operon Is a Repressible Operon with Three Transcription Units665

24.13 The trp Operon Is Also Controlled by Attenuation666

24.14 Attenuation Can Be Controlled by Translation668

24.15 Stringent Control by Stable RNA Transcription670

24.16 r-Protein Synthesis Is Controlled by Autoregulation671

Chapter 25 Phage Strategies677

25.1 Introduction677

25.2 Lytic Development Is Divided into Two Periods679

25.3 Lytic Development Is Controlled by a Cascade679

25.4 Two Types of Regulatory Events Control the Lytic Cascade681

25.5 The Phage T7 and T4 Genomes Show Functional Clustering681

25.6 Lambda Immediate Early and Delayed Early Genes Are Needed for Both Lysogeny and the Lytic Cycle683

25.7 The Lytic Cycle Depends on Antitermination by pN684

25.8 Lysogeny Is Maintained by the Lambda Repressor Protein685

25.9 The Lambda Repressor and Its Operators Define the Immunity Region686

25.10 The DNA-Binding Form of the Lambda Repressor Is a Dimer687

25.11 The Lambda Repressor Uses a Helix-Turn-Helix Motif to Bind DNA688

25.12 Lambda Repressor Dimers Bind Cooperatively to the Operator689

25.13 The Lambda Repressor Maintains an Autoregulatory Circuit690

25.14 Cooperative Interactions Increase the Sensitivity of Regulation692

25.15 The cll and clll Genes Are Needed to Establish Lysogeny692

25.16 A Poor Promoter Requires cll Protein693

25.17 Lysogeny Requires Several Events694

25.18 The Cro Repressor Is Needed for Lytic Infection694

25.19 What Determines the Balance Between Lysogeny and the Lytic Cycle？697

Chapter 26 Eukaryotic Transcription Regulation701

26.1 Introduction702

26.2 How Is a Gene Turned On？703

26.3 Mechanism of Action of Activators and Repressors704

26.4 Independent Domains Bind DNA and Activate Transcription707

26.5 The Two-Hybrid Assay Detects Protein-Protein Interactions707

26.6 Activators Interact with the Basal Apparatus708

26.7 Many Types of DNA-Binding Domains Have Been Identified711

26.8 Chromatin Remodeling Is an Active Process712

26.9 Nucleosome Organization or Content Can Be Changed at the Promoter715

26.10 Histone Acetylation Is Associated with Transcription Activation716

26.11 Methylation of Histones and DNA Is Connected719

26.12 Promoter Activation Involves Multiple Changes to Chromatin720

26.13 Histone Phosphorylation Affects Chromatin Structure722

26.14 Yeast GAL Genes：A Model for Activation and Repression722

Chapter 27 Epigenetics Ⅰ&Edited by Trygve Tollefsbol731

27.1 Introduction731

27.2 Heterochromatin Propagates from a Nucleation Event732

27.3 Heterochromatin Depends on Interactions with Histones734

27.4 Polycomb and Trithorax Are Antagonistic Repressors and Activators737

27.5 CpG Islands Are Subject to Methylation738

27.6 Epigenetic Effects Can Be Inherited741

27.7 Yeast Prions Show Unusual Inheritance743

Chapter 28 Epigenetics Ⅱ&Edited by Trygve Tollefsbol749

28.1 Introduction749

28.2 X Chromosomes Undergo Global Changes750

28.3 Chromosome Condensation Is Caused by Condensins752

28.4 DNA Methylation Is Responsible for Imprinting755

28.5 Oppositely Imprinted Genes Can Be Controlled by a Single Center756

28.6 Prions Cause Diseases in Mammals757

Chapter 29 Noncoding RNA761

29.1 Introduction761

29.2 A Riboswitch Can Alter Its Structure According to Its Environment762

29.3 Noncoding RNAs Can Be Used to Regulate Gene Expression763

Chapter 30 Regulatory RNA769

30.1 Introduction769

30.2 Bacteria Contain Regulator RNAs770

30.3 MicroRNAs Are Widespread Regulators in Eukaryotes772

30.4 How Does RNA Interference Work？775

30.5 Heterochromatin Formation Requires MicroRNAs778

Glossary783

Index809