Genes IX / Benjamin Lewin.

Format:

Book

Author/Creator:

Lewin, Benjamin.

Contributor:

Clarence J. Marshall Memorial Library Fund.

Language:

English

Subjects (All):

Genetics.

Genes.

Genes--physiology.

DNA--genetics.

Genetic Phenomena.

Genome.

Proteins--genetics.

RNA--genetics.

Medical Subjects:

Genes--physiology.

DNA--genetics.

Genetic Phenomena.

Genome.

Proteins--genetics.

RNA--genetics.

Physical Description:

xvii, 892 pages : color illustrations ; 29 cm

Other Title:

Genes 9

Genes nine

Place of Publication:

Sudbury, MA : Jones and Bartlett Publishers, [2008]

Summary:

When the first edition of Genes published, Benjamin Lewin set the standard for teaching molecular biology and molecular genetics with a unified approach. The Ninth Edition of this classic text continues this tradition, presenting gene structure and function in both eukaryotic and prokaryotic organisms. Dr. Lewin maintains his commitment to providing students, researchers, and educators with the most current presentation of concepts in this rapidly changing field. The Ninth Edition of Genes includes updated content and expanded coverage of critical topics with a new organization that allows the student to focus more sharply on genes and their expression. Genes IX also boasts a fresh, modern design and a contemporary art program.

New and Key Features of Genes IX: Expanded coverage in many areas including: DNA replication, Recombination and repair, The replicon, Chromatin regulation and gene regulation, Evolution of genes, The Y chromosome. Reorganized to allow instructors to build on critical concepts throughout the course, New contemporary design and stunning 4-color art program, New updates throughout, including the most current information on genome, organization, DNA replication, gene regulation, and much more Resources include an Instructor's ToolKit CD-ROM with Image Bank, PowerPoint[Registered] Lecture Outline Slides, and an all-new Test Bank, as well as the Genes IX companion website with numerous eLearning Tools.

Contents:

1 Genes Are DNA 1

1.2 DNA Is the Genetic Material of Bacteria 3

1.3 DNA Is the Genetic Material of Viruses 4

1.4 DNA Is the Genetic Material of Animal Cells 5

1.5 Polynucleotide Chains Have Nitrogenous Bases Linked to a Sugar-Phosphate Backbone 6

1.6 DNA Is a Double Helix 6

1.7 DNA Replication Is Semiconservative 8

1.8 DNA Strands Separate at the Replication Fork 9

1.9 Genetic Information Can Be Provided by DNA or RNA 10

1.10 Nucleic Acids Hybridize by Base Pairing 12

1.11 Mutations Change the Sequence of DNA 14

1.12 Mutations May Affect Single Base Pairs or Longer Sequences 15

1.13 The Effects of Mutations Can Be Reversed 16

1.14 Mutations Are Concentrated at Hotspots 17

1.15 Many Hotspots Result from Modified Bases 18

1.16 Some Hereditary Agents Are Extremely Small 19

2 Genes Code for Proteins 23

2.2 A Gene Codes for a Single Polypeptide 24

2.3 Mutations in the Same Gene Cannot Complement 25

2.4 Mutations May Cause Loss-of-Function or Gain-of-Function 26

2.5 A Locus May Have Many Different Mutant Alleles 27

2.6 A Locus May Have More than One Wild-type Allele 28

2.7 Recombination Occurs by Physical Exchange of DNA 28

2.8 The Genetic Code Is Triplet 30

2.9 Every Sequence Has Three Possible Reading Frames 31

2.10 Prokaryotic Genes Are Colinear with Their Proteins 32

2.11 Several Processes Are Required to Express the Protein Product of a Gene 33

2.12 Proteins Are Trans-acting, but Sites on DNA Are Cis-acting 35

3 The Interrupted Gene 37

3.2 An Interrupted Gene Consists of Exons and Introns 38

3.3 Restriction Endonucleases Are a Key Tool in Mapping DNA 39

3.4 Organization of Interrupted Genes May Be Conserved 40

3.5 Exon Sequences Are Conserved but Introns Vary 42

3.6 Genes Show a Wide Distribution of Sizes 43

3.7 Some DNA Sequences Code for More Than One Protein 45

3.8 How Did Interrupted Genes Evolve? 47

3.9 Some Exons Can Be Equated with Protein Functions 49

3.10 The Members of a Gene Family Have a Common Organization 51

3.11 Is All Genetic Information Contained in DNA? 53

4 The Content of the Genome 55

4.2 Genomes Can Be Mapped by Linkage, Restriction Cleavage, or DNA Sequence 56

4.3 Individual Genomes Show Extensive Variation 57

4.4 RFLPs and SNPs Can Be Used for Genetic Mapping 58

4.5 Why Are Genomes So Large? 60

4.6 Eukaryotic Genomes Contain Both Nonrepetitive and Repetitive DNA Sequences 61

4.7 Genes Can Be Isolated by the Conservation of Exons 63

4.8 The Conservation of Genome Organization Helps to Identify Genes 65

4.9 Organelles Have DNA 67

4.10 Organelle Genomes Are Circular DNAs That Code for Organelle Proteins 69

4.11 Mitochondrial DNA Organization Is Variable 70

4.12 The Chloroplast Genome Codes for Many Proteins and RNAs 71

4.13 Mitochondria Evolved by Endosymbiosis 72

5 Genome Sequences and Gene Numbers 76

5.2 Bacterial Gene Numbers Range Over an Order of Magnitude 77

5.3 Total Gene Number Is Known for Several Eukaryotes 79

5.4 How Many Different Types of Genes Are There? 81

5.5 The Human Genome Has Fewer Genes Than Expected 83

5.6 How Are Genes and Other Sequences Distributed in the Genome? 85

5.7 The Y Chromosome Has Several Male-Specific Genes 86

5.8 More Complex Species Evolve by Adding New Gene Functions 87

5.9 How Many Genes Are Essential? 89

5.10 Genes Are Expressed at Widely Differing Levels 92

5.11 How Many Genes Are Expressed? 93

5.12 Expressed Gene Number Can Be Measured En Masse 93

6 Clusters and Repeats 98

6.2 Gene Duplication Is a Major Force in Evolution 100

6.3 Globin Clusters Are Formed by Duplication and Divergence 101

6.4 Sequence Divergence Is the Basis for the Evolutionary Clock 104

6.5 The Rate of Neutral Substitution Can Be Measured from Divergence of Repeated Sequences 107

6.6 Pseudogenes Are Dead Ends of Evolution 108

6.7 Unequal Crossing-over Rearranges Gene Clusters 109

6.8 Genes for rRNA Form Tandem Repeats 112

6.9 The Repeated Genes for rRNA Maintain Constant Sequence 114

6.10 Crossover Fixation Could Maintain Identical Repeats 115

6.11 Satellite DNAs Often Lie in Heterochromatin 117

6.12 Arthropod Satellites Have Very Short Identical Repeats 119

6.13 Mammalian Satellites Consist of Hierarchical Repeats 120

6.14 Minisatellites Are Useful for Genetic Mapping 123

7 Messenger RNA 127

7.2 mRNA Is Produced by Transcription and Is Translated 129

7.3 Transfer RNA Forms a Cloverleaf 130

7.4 The Acceptor Stem and Anticodon Are at Ends of the Tertiary Structure 131

7.5 Messenger RNA Is Translated by Ribosomes 132

7.6 Many Ribosomes Bind to One mRNA 133

7.7 The Life Cycle of Bacterial Messenger RNA 135

7.8 Eukaryotic mRNA Is Modified During or after Its Transcription 137

7.9 The 5' End of Eukaryotic mRNA Is Capped 138

7.10 The 3' Terminus Is Polyadenylated 139

7.11 Bacterial mRNA Degradation Involves Multiple Enzymes 140

7.12 mRNA Stability Depends on Its Structure and Sequence 141

7.13 mRNA Degradation Involves Multiple Activities 143

7.14 Nonsense Mutations Trigger a Surveillance System 144

7.15 Eukaryotic RNAs Are Transported 145

7.16 mRNA Can Be Specifically Localized 146

8 Protein Synthesis 151

8.2 Protein Synthesis Occurs by Initiation, Elongation, and Termination 153

8.3 Special Mechanisms Control the Accuracy of Protein Synthesis 155

8.4 Initiation in Bacteria Needs 30S Subunits and Accessory Factors 157

8.5 A Special Initiator tRNA Starts the Polypeptide Chain 158

8.6 Use of fMet-tRNA[subscript f] Is Controlled by IF-2 and the Ribosome 150

8.7 Initiation Involves Base Pairing Between mRNA and rRNA 161

8.8 Small Subunits Scan for Initiation Sites on Eukaryotic mRNA 162

8.9 Eukaryotes Use a Complex of Many Initiation Factors 164

8.10 Elongation Factor Tu Loads Aminoacyl-tRNA into the A Site 167

8.11 The Polypeptide Chain Is Transferred to Aminoacyl-tRNA 168

8.12 Translocation Moves the Ribosome 169

8.13 Elongation Factors Bind Alternately to the Ribosome 170

8.14 Three Codons Terminate Protein Synthesis 172

8.15 Termination Codons Are Recognized by Protein Factors 173

8.16 Ribosomal RNA Pervades Both Ribosomat Subunits 175

8.17 Ribosomes Have Several Active Centers 177

8.18 16S rRNA Plays an Active Role in Protein Synthesis 179

8.19 23S rRNA Has Peptidyl Transferase Activity 182

8.20 Ribosomal Structures Change When the Subunits Come Together 183

9 Using the Genetic Code 189

9.2 Related Codons Represent Related Amino Acids 190

9.3 Codon-Anticodon Recognition Involves Wobbling 192

9.4 tRNAs Are Processed from Longer Precursors 194

9.5 tRNA Contains Modified Bases 194

9.6 Modified Bases Affect Anticodon-Codon Pairing 196

9.7 There Are Sporadic Alterations of the Universal Code 197

9.8 Novel Amino Acids Can Be Inserted at Certain Stop Codons 199

9.9 tRNAs Are Charged with Amino Acids by Synthetases 200

9.10 Aminoacyl-tRNA Synthetases Fall into Two Groups 201

9.11 Synthetases Use Proofreading to Improve Accuracy 203

9.12 Suppressor tRNAs Have Mutated Anticodons That Read New Codons 206

9.13 There Are Nonsense Suppressors for Each Termination Codon 207

9.14 Suppressors May Compete with Wild-Type Reading of the Code 208

9.15 The Ribosome Influences the Accuracy of Translation 209

9.16 Recoding Changes Codon Meanings 211

9.17 Frameshifting Occurs at Slippery Sequences 213

9.18 Bypassing Involves Ribosome Movement 214

10 Protein Localization 218

10.2 Passage Across a Membrane Requires a Special Apparatus 220

10.3 Protein Translocation May Be Posttranslational or Cotranslational 221

10.4 Chaperones May Be Required for Protein Folding 223

10.5 Chaperones Are Needed by Newly Synthesized and by Denatured Proteins 224

10.6 The Hsp70 Family Is Ubiquitous 226

10.7 Signal Sequences Initiate Translocation 227

10.8 The Signal Sequence Interacts with the SRP 228

10.9 The SRP

Interacts with the SRP Receptor 229

10.10 The Translocon Forms a Pore 231

10.11 Translocation Requires Insertion into the Translocon and (Sometimes) a Ratchet in the ER 233

10.12 Reverse Translocation Sends Proteins to the Cytosol for Degradation 234

10.13 Proteins Reside in Membranes by Means of Hydrophobic Regions 235

10.14 Anchor Sequences Determine Protein Orientation 236

10.15 How Do Proteins Insert into Membranes? 238

10.16 Posttranslational Membrane Insertion Depends on Leader Sequences 240

10.17 A Hierarchy of Sequences Determines Location within Organelles 241

10.18 Inner and Outer Mitochondrial Membranes Have Different Translocons 243

10.19 Peroxisomes Employ Another Type of Translocation System 245

10.20 Bacteria Use Both Cotranslational and Posttranslational Translocation 246

10.21 The Sec System Transports Proteins into and Through the Inner Membrane 247

10.22 Sec-Independent Translocation Systems in E. coli 249

11 Transcription 256

11.2 Transcription Occurs by Base Pairing in a "Bubble" of Unpaired DNA 259

11.3 The Transcription Reaction Has Three Stages 260

11.4 Phage T7 RNA Polymerase Is a Useful Model System 251

11.5 A Model for Enzyme Movement Is Suggested by the Crystal Structure 262

11.6 Bacterial RNA Polymerase Consists of Multiple Subunits 265

11.7 RNA Polymerase Consists of the Core Enzyme and Sigma Factor 267

11.8 The Association with Sigma Factor Changes at Initiation 267

11.9 A Stalled RNA Polymerase Can Restart 269

11.10 How Does RNA Polymerase Find Promoter Sequences? 270

11.11 Sigma Factor Controls Binding to DNA 271

11.12 Promoter Recognition Depends on Consensus Sequences 272

11.13 Promoter Efficiencies Can Be Increased or Decreased by Mutation 274

11.14 RNA Polymerase Binds to One Face of DNA 275

11.15 Supercoiling Is an Important Feature of Transcription 277

11.16 Substitution of Sigma Factors May Control Initiation 278

11.17 Sigma Factors Directly Contact DNA 280

11.18 Sigma Factors May Be Organized into Cascades 282

11.19 Sporulation Is Controlled by Sigma Factors 283

11.20 Bacterial RNA Polymerase Terminates at Discrete Sites 286

11.21 There Are Two Types of Terminators in E. coli 287

11.22 How Does Rho Factor Work? 288

11.23 Antitermination Is a Regulatory Event 291

11.24 Antitermination Requires Sites That Are Independent of the Terminators 292

11.25 Termination and Antitermination Factors Interact with RNA Polymerase 293

12 The Operon 300

12.2 Regulation Can Be Negative or Positive 303

12.3 Structural Gene Clusters Are Coordinately Controlled 304

12.4 The lac Genes Are Controlled by a Repressor 304

12.5 The lac Operon Can Be Induced 305

12.6 Repressor Is Controlled by a Small-Molecule Inducer 306

12.7 cis-Acting Constitutive Mutations Identify the Operator 308

12.8 trans-Acting Mutations Identify the Regulator Gene 309

12.9 Multimeric Proteins Have Special Genetic Properties 309

12.10 The Repressor Monomer Has Several Domains 310

12.11 Repressor Is a Tetramer Made of Two Dimers 311

12.12 DNA-Binding Is Regulated by an Allosteric Change in Conformation 312

12.13 Mutant Phenotypes Correlate with the Domain Structure 312

12.14 Repressor Protein Binds to the Operator 313

12.15 Binding of Inducer Releases Repressor from the Operator 314

12.16 Repressor Binds to Three Operators and Interacts with RNA Polymerase 315

12.17 Repressor Is Always Bound to DNA 316

12.18 The Operator Competes with Low-Affinity Sites to Bind Repressor 317

12.19 Repression Can Occur at Multiple Loci 319

12.20 Cyclic AMP Is an Effector That Activates CRP to Act at Many Operons 320

12.21 CRP Functions in Different Ways in Different Target Operons 321

12.22 Translation Can Be Regulated 323

12.23 r-Protein Synthesis Is Controlled by Autogenous Regulation 325

12.24 Phage T4 p32 Is Controlled by an Autogenous Circuit 326

12.25 Autogenous Regulation Is Often Used to Control Synthesis of Macromolecular Assemblies 327

13 Regulatory RNA 331

13.2 Alternative Secondary Structures Control Attenuation 333

13.3 Termination of Bacillus subtilis trp Genes Is Controlled by Tryptophan and by tRNA[superscript Trp] 333

13.4 The Escherichia coli tryptophan Operon Is Controlled by Attenuation 335

13.5 Attenuation Can Be Controlled by Translation 336

13.6 Antisense RNA Can Be Used to Inactivate Gene Expression 338

13.7 Small RNA Molecules Can Regulate Translation 339

13.8 Bacteria Contain Regulator RNAs 341

13.9 MicroRNAs Are Regulators in Many Eukaryotes 342

13.10 RNA Interference Is Related to Gene Silencing 343

14 Phage Strategies 349

14.2 Lytic Development Is Divided into Two Periods 352

14.3 Lytic Development Is Controlled by a Cascade 353

14.4 Two Types of Regulatory Event Control the Lytic Cascade 354

14.5 The T7 and T4 Genomes Show Functional Clustering 355

14.6 Lambda Immediate Early and Delayed Early Genes Are Needed for Both Lysogeny and the Lytic Cycle 356

14.7 The Lytic Cycle Depends on Antitermination 357

14.8 Lysogeny Is Maintained by Repressor Protein 359

14.9 The Repressor and Its Operators Define the Immunity Region 360

14.10 The DNA-Binding Form of Repressor Is a Dimer 361

14.11 Repressor Uses a Helix-Turn-Helix Motif to Bind DNA 362

14.12 The Recognition Helix Determines Specificity for DNA 363

14.13 Repressor Dimers Bind Cooperatively to the Operator 364

14.14 Repressor at 0[subscript R]2 Interacts with RNA Polymerase at P[subscript RM] 365

14.15 Repressor Maintains an Autogenous Circuit 366

14.16 Cooperative Interactions Increase the Sensitivity of Regulation 367

14.17 The cII and cIII Genes Are Needed to Establish Lysogeny 368

14.18 A Poor Promoter Requires cII Protein 369

14.19 Lysogeny Requires Several Events 369

14.20 The cro Repressor Is Needed for Lytic Infection 371

14.21 What Determines the Balance Between Lysogeny and the Lytic Cycle? 373

15 The Replicon 376

15.2 Replicons Can Be Linear or Circular 378

15.3 Origins Can Be Mapped by Autoradiography and Electrophoresis 379

15.4 Does Methylation at the Origin Regulate Initiation? 380

15.5 Origins May Be Sequestered after Replication 381

15.6 Each Eukaryotic Chromosome Contains Many Replicons 383

15.7 Replication Origins Can Be Isolated in Yeast 384

15.8 Licensing Factor Controls Eukaryotic Rereplication 385

15.9 Licensing Factor Consists of MCM Proteins 386

15.10 D Loops Maintain Mitochondrial Origins 388

16 Extrachromosomal Replicons 392

16.2 The Ends of Linear DNA Are a Problem for Replication 393

16.3 Terminal Proteins Enable Initiation at the Ends of Viral DNAs 394

16.4 Rolling Circles Produce Multimers of a Replicon 396

16.5 Rolling Circles Are Used to Replicate Phage Genomes 397

16.6 The F Plasmid Is Transferred by Conjugation between Bacteria 398

16.7 Conjugation Transfers Single-Stranded DNA 400

16.8 The Bacterial Ti Plasmid Causes Crown Gall Disease in Plants 401

16.9 T-DNA Carries Genes Required for Infection 402

16.10 Transfer of T-DNA Resembles Bacterial Conjugation 405

17 Bacterial Replication Is Connected to the Cell Cycle 408

17.2 Replication Is Connected to the Cell Cycle 410

17.3 The Septum Divides a Bacterium into Progeny That Each Contain a Chromosome 411

17.4 Mutations in Division or Segregation Affect Cell Shape 412

17.5 FtsZ Is Necessary for Septum Formation 413

17.6 min Genes Regulate the Location of the Septum 415

17.7 Chromosomal Segregation May Require Site-Specific Recombination 415

17.8 Partitioning Involves Separation of the Chromosomes 417

17.9 Single-Copy Plasmids Have a Partitioning System 419

17.10 Plasmid Incompatibility Is Determined by the Replicon 421

17.11 The ColE1 Compatibility System Is Controlled by an RNA Regulator 422

17.12 How Do Mitochondria Replicate and Segregate? 424

18 DNA Replication 428

18.2 DNA Polymerases Are the Enzymes That Make DNA 430

18.3 DNA Polymerases Have Various Nuclease Activities 431

18.4 DNA Polymerases Control the Fidelity of Replication 432

18.5 DNA Polymerases Have a Common Structure 433

18.6 DNA Synthesis Is Semidiscontinuous 434

18.7 The [phi]X Model System Shows How Single-Stranded DNA Is Generated for Replication 435

18.8 Priming Is Required to Start DNA Synthesis 437

18.9 DNA Polymerase Holoenzyme Has Three Subcomplexes 439

18.10 The Clamp Controls

Association of Core Enzyme with DNA 440

18.11 Coordinating Synthesis of the Lagging and Leading Strands 442

18.12 Okazaki Fragments Are Linked by Ligase 443

18.13 Separate Eukaryotic DNA Polymerases Undertake Initiation and Elongation 444

18.14 Phage T4 Provides Its Own Replication Apparatus 445

18.15 Creating the Replication Forks at an Origin 448

18.16 Common Events in Priming Replication at the Origin 450

18.17 The Primosome Is Needed to Restart Replication 451

19 Homologous and Site-Specific Recombination 457

19.2 Homologous Recombination Occurs between Synapsed Chromosomes 460

19.3 Breakage and Reunion Involves Heteroduplex DNA 462

19.4 Double-Strand Breaks Initiate Recombination 464

19.5 Recombining Chromosomes Are Connected by the Synaptonemal Complex 465

19.6 The Synaptonemal Complex Forms after Double-Strand Breaks 467

19.7 Pairing and Synaptonemal Complex Formation Are Independent 469

19.8 The Bacterial RecBCD System Is stimulated by chi Sequences 470

19.9 Strand-Transfer Proteins Catalyze Single-Strand Assimilation 471

19.10 The Ruv System Resolves Holliday Junctions 473

19.11 Gene Conversion Accounts for Interallelic Recombination 475

19.12 Supercoiling Affects the Structure of DNA 476

19.13 Topoisomerases Relax or Introduce Supercoils in DNA 478

19.14 Topoisomerases Break and Reseal Strands 480

19.15 Gyrase Functions by Coil Inversion 481

19.16 Specialized Recombination Involves Specific Sites 482

19.17 Site-Specific Recombination Involves Breakage and Reunion 484

19.18 Site-Specific Recombination Resembles Topoisomerase Activity 484

19.19 Lambda Recombination Occurs in an Intasome 486

19.20 Yeast Can Switch Silent and Active Loci for Mating Type 488

19.21 The MAT Locus Codes for Regulator Proteins 490

19.22 Silent Cassettes at HML and HMR Are Repressed 492

19.23 Unidirectional Transposition Is Initiated by the Recipient MAT Locus 493

19.24 Regulation of HO Expression Controls Switching 494

20 Repair Systems 499

20.2 Repair Systems Correct Damage to DNA 502

20.3 Excision Repair Systems in E. coli 503

20.4 Excision-Repair Pathways in Mammalian Cells 504

20.5 Base Flipping Is Used by Methylases and Glycosylases 506

20.6 Error-Prone Repair and Mutator Phenotypes 507

20.7 Controlling the Direction of Mismatch Repair 507

20.8 Recombination-Repair Systems in E. coli 510

20.9 Recombination Is an Important Mechanism to Recover from Replication Errors 511

20.10 RecA Triggers the SOS System 513

20.11 Eukaryotic Cells Have Conserved Repair Systems 515

20.12 A Common System Repairs Double-Strand Breaks 516

21 Transposons 521

21.2 Insertion Sequences Are Simple Transposition Modules 524

21.3 Composite Transposons Have IS Modules 525

21.4 Transposition Occurs by Both Replicative and Nonreplicative Mechanisms 527

21.5 Transposons Cause Rearrangement of DNA 528

21.6 Common Intermediates for Transposition 530

21.7 Replicative Transposition Proceeds through a Cointegrate 531

21.8 Nonreplicative Transposition Proceeds by Breakage and Reunion 533

21.9 TnA Transposition Requires Transposase and Resolvase 534

21.10 Transposition of Tn10 Has Multiple Controls 536

21.11 Controlling Elements in Maize Cause Breakage and Rearrangements 538

21.12 Controlling Elements Form Families of Transposons 540

21.13 Spm Elements Influence Gene Expression 542

21.14 The Role of Transposable Elements in Hybrid Dysgenesis 544

21.15 P Elements Are Activated in the Germline 545

22 Retroviruses and Retroposons 550

22.2 The Retrovirus Life Cycle Involves Transposition-Like Events 551

22.3 Retroviral Genes Code for Polyproteins 552

22.4 Viral DNA Is Generated by Reverse Transcription 554

22.5 Viral DNA Integrates into the Chromosome 556

22.6 Retroviruses May Transduce Cellular Sequences 558

22.7 Yeast Ty Elements Resemble Retroviruses 559

22.8 Many Transposable Elements Reside in Drosophila melanogaster 561

22.9 Retroposons Fall into Three Classes 562

22.10 The Alu Family Has Many Widely Dispersed Members 564

22.11 Processed Pseudogenes Originated as Substrates for Transposition 565

22.12 LINES Use an Endonuclease to Generate a Priming End 566

23 Immune Diversity 570

23.2 Clonal Selection Amplifies Lymphocytes That Respond to Individual Antigens 574

23.3 Immunoglobulin Genes Are Assembled from Their Parts in Lymphocytes 575

23.4 Light Chains Are Assembled by a Single Recombination 577

23.5 Heavy Chains Are Assembled by Two Recombinations 579

23.6 Recombination Generates Extensive Diversity 580

23.7 Immune Recombination Uses Two Types of Consensus Sequence 581

23.8 Recombination Generates Deletions or Inversions 582

23.9 Allelic Exclusion Is Triggered by Productive Rearrangement 582

23.10 The RAG Proteins Catalyze Breakage and Reunion 584

23.11 Early Heavy Chain Expression Can Be Changed by RNA Processing 586

23.12 Class Switching Is Caused by DNA Recombination 587

23.13 Switching Occurs by a Novel Recombination Reaction 589

23.14 Somatic Mutation Generates Additional Diversity in Mouse and Human Being 590

23.15 Somatic Mutation Is Induced by Cytidine Deaminase and Uracil Glycosylase 591

23.16 Avian Immunoglobulins Are Assembled from Pseudogenes 593

23.17 B Cell Memory Allows a Rapid Secondary Response 594

23.18 T Cell Receptors Are Related to Immunoglobulins 595

23.19 The T Cell Receptor Functions in Conjunction with the MHC 597

23.20 The Major Histocompatibility Locus Codes for Many Genes of the Immune System 599

23.21 Innate Immunity Utilizes Conserved Signaling Pathways 602

24 Promoters and Enhancers 609

24.2 Eukaryotic RNA Polymerases Consist of Many Subunits 612

24.3 Promoter Elements Are Defined by Mutations and Footprinting 613

24.4 RNA Polymerase I Has a Bipartite Promoter 614

24.5 RNA Polymerase III Uses Both Downstream and Upstream Promoters 615

24.6 TF[subscript III]B Is the Commitment Factor for Pol III Promoters 616

24.7 The Startpoint for RNA Polymerase II 618

24.8 TBP Is a Universal Factor 619

24.9 TBP Binds DNA in an Unusual Way 620

24.10 The Basal Apparatus Assembles at the Promoter 621

24.11 Initiation Is Followed by Promoter Clearance 623

24.12 A Connection between Transcription and Repair 625

24.13 Short Sequence Elements Bind Activators 627

24.14 Promoter Construction Is Flexible but Context Can Be Important 628

24.15 Enhancers Contain Bidirectional Elements That Assist Initiation 629

24.16 Enhancers Contain the Same Elements That Are Found at Promoters 630

24.17 Enhancers Work by Increasing the Concentration of Activators Near the Promoter 631

24.18 Gene Expression Is Associated with Demethylation 632

24.19 CpG Islands Are Regulatory Targets 634

25 Activating Transcription 640

25.2 There Are Several Types of Transcription Factors 642

25.3 Independent Domains Bind DNA and Activate Transcription 643

25.4 The Two Hybrid Assay Detects Protein-Protein Interactions 645

25.5 Activators Interact with the Basal Apparatus 646

25.6 Some Promoter-Binding Proteins Are Repressors 648

25.7 Response Elements Are Recognized by Activators 649

25.8 There Are Many Types of DNA-Binding Domains 651

25.9 A Zinc Finger Motif Is a DNA-Binding Domain 652

25.10 Steroid Receptors Are Activators 653

25.11 Steroid Receptors Have Zinc Fingers 655

25.12 Binding to the Response Element Is Activated by Ligand-Binding 656

25.13 Steroid Receptors Recognize Response Elements by a Combinatorial Code 657

25.14 Homeodomains Bind Related Targets in DNA 658

25.15 Helix-Loop-Helix Proteins Interact by Combinatorial Association 660

25.16 Leucine Zippers Are Involved in Dimer Formation 662

26 RNA Splicing and Processing 667

26.2 Nuclear Splice Junctions Are Short Sequences 670

26.3 Splice Junctions Are Read in Pairs 671

26.4 Pre-mRNA Splicing Proceeds through a Lariat 673

26.5 snRNAs Are Required for Splicing 674

26.6 U1 snRNP Initiates Splicing 676

26.7 The E Complex Can Be Formed by Intron Definition or Exon Definition 678

26.8 5 snRNPs Form the Spliceosome 679

26.9 An Alternative Splicing Apparatus Uses Different snRNPs 681

26.10 Splicing Is Connected to Export of mRNA 682

26.11 Group II Introns Autosplice via Lariat Formation 683

26.12 Alternative Splicing Involves Differential Use of Splice Junctions 685

26.13 trans-Splicing Reactions Use Small RNAs 688

26.14 Yeast tRNA Splicing Involves Cutting and Rejoining 690

26.15 The Splicing Endonuclease Recognizes tRNA 691

26.16 tRNA Cleavage and Ligation Are Separate Reactions 692

26.17 The Unfolded Protein Response Is Related to tRNA Splicing 693

26.18 The 3' Ends of polI and polIII Transcripts Are Generated by Termination 694

26.19 The 3' Ends of mRNAs Are Generated by Cleavage and Polyadenylation 695

26.20 Cleavage of the 3' End of Histone mRNA May Require a Small RNA 697

26.21 Production of rRNA Requires Cleavage Events 697

26.22 Small RNAs Are Required for rRNA Processing 699

27 Catalytic RNA 706

27.2 Group I Introns Undertake Self-Splicing by Transesterification 707

27.3 Group I Introns Form a Characteristic Secondary Structure 709

27.4 Ribozymes Have Various Catalytic Activities 711

27.5 Some Group I Introns Code for Endonucleases That Sponsor Mobility 715

27.6 Group II Introns May Code for Multifunction Proteins 716

27.7 Some Autosplicing Introns Require Maturases 717

27.8 The Catalytic Activity of RNAase P Is Due to RNA 718

27.9 Viroids Have Catalytic Activity 718

27.10 RNA Editing Occurs at Individual Bases 720

27.11 RNA Editing Can Be Directed by Guide RNAs 721

27.12 Protein Splicing Is Autocatalytic 724

28 Chromosomes 729

28.2 Viral Genomes Are Packaged into Their Coats 731

28.3 The Bacterial Genome Is a Nucleoid 734

28.4 The Bacterial Genome Is Supercoiled 735

28.5 Eukaryotic DNA Has Loops and Domains Attached to a Scaffold 736

28.6 Specific Sequences Attach DNA to an Interphase Matrix 737

28.7 Chromatin Is Divided into Euchromatin and Heterochromatin 738

28.8 Chromosomes Have Banding Patterns 740

28.9 Lampbrush Chromosomes Are Extended 741

28.10 Polytene Chromosomes Form Bands 742

28.11 Polytene Chromosomes Expand at Sites of Gene Expression 743

28.12 The Eukaryotic Chromosome Is a Segregation Device 744

28.13 Centromeres May Contain Repetitive DNA 746

28.14 Centromeres Have Short DNA Sequences in S. cerevisiae 747

28.15 The Centromere Binds a Protein Complex 748

28.16 Telomeres Have Simple Repeating Sequences 748

28.17 Telomeres Seat the Chromosome Ends 749

28.18 Telomeres Are Synthesized by a Ribonucleoprotein Enzyme 750

28.19 Telomeres Are Essential for Survival 752

29 Nucleosomes 757

29.2 The Nucleosome Is the Subunit of All Chromatin 759

29.3 DNA Is Coiled in Arrays of Nucleosomes 761

29.4 Nucleosomes Have a Common Structure 762

29.5 DNA Structure Varies on the Nucleosomal Surface 763

29.6 The Periodicity of DNA Changes on the Nucleosome 766

29.7 Organization of the Histone Octamer 767

29.8 The Path of Nucleosomes in the Chromatin Fiber 769

29.9 Reproduction of Chromatin Requires Assembly of Nucleosomes 771

29.10 Do Nucleosomes Lie at Specific Positions? 774

29.11 Are Transcribed Genes Organized in Nucleosomes? 777

29.12 Histone Octamers Are Displaced by Transcription 779

29.13 Nucleosome Displacement and Reassembly Require Special Factors 781

29.14 Insulators Block the Actions of Enhancers and Heterochromatin 781

29.15 Insulators Can Define a Domain 783

29.16 Insulators May Act in One Direction 784

29.17 Insulators Can Vary in Strength 785

29.18 DNAase Hypersensitive Sites Reflect Changes in Chromatin Structure 786

29.19 Domains Define Regions That Contain Active Genes 788

29.20 An LCR May Control a Domain 789

29.21 What Constitutes a Regulatory Domain? 790

30 Controlling Chromatin Structure 796

30.2 Chromatin Can Have Alternative States 797

30.3 Chromatin Remodeling Is an Active Process 798

30.4 Nucleosome Organization May Be Changed at the Promoter 801

30.5 Histone Modification Is a Key Event 802

30.6 Histone Acetylation Occurs in Two Circumstances 805

30.7 Acetylases Are Associated with Activators 806

30.8 Deacetylases Are Associated with Repressors 808

30.9 Methylation of Histones and DNA Is Connected 808

30.10 Chromatin States Are Interconverted by Modification 809

30.11 Promoter Activation Involves an Ordered Series of Events 809

30.12 Histone Phosphorylation Affects Chromatin Structure 810

30.13 Some Common Motifs Are Found in Proteins That Modify Chromatin 811

31 Epigenetic Effects Are Inherited 818

31.2 Heterochromatin Propagates from a Nucleation Event 820

31.3 Heterochromatin Depends on Interactions with Histones 822

31.4 Polycomb and Trithorax Are Antagonistic Repressors and Activators 824

31.5 X Chromosomes Undergo Global Changes 826

31.6 Chromosome Condensation Is Caused by Condensins 828

31.7 DNA Methylation Is Perpetuated by a Maintenance Methylase 830

31.8 DNA Methylation Is Responsible for Imprinting 832

31.9 Oppositely Imprinted Genes Can Be Controlled by a Single Center 834

31.10 Epigenetic Effects Can Be Inherited 835

31.11 Yeast Prions Show Unusual Inheritance 836

31.12 Prions Cause Diseases in Mammals 839.

Notes:

Includes bibliographical references and index.

Local Notes:

Acquired for the Penn Libraries with assistance from the Clarence J. Marshall Memorial Library Fund.

ISBN:

0763740632

9780763740634

OCLC:

65617431