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E-raamat: Lewin's GENES XII

  • Formaat: 838 pages
  • Ilmumisaeg: 02-Mar-2017
  • Kirjastus: Jones and Bartlett Publishers, Inc
  • Keel: eng
  • ISBN-13: 9781284104516
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  • Formaat: 838 pages
  • Ilmumisaeg: 02-Mar-2017
  • Kirjastus: Jones and Bartlett Publishers, Inc
  • Keel: eng
  • ISBN-13: 9781284104516
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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.
Preface xv
About the Authors xxiii
PART I Genes and Chromosomes
1(226)
Chapter 1 Genes Are DNA and Encode RNAs and Polypeptides
2(33)
Esther Siegfried
1.1 Introduction
3(1)
1.2 DNA Is the Genetic Material of Bacteria and Viruses
4(2)
1.3 DNA Is the Genetic Material of Eukaryotic Cells
6(1)
1.4 Polynucleotide Chains Have Nitrogenous Bases Linked to a Sugar-Phosphate Backbone
6(1)
1.5 Supercoiling Affects the Structure of DNA
7(2)
1.6 DNA Is a Double Helix
9(2)
1.7 DNA Replication Is Semiconservative
11(1)
1.8 Polymerases Act on Separated DNA Strands at the Replication Fork
12(1)
1.9 Genetic Information Can Be Provided by DNA or RNA
13(2)
1.10 Nucleic Acids Hybridize by Base Pairing
15(1)
1.11 Mutations Change the Sequence of DNA
16(1)
1.12 Mutations Can Affect Single Base Pairs or Longer Sequences
17(1)
1.13 The Effects of Mutations Can Be Reversed
18(1)
1.14 Mutations Are Concentrated at Hotspots
19(1)
1.15 Many Hotspots Result from Modified Bases
19(1)
1.16 Some Hereditary Agents Are Extremely Small
20(1)
1.17 Most Genes Encode Polypeptides
21(1)
1.18 Mutations in the Same Gene Cannot Complement
22(1)
1.19 Mutations May Cause Loss of Function or Gain of Function
23(1)
1.20 A Locus Can Have Many Different Mutant Alleles
24(1)
1.21 A Locus Can Have More Than One Wild-Type Allele
25(1)
1.22 Recombination Occurs by Physical Exchange of DNA
25(2)
1.23 The Genetic Code Is Triplet
27(2)
1.24 Every Coding Sequence Has Three Possible Reading Frames
29(1)
1.25 Bacterial Genes Are Colinear with Their Products
29(1)
1.26 Several Processes Are Required to Express the Product of a Gene
30(1)
1.27 Proteins Are trans-Acting but Sites on DNA Are c/'s-Acting
31(4)
Chapter 2 Methods in Molecular Biology and Genetic Engineering
35(36)
2.1 Introduction
35(1)
2.2 Nucleases
36(2)
2.3 Cloning
38(2)
2.4 Cloning Vectors Can Be Specialized for Different Purposes
40(3)
2.5 Nucleic Acid Detection
43(2)
2.6 DNA Separation Techniques
45(3)
2.7 DNA Sequencing
48(2)
2.8 PCR and RT-PCR
50(5)
2.9 Blotting Methods
55(3)
2.10 DNA Microarrays
58(3)
2.11 Chromatin Immunoprecipitation
61(1)
2.12 Gene Knockouts, Transgenics, and Genome Editing
62(9)
Chapter 3 The Interrupted Gene
71(30)
3.1 Introduction
71(1)
3.2 An Interrupted Gene Has Exons and Introns
72(1)
3.3 Exon and Intron Base Compositions Differ
73(1)
3.4 Organization of Interrupted Genes Can Be Conserved
73(1)
3.5 Exon Sequences Under Negative Selection Are Conserved but Introns Vary
74(1)
3.6 Exon Sequences Under Positive Selection Vary but Introns Are Conserved
75(1)
3.7 Genes Show a Wide Distribution of Sizes Due Primarily to Intron Size and Number Variation
76(2)
3.8 Some DNA Sequences Encode More Than One Polypeptide
78(1)
3.9 Some Exons Correspond to Protein Functional Domains
79(2)
3.10 Members of a Gene Family Have a Common Organization
81(1)
3.11 There Are Many Forms of Information in DNA
82(5)
3.12 The Content of the Genome
87(1)
4.1 Introduction
87(1)
4.2 Genome Mapping Reveals That Individual Genomes Show Extensive Variation
88(1)
4.3 SNPs Can Be Associated with Genetic Disorders
89(1)
4.4 Eukaryotic Genomes Contain Nonrepetitive and Repetitive DNA Sequences
90(2)
4.5 Eukaryotic Protein-Coding Genes Can Be Identified by the Conservation of Exons and of Genome Organization
92(2)
4.6 Some Eukaryotic Organelles Have DNA
94(1)
4.7 Organelle Genomes Are Circular DNAs That Encode Organelle Proteins
95(2)
4.8 The Chloroplast Genome Encodes Many Proteins and RNAs
97(1)
4.9 Mitochondria and Chloroplasts Evolved by Endosymbiosis
98(3)
Chapter 5 Genome Sequences and Evolution
101(42)
5.1 Introduction
102(1)
5.2 Prokaryotic Gene Numbers Range Over an Order of Magnitude
103(1)
5.3 Total Gene Number Is Known for Several Eukaryotes
104(2)
5.4 How Many Different Types of Genes Are There?
106(2)
5.5 The Human Genome Has Fewer Genes Than Originally Expected
108(2)
5.6 How Are Genes and Other Sequences Distributed in the Genome?
110(1)
5.7 The Y Chromosome Has Several Male-Specific Genes
111(1)
5.8 How Many Genes Are Essential?
112(3)
5.9 About 10,000 Genes Are Expressed at Widely Differing Levels in a Eukaryotic Cell
115(1)
5.10 Expressed Gene Number Can Be Measured En Masse
116(1)
5.11 DNA Sequences Evolve by Mutation and a Sorting Mechanism
117(2)
5.12 Selection Can Be Detected by Measuring Sequence Variation
119(3)
5.13 A Constant Rate of Sequence Divergence Is a Molecular Clock
122(3)
5.14 The Rate of Neutral Substitution Can Be Measured from Divergence of Repeated Sequences
125(1)
5.15 How Did Interrupted Genes Evolve?
126(2)
5.16 Why Are Some Genomes So Large?
128(2)
5.17 Morphological Complexity Evolves by Adding New Gene Functions
130(1)
5.18 Gene Duplication Contributes to Genome Evolution
131(1)
5.19 Globin Clusters Arise by Duplication and Divergence
132(2)
8.20 Pseudogenes Have Lost Their Original Functions
134(1)
5.21 Genome Duplication Has Played a Role in Plant and Vertebrate Evolution
135(2)
5.22 What is the Role of Transposable Elements in Genome Evolution
137(1)
5.23 There Can Be Biases in Mutation, Gene Conversion, and Codon Usage
137(6)
Chapter 6 Clusters and Repeats
143(46)
6.1 Introduction
143(2)
6.2 Unequal Crossing-Over Rearranges Gene Clusters
145(2)
6.3 Genes for rRNA Form Tandem Repeats Including an Invariant Transcription Unit
147(3)
6.4 Crossover Fixation Could Maintain Identical Repeats
150(2)
6.5 Satellite DNAs Often Lie in Heterochromatin
152(1)
6.6 Arthropod Satellites Have Very Short Identical Repeats
153(1)
6.7 Mammalian Satellites Consist of Hierarchical Repeats
154(3)
6.8 Minisatellites Are Useful for DNA Profiling
157(4)
6.9 Chromosomes
161(1)
Hank W. Bass
7.1 Introduction
162(1)
7.2 Viral Genomes Are Packaged into Their Coats
163(2)
7.3 The Bacterial Genome Is a Nucleoid with Dynamic Structural Properties
165(2)
7.4 The Bacterial Genome Is Supercoiled and Has Four Macrodomains
167(1)
7.5 Eukaryotic DNA Has Loops and Domains Attached to a Scaffold
168(1)
7.6 Specific Sequences Attach DNA to an Interphase Matrix
169(1)
7.7 Chromatin Is Divided into Euchromatin and Heterochromatin
170(2)
7.8 Chromosomes Have Banding Patterns
172(1)
7.9 Lampbrush Chromosomes Are Extended
173(1)
7.10 Polytene Chromosomes Form Bands
174(1)
7.11 Polytene Chromosomes Expand at Sites of Gene Expression
175(1)
7.12 The Eukaryotic Chromosome Is a Segregation Device
176(1)
7.13 Regional Centromeres Contain a Centromeric Histone H3 Variant and Repetitive DNA
177(2)
7.14 Point Centromeres in S, cerevisiae Contain Short, Essential DNA Sequences
179(1)
7.15 The S. cerevisiae Centromere Binds a Protein Complex
179(1)
7.16 Telomeres Have Simple Repeating Sequences
180(1)
7.17 Telomeres Seal the Chromosome Ends and Function in Meiotic Chromosome Pairing
181(1)
7.18 Telomeres Are Synthesized by a Ribonucleoprotein Enzyme
182(2)
7.19 Telomeres Are Essential for Survival
184(5)
Chapter 8 Chromatin
189(38)
Craig Peterson
8.1 Introduction
189(1)
8.2 DNA Is Organized in Arrays of Nucleosomes
190(2)
8.3 The Nucleosome Is the Subunit of All Chromatin
192(4)
8.4 Nucleosomes Are Covalently Modified
196(3)
8.5 Histone Variants Produce Alternative Nucleosomes
199(3)
8.6 DNA Structure Varies on the Nucleosomal Surface
202(3)
8.7 The Path of Nucleosomes in the Chromatin Fiber
205(2)
8.8 Replication of Chromatin Requires Assembly of Nucleosomes
207(2)
8.9 Do Nucleosomes Lie at Specific Positions?
209(3)
8.10 Nucleosomes Are Displaced and Reassembled During Transcription
212(3)
8.11 DNase Sensitivity Detects Changes in Chromatin Structure
215(2)
8.12 An LCR Can Control a Domain
217(1)
8.13 Insulators Define Transcriptionally Independent Domains
218(9)
PART II DNA Replication and Recombination
227(214)
Chapter 9 Replication Is Connected to the Cell Cycle
228(17)
Barbara Funnell
9.1 Introduction
228(2)
9.2 Bacterial Replication Is Connected to the Cell Cycle
230(1)
9.3 The Shape and Spatial Organization of a Bacterium Are Important During Chromosome Segregation and Cell Division
231(1)
9.4 Mutations in Division or Segregation Affect Cell Shape
232(1)
9.5 FtsZ Is Necessary for Septum Formation
233(1)
9.6 Min and noc/slm Genes Regulate the Location of the Septum
233(1)
9.7 Partition Involves Separation of the Chromosomes
234(1)
9.8 Chromosomal Segregation Might Require Site-Specific Recombination
235(2)
9.9 The Eukaryotic Growth Factor Signal Transduction Pathway Promotes Entry to S Phase
237(2)
9.10 Checkpoint Control for Entry into S Phase: p53, a Guardian of the Checkpoint
239(1)
9.11 Checkpoint Control for Entry into S Phase: Rb, a Guardian of the Checkpoint
240(5)
Chapter 10 The Replicon: Initiation of Replication
245(16)
10.1 Introduction
245(1)
10.2 An Origin Usually Initiates Bidirectional Replication
246(1)
10.3 The Bacterial Genome Is (Usually) a Single Circular Replicon
247(1)
10.4 Methylation of the Bacterial Origin Regulates Initiation
248(1)
10.5 Initiation: Creating the Replication Forks at the Origin oriC
249(2)
10.6 Multiple Mechanisms Exist to Prevent Premature Reinitiation of Replication
251(1)
10.7 Archaeal Chromosomes Can Contain Multiple Replicons
252(1)
10.8 Each Eukaryotic Chromosome Contains Many Replicons
252(1)
10.9 Replication Origins Can Be Isolated in Yeast
253(2)
10.10 Licensing Factor Controls Eukaryotic Rereplication
255(1)
10.11 Licensing Factor Binds to ORC
256(5)
Chapter 11 DNA Replication
261(22)
11.1 Introduction
261(1)
11.2 DNA Polymerases Are the Enzymes That Make DNA
262(2)
11.3 DNA Polymerases Have Various Nuclease Activities
264(1)
11.4 DNA Polymerases Control the Fidelity of Replication
264(1)
11.5 DNA Polymerases Have a Common Structure
265(1)
11.6 The Two New DNA Strands Have Different Modes of Synthesis
266(1)
11.7 Replication Requires a Helicase and a Single-Stranded Binding Protein
267(1)
11.8 Priming Is Required to Start DNA Synthesis
268(2)
11.9 Coordinating Synthesis of the Lagging and Leading Strands
270(1)
11.10 DNA Polymerase Holoenzyme Consists of Subcomplexes
270(1)
11.11 The Clamp Controls Association of Core Enzyme with DNA
271(3)
11.12 Okazaki Fragments Are Linked by Ligase
274(2)
11.13 Separate Eukaryotic DNA Polymerases Undertake Initiation and Elongation
276(2)
11.14 Lesion Bypass Requires Polymerase Replacement
278(1)
11.15 Termination of Replication
279(4)
Chapter 12 Extrachromosomal Replicons
283(22)
12.1 Introduction
283(1)
12.2 The Ends of Linear DNA Are a Problem for Replication
284(1)
12.3 Terminal Proteins Enable Initiation at the Ends of Viral DNAs
285(1)
12.4 Rolling Circles Produce Multimers of a Replicon
286(1)
12.5 Rolling Circles Are Used to Replicate Phage Genomes
287(1)
12.6 The F Plasmid Is Transferred by Conjugation Between Bacteria
288(2)
12.7 Conjugation Transfers Single-Stranded DNA
290(1)
12.8 Single-Copy Plasmids Have a Partitioning System
291(2)
12.9 Plasmid Incompatibility Is Determined by the Replicon
293(1)
12.10 The ColE1 Compatibility System Is Controlled by an RNA Regulator
293(3)
12.11 How Do Mitochondria Replicate and Segregate?
296(1)
12.12 D Loops Maintain Mitochondrial Origins
297(1)
12.13 The Bacterial Ti Plasmid Causes Crown Gall Disease in Plants
298(1)
12.14 T-DNA Carries Genes Required for Infection
299(2)
12.15 Transfer of T-DNA Resembles Bacterial Conjugation
301(4)
Chapter 13 Homologous and Site-Specific Recombination
305(34)
Hannah L. Klein
Samantha Hoot
13.1 Introduction
306(1)
13.2 Homologous Recombination Occurs Between Synapsed Chromosomes in Meiosis
306(2)
13.3 Double-Strand Breaks Initiate Recombination
308(2)
13.4 Gene Conversion Accounts for Interallelic Recombination
310(1)
13.5 The Synthesis-Dependent Strand-Annealing Model
311(1)
13.6 The Single-Strand Annealing Mechanism Functions at Some Double-Strand Breaks
312(1)
13.7 Break-Induced Replication Can Repair Double-Strand Breaks
313(1)
13.8 Recombining Meiotic Chromosomes Are Connected by the Synaptonemal Complex
314(1)
13.9 The Synaptonemal Complex Forms After Double-Strand Breaks
315(1)
13.10 Pairing and Synaptonemal Complex Formation Are Independent
316(1)
13.11 The Bacterial RecBCD System Is Stimulated by chi Sequences
317(1)
13.12 Strand-Transfer Proteins Catalyze Single-Strand Assimilation
318(3)
13.13 Holliday Junctions Must Be Resolved
321(1)
13.14 Eukaryotic Genes Involved in Homologous Recombination
322(3)
1 End Processing/Presynapsis
322(2)
2 Synapsis
324(1)
3 DNA Heteroduplex Extension and Branch Migration
324(1)
4 Resolution
324(1)
13.15 Specialized Recombination Involves Specific Sites
325(1)
13.16 Site-Specific Recombination Involves Breakage and Reunion
326(1)
13.17 Site-Specific Recombination Resembles Topoisomerase Activity
327(1)
13.18 Lambda Recombination Occurs in an Intasome
328(1)
13.19 Yeast Can Switch Silent and Active Mating-Type Loci
329(2)
13.20 Unidirectional Gene Conversion Is Initiated by the Recipient MAT Locus
331(1)
13.21 Antigenic Variation in Trypanosomes Uses Homologous Recombination
332(1)
13.22 Recombination Pathways Adapted for Experimental Systems
332(7)
Chapter 14 Repair Systems
339(28)
14.1 Introduction
339(2)
14.2 Repair Systems Correct Damage to DNA
341(2)
14.3 Excision Repair Systems in E. coli
343(1)
14.4 Eukaryotic Nucleotide Excision Repair Pathways
344(1)
14.5 Base Excision Repair Systems Require Glycosylases
345(4)
14.6 Error-Prone Repair and Translesion Synthesis
349(1)
14.7 Controlling the Direction of Mismatch Repair
349(3)
14.8 Recombination-Repair Systems in E. coli
352(1)
14.9 Recombination Is an Important Mechanism to Recover from Replication Errors
353(1)
14.10 Recombination-Repair of Double-Strand Breaks in Eukaryotes
354(2)
14.11 Nonhomologous End Joining Also Repairs Double-Strand Breaks
356(1)
14.12 DNA Repair in Eukaryotes Occurs in the Context of Chromatin
357(4)
14.13 RecA Triggers the SOS System
361(6)
Chapter 15 Transposable Elements and Retroviruses
367(30)
Damon Lisch
15.1 Introduction
368(1)
15.2 Insertion Sequences Are Simple Transposition Modules
369(1)
15.3 Transposition Occurs by Both Replicative and Nonreplicative Mechanisms
370(2)
15.4 Transposons Cause Rearrangement of DNA
372(1)
15.5 Replicative Transposition Proceeds Through a Cointegrate
373(1)
15.6 Nonreplicative Transposition Proceeds by Breakage and Reunion
374(1)
15.7 Transposons Form Superfamilies and Families
375(3)
15.8 The Role of Transposable Elements in Hybrid Dysgenesis
378(1)
15.9 P Elements Are Activated in the Germ line
379(2)
15.10 The Retrovirus Life Cycle Involves Transposition-Like Events
381(1)
15.11 Retroviral Genes Code for Polyproteins
381(2)
15.12 Viral DNA Is Generated by Reverse Transcription
383(2)
15.13 Viral DNA Integrates into the Chromosome
385(1)
15.14 Retroviruses May Transduce Cellular Sequences
386(2)
15.15 Retroelements Fall into Three Classes
388(1)
15.16 Yeast Ty Elements Resemble Retroviruses
389(2)
15.17 The Alu Family Has Many Widely Dispersed Members
391(1)
15.18 LINEs Use an Endonuclease to Generate a Priming End
392(5)
Chapter 16 Somatic DNA Recombination and Hypermutation in the Immune System
397(44)
Paolo Casali
16.1 The Immune System: Innate and Adaptive Immunity
398(1)
16.2 The Innate Response Utilizes Conserved Recognition Molecules and Signaling Pathways
399(2)
16.3 Adaptive Immunity
401(1)
16.4 Clonal Selection Amplifies Lymphocytes That Respond to a Given Antigen
402(2)
16.5 Ig Genes Are Assembled from Discrete DNA Segments in B Lymphocytes
404(1)
16.6 L Chains Are Assembled by a Single Recombination Event
405(1)
16.7 H Chains Are Assembled by Two Sequential Recombination Events
406(1)
16.8 Recombination Generates Extensive Diversity
407(1)
16.9 V(D)J DNA Recombination Relies on RSS and Occurs by Deletion or Inversion
408(2)
16.10 Allelic Exclusion Is Triggered by Productive Rearrangements
410(1)
16.11 RAG1/RAG2 Catalyze Breakage and Religation of V(D)J Gene Segments
411(2)
16.12 B Cell Development in the Bone Marrow: From Common Lymphoid Progenitor to Mature B Cell
413(2)
16.13 Class Switch DNA Recombination
415(1)
16.14 CSR Involves AID and Elements of the NHEJ Pathway
416(2)
16.15 Somatic Hypermutation Generates Additional Diversity and Provides the Substrate for Higher-Affinity Submutants
418(1)
16.16 SHM Is Mediated by AID, Ung, Elements of the Mismatch DNA Repair Machinery, and Translesion DNA Synthesis Polymerases
419(1)
16.17 Igs Expressed in Avians Are Assembled from Pseudogenes
420(1)
16.18 Chromatin Architecture Dynamics of the IgH Locus in V(D) Recombination, CSR, and SHM
421(2)
16.19 Epigenetics of V(D)J Recombination, CSR, and SHM
423(2)
16.20 B Cell Differentiation Results in Maturation of the Antibody Response and Generation of Long-lived Plasma Cells and Memory B Cells
425(1)
16.21 The T Cell Receptor Antigen Is Related to the BCR
426(1)
16.22 The TCR Functions in Conjunction with the MHC
427(1)
16.23 The MHC Locus Comprises a Cohort of Genes Involved in Immune Recognition
428(13)
PART III Transcription and Posttranscriptional Mechanisms
441(206)
Chapter 17 Prokaryotic Transcription
442(37)
17.1 Introduction
443(1)
17.2 Transcription Occurs by Base Pairing in a "Bubble" of Unpaired DNA
444(1)
17.3 The Transcription Reaction Has Three Stages
445(1)
17.4 Bacterial RNA Polymerase Consists of Multiple Subunits
446(1)
17.5 RNA Polymerase Holoenzyme Consists of the Core Enzyme and Sigma Factor
446(2)
17.6 How Does RNA Polymerase Find Promoter Sequences?
448(1)
17.7 The Holoenzyme Goes Through Transitions in the Process of Recognizing and Escaping from Promoters
448(3)
17.8 Sigma Factor Controls Binding to DNA by Recognizing Specific Sequences in Promoters
451(1)
17.9 Promoter Efficiencies Can Be Increased or Decreased by Mutation
452(1)
17.10 Multiple Regions in RNA Polymerase Directly Contact Promoter DNA
453(3)
17.11 RNA Polymerase--Promoter and DNA--Protein Interactions Are the Same for Promoter Recognition and DNA Melting
456(2)
17.12 Interactions Between Sigma Factor and Core RNA Polymerase Change During Promoter Escape
458(1)
17.13 A Model for Enzyme Movement Is Suggested by the Crystal Structure
459(2)
17.14 A Stalled RNA Polymerase Can Restart
461(1)
17.15 Bacterial RNA Polymerase Terminates at Discrete Sites
461(2)
17.16 How Does Rho Factor Work?
463(2)
17.17 Supercoiling Is an Important Feature of Transcription
465(1)
17.18 Phage T7 RNA Polymerase Is a Useful Model System
466(1)
17.19 Competition for Sigma Factors Can Regulate Initiation
466(2)
17.20 Sigma Factors Can Be Organized into Cascades
468(1)
17.21 Sporulation Is Controlled by Sigma Factors
469(2)
17.22 Antitermination Can Be a Regulatory Event
471(8)
Chapter 18 Eukaryotic Transcription
479(24)
18.1 Introduction
479(2)
18.2 Eukaryotic RNA Polymerases Consist of Many Subunits
481(1)
18.3 RNA Polymerase I Has a Bipartite Promoter
482(1)
18.4 RNA Polymerase III Uses Downstream and Upstream Promoters
483(2)
18.5 The Start Point for RNA Polymerase II
485(1)
18.6 TBP Is a Universal Factor
486(2)
18.7 The Basal Apparatus Assembles at the Promoter
488(2)
18.8 Initiation Is Followed by Promoter Clearance and Elongation
490(3)
18.9 Enhancers Contain Bidirectional Elements That Assist Initiation
493(1)
18.10 Enhancers Work by Increasing the Concentration of Activators Near the Promoter
494(1)
18.11 Gene Expression Is Associated with Demethylation
495(1)
18.12 CpG Islands Are Regulatory Targets
496(7)
Chapter 19 RNA Splicing and Processing
503(40)
19.1 Introduction
503(2)
19.2 The 5' End of Eukaryotic mRNA Is Capped
505(1)
19.3 Nuclear Splice Sites Are Short Sequences
506(1)
19.4 Splice Sites Are Read in Pairs
507(1)
19.5 Pre-mRNA Splicing Proceeds Through a Lariat
508(1)
19.6 snRNAs Are Required for Splicing
509(1)
19.7 Commitment of Pre-mRNA to the Splicing Pathway
510(3)
19.8 The Spliceosome Assembly Pathway
513(2)
19.9 An Alternative Spliceosome Uses Different snRNPs to Process the Minor Class of Introns
515(1)
19.10 Pre-mRNA Splicing Likely Shares the Mechanism with Group II Autocatalytic Introns
516(2)
19.11 Splicing Is Temporally and Functionally Coupled with Multiple Steps in Gene Expression
518(1)
19.12 Alternative Splicing Is a Rule, Rather Than an Exception, in Multicellular Eukaryotes
519(3)
19.13 Splicing Can Be Regulated by Exonic and Intronic Splicing Enhancers and Silencers
522(2)
19.14 Trans-Splicing Reactions Use Small RNAs
524(2)
19.15 The 3' Ends of mRNAs Are Generated by Cleavage and Polyadenylation
526(2)
19.16 3' mRNA End Processing Is Critical for Termination of Transcription
528(1)
19.17 The 3' End Formation of Histone mRNA Requires U7 snRNA
529(1)
19.18 tRNA Splicing Involves Cutting and Rejoining in Separate Reactions
530(3)
19.19 The Unfolded Protein Response Is Related to tRNA Splicing
533(1)
19.20 Production of rRNA Requires Cleavage Events and Involves Small RNAs
534(9)
Chapter 20 mRNA Stability and Localization
543(20)
Ellen Baker
20.1 Introduction
543(1)
20.2 Messenger RNAs Are Unstable Molecules
544(2)
20.3 Eukaryotic mRNAs Exist in the Form of mRNPs from Their Birth to Their Death
546(1)
20.4 Prokaryotic mRNA Degradation Involves Multiple Enzymes
546(2)
20.5 Most Eukaryotic mRNA Is Degraded via Two Deadenylation-Dependent Pathways
548(2)
20.6 Other Degradation Pathways Target Specific mRNAs
550(2)
20.7 mRNA-Specific Half-Lives Are Controlled by Sequences or Structures Within the mRNA
552(1)
20.8 Newly Synthesized RNAs Are Checked for Defects via a Nuclear Surveillance System
553(2)
20.9 Quality Control of mRNA Translation Is Performed by Cytoplasmic Surveillance Systems
555(2)
20.10 Translationally Silenced mRNAs Are Sequestered in a Variety of RNA Granules
557(1)
20.11 Some Eukaryotic mRNAs Are Localized to Specific Regions of a Cell
558(5)
Chapter 21 Catalytic RNA
563(20)
Douglas J. Briant
21.1 Introduction
563(1)
21.2 Group I Introns Undertake Self-Splicing by Transesterification
564(3)
21.3 Group I Introns Form a Characteristic Secondary Structure
567(1)
21.4 Ribozymes Have Various Catalytic Activities
568(2)
21.5 Some Group I Introns Encode Endonucleases That Sponsor Mobility
570(1)
21.6 Group II Introns May Encode Multifunction Proteins
571(1)
21.7 Some Autosplicing Introns Require Maturases
572(1)
21.8 The Catalytic Activity of RNase P Is Due to RNA
573(1)
21.9 Viroids Have Catalytic Activity
573(2)
21.10 RNA Editing Occurs at Individual Bases
575(1)
21.11 RNA Editing Can Be Directed by Guide RNAs
576(2)
21.12 Protein Splicing Is Autocatalytic
578(5)
Chapter 22 Translation
583(38)
22.1 Introduction
583(1)
22.2 Translation Occurs by Initiation, Elongation, and Termination
584(2)
22.3 Special Mechanisms Control the Accuracy of Translation
586(1)
22.4 Initiation in Bacteria Needs 30S Subunits and Accessory Factors
587(2)
22.5 Initiation Involves Base Pairing Between mRNA and rRNA
589(1)
22.6 A Special Initiator tRNA Starts the Polypeptide Chain
590(1)
22.7 Use of fMet-tRNAf Is Controlled by IF-2 and the Ribosome
591(1)
22.8 Small Subunits Scan for Initiation Sites on Eukaryotic mRNA
592(1)
22.9 Eukaryotes Use a Complex of Many Initiation Factors
593(4)
22.10 Elongation Factor Tu Loads Aminoacyl-tRNA into the A Site
597(1)
22.11 The Polypeptide Chain Is Transferred to Aminoacyl-tRNA
598(1)
22.12 Translocation Moves the Ribosome
599(1)
22.13 Elongation Factors Bind Alternately to the Ribosome
600(1)
22.14 Three Codons Terminate Translation
601(1)
22.15 Termination Codons Are Recognized by Protein Factors
602(2)
22.16 Ribosomal RNA Is Found Throughout Both Ribosomal Subunits
604(2)
22.17 Ribosomes Have Several Active Centers
606(2)
22.18 16S rRNA Plays an Active Role in Translation
608(2)
22.19 23S rRNA Has Peptidyl Transferase Activity
610(1)
22.20 Ribosomal Structures Change When the Subunits Come Together
611(1)
22.21 Translation Can Be Regulated
612(1)
22.22 The Cycle of Bacterial Messenger RNA
613(8)
Chapter 23 Using the Genetic Code
621(26)
23.1 Introduction
621(1)
23.2 Related Codons Represent Chemically Similar Amino Acids
622(1)
23.3 Codon-Anticodon Recognition Involves Wobbling
623(1)
23.4 tRNAs Are Processed from Longer Precursors
624(1)
23.5 tRNA Contains Modified Bases
625(2)
23.6 Modified Bases Affect Anticodon-Codon Pairing
627(1)
23.7 The Universal Code Has Experienced Sporadic Alterations
628(2)
23.8 Novel Amino Acids Can Be Inserted at Certain Stop Codons
630(1)
23.9 tRNAs Are Charged with Amino Acids by Aminoacyl-tRNA Synthetases
631(1)
23.10 Aminoacyl-tRNA Synthetases Fall into Two Classes
632(2)
23.11 Synthetases Use Proofreading to Improve Accuracy
634(2)
23.12 Suppressor tRNAs Have Mutated Anticodons That Read New Codons
636(1)
23.13 Each Termination Codon Has Nonsense Suppressors
637(1)
23.14 Suppressors May Compete with Wild-Type Reading of the Code
638(1)
23.15 The Ribosome Influences the Accuracy of Translation
639(2)
23.16 Frameshifting Occurs at Slippery Sequences
641(1)
23.17 Other Recoding Events: Translational Bypassing and the tmRNA Mechanism to Free Stalled Ribosomes
642(5)
PART IV Gene Regulation
647(136)
Chapter 24 The Operon
648(29)
Lishin Swint-Kruse
24.1 Introduction
649(2)
24.2 Structural Gene Clusters Are Coordinately Controlled
651(1)
24.3 The lac Operon Is Negative Inducible
652(1)
24.4 The lac Repressor Is Controlled by a Small-Molecule Inducer
653(2)
24.5 c/s-Acting Constitutive Mutations Identify the Operator
655(1)
24.6 trans-Acting Mutations Identify the Regulator Gene
655(1)
24.7 The lac Repressor Is a Tetramer Made of Two Dimers
656(2)
24.8 Lac Repressor Binding to the Operator Is Regulated by an Allosteric Change in Conformation
658(2)
24.9 The lac Repressor Binds to Three Operators and Interacts with RNA Polymerase
660(1)
24.10 The Operator Competes with Low-Affinity Sites to Bind Repressor
661(1)
24.11 The lac Operon Has a Second Layer of Control: Catabolite Repression
662(3)
24.12 The trp Operon Is a Repressible Operon with Three Transcription Units
665(1)
24.13 The trp Operon Is Also Controlled by Attenuation
666(2)
24.14 Attenuation Can Be Controlled by Translation
668(2)
24.15 Stringent Control by Stable RNA Transcription
670(1)
24.16 r-Protein Synthesis Is Controlled by Autoregulation
671(6)
Chapter 25 Phage Strategies
677(24)
25.1 Introduction
677(2)
25.2 Lytic Development Is Divided into Two Periods
679(1)
25.3 Lytic Development Is Controlled by a Cascade
679(2)
25.4 Two Types of Regulatory Events Control the Lytic Cascade
681(1)
25.5 The Phage T7 and T4 Genomes Show Functional Clustering
681(2)
25.6 Lambda Immediate Early and Delayed Early Genes Are Needed for Both Lysogeny and the Lytic Cycle
683(1)
25.7 The Lytic Cycle Depends on Antitermination by pN
684(1)
25.8 Lysogeny Is Maintained by the Lambda Repressor Protein
685(1)
25.9 The Lambda Repressor and Its Operators Define the Immunity Region
686(1)
25.10 The DNA-Binding Form of the Lambda Repressor Is a Dimer
687(1)
25.11 The Lambda Repressor Uses a Helix-Turn-Helix Motif to Bind DNA
688(1)
25.12 Lambda Repressor Dimers Bind Cooperatively to the Operator
689(1)
25.13 The Lambda Repressor Maintains an Autoregulatory Circuit
690(2)
25.14 Cooperative Interactions Increase the Sensitivity of Regulation
692(1)
25.15 The cII and cIII Genes Are Needed to Establish Lysogeny
692(1)
25.16 A Poor Promoter Requires cII Protein
693(1)
25.17 Lysogeny Requires Several Events
694(1)
25.18 The Cro Repressor Is Needed for Lytic Infection
694(3)
25.19 What Determines the Balance Between Lysogeny and the Lytic Cycle?
697(4)
Chapter 26 Eukaryotic Transcription Regulation
701(30)
26.1 Introduction
702(1)
26.2 How Is a Gene Turned On?
703(1)
26.3 Mechanism of Action of Activators and Repressors
704(3)
26.4 Independent Domains Bind DNA and Activate Transcription
707(1)
26.5 The Two-Hybrid Assay Detects Protein-Protein Interactions
707(1)
26.6 Activators Interact with the Basal Apparatus
708(3)
26.7 Many Types of DNA-Binding Domains Have Been Identified
711(1)
26.8 Chromatin Remodeling Is an Active Process
712(3)
26.9 Nucleosome Organization or Content Can Be Changed at the Promoter
715(1)
26.10 Histone Acetylation Is Associated with Transcription Activation
716(3)
26.11 Methylation of Histones and DNA Is Connected
719(1)
26.12 Promoter Activation Involves Multiple Changes to Chromatin
720(2)
26.13 Histone Phosphorylation Affects Chromatin Structure
722(1)
26.14 Yeast GAL Genes: A Model for Activation and Repression
722(9)
Chapter 27 Epigenetics I
731(18)
Trygve Tollefsbol
27.1 Introduction
731(1)
27.2 Heterochromatin Propagates from a Nucleation Event
732(2)
27.3 Heterochromatin Depends on Interactions with Histones
734(3)
27.4 Polycomb and Trithorax Are Antagonistic Repressors and Activators
737(1)
27.5 CpG Islands Are Subject to Methylation
738(3)
27.6 Epigenetic Effects Can Be Inherited
741(2)
27.7 Yeast Prions Show Unusual Inheritance
743(6)
Chapter 28 Epigenetics II
749(12)
Trygve Tollefsbol
28.1 Introduction
749(1)
28.2 X Chromosomes Undergo Global Changes
750(2)
28.3 Chromosome Condensation Is Caused by Condensins
752(3)
28.4 DNA Methylation Is Responsible for Imprinting
755(1)
28.5 Oppositely Imprinted Genes Can Be Controlled by a Single Center
756(1)
28.6 Prions Cause Diseases in Mammals
757(4)
Chapter 29 Noncoding RNA
761(8)
29.1 Introduction
761(1)
29.2 A Riboswitch Can Alter Its Structure According to Its Environment
762(1)
29.3 Noncoding RNAs Can Be Used to Regulate Gene Expression
763(6)
Chapter 30 Regulatory RNA
769(14)
30.1 Introduction
769(1)
30.2 Bacteria Contain Regulator RNAs
770(2)
30.3 MicroRNAs Are Widespread Regulators in Eukaryotes
772(3)
30.4 How Does RNA Interference Work?
775(3)
30.5 Heterochromatin Formation Requires MicroRNAs
778(5)
Glossary 783(26)
Index 809
Jocelyn E. Krebs received a B.A. in Biology from Bard College, Annandale-on-Hudson, New York, and a Ph.D. in Molecular and Cell Biology from the University of California, Berkeley. For her Ph.D. thesis, she studied the roles of DNA topology and insulator elements in transcriptional regulation. She performed her postdoctoral training as an American Cancer Society Fellow at the University of Massachusetts Medical School in the laboratory of Dr. Craig Peterson, where she focused on the roles of histone acetylation and chromatin remodeling in transcription. In 2000, Dr. Krebs joined the faculty in the Department of Biological Sciences at the University of Alaska, Anchorage, where she is now a Full Professor. Her most recent research focus has been on the role of the Williams syndrome transcription factor (one of the genes lost in the human neurodevelopmental syndrome Williams syndrome) in early embryonic development in the frog Xenopus. She teaches courses in introductory biology, genetics, and molecular biology for undergraduates, graduate students, and first-year medical students. She also teaches courses on the molecular biology of cancer and epigenetics. Although working in Anchorage, she lives in Portland, Oregon, with her wife and two sons, a dog, and three cats. Her nonwork passions include hiking, gardening, and fused glass work.'

Elliott S. Goldstein earned his B.S. in Biology from the University of Hartford in Connecticut and his Ph.D. in Genetics from the University of Minnesota, Department of Genetics and Cell Biology. Following this, he was awarded an NIH Postdoctoral Fellowship to work with Dr. Sheldon Penman at the Massachusetts Institute of Technology. After leaving Boston, he joined the faculty at Arizona State University in Tempe, Arizona, where he is an Associate Professor, Emeritus, in the Cellular, Molecular, and Biosciences program in the School of Life Sciences and in the Honors Disciplinary Program. His research interests are in the area of molecular and developmental genetics of early embryogenesis in Drosophila melanogaster. In recent years, he has focused on the Drosophila counterparts of the human protooncogenes jun and fos. His primary teaching responsibilities are in the undergraduate general genetics course as well as the graduate-level molecular genetics course. Dr. Goldstein lives in Tempe with his wife, his high school sweetheart. They have three children and two grandchildren. He is a bookworm who loves reading as well as underwater photography. His pictures can be found at http://www.public.asu.edu/~elliotg/.

Stephen T. Kilpatrick received a B.S. in Biology from Eastern College (now Eastern University) in St. Davids, Pennsylvania, and a Ph.D. from the Program in Ecology and Evolutionary Biology at Brown University. His thesis research was an investigation of the population genetics of interactions between the mitochondrial and nuclear genomes of Drosophila melanogaster. Since 1995, Dr. Kilpatrick has taught at the University of Pittsburgh at Johnstown in Johnstown, Pennsylvania, where he is currently chair of the Department of Biology. His regular teaching duties include undergraduate courses in introductory biology for biology majors and advanced undergraduate courses in genetics (for both majors and nursing students), evolution, and molecular genetics. He has also supervised a number of undergraduate research projects in evolutionary genetics. Dr. Kilpatricks major professional focus has been in biology education. He has participated in the development and authoring of ancillary materials for several introductory biology, genetics, and molecular genetics texts and online educational review sites as well as writing articles for educational reference publications. For his classes at Pitt-Johnstown, Dr. Kilpatrick has developed many active learning exercises in introductory biology, genetics, and evolution. Dr. Kilpatrick resides in Johnstown with his wife and four cats. Outside of scientific interests, he enjoys music, literature, and theater.