5
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9780127114200
$72.95
Preface
1 Introduction
Text
2 Virulence Structure of Puccinia graminis Populations
2.1 Introduction
2.2 The Dissociation of Virulence for Genes Sr6 and Sr9d in Canada
2.3 The Association of Virulence for Genes Sr6 and Sr9d in the United States and Mexico
2.4 The Association and Dissociation of Virulence for Gene Sr9d, on the One Hand, and Genes Sr9a, Sr9b, or Sri5, on the Other
2.5 The Involvement of Dates and Temperature
2.6 Loss of Virulence Associations in Race 15B-1
2.7 The Dissociation of Virulence for Genes Sr6 and Sr9e
2.8 The Concept of Fitness
2.9 The Dissociation of Virulence for Gene Sr9e from Virulence for Genes Sr9a, Sr9b, and Sri15
2.10 Matching Virulence and the ABC-XYZ System
2.11 Genes Sr7b, SrlO, Srll, and SrTtl in the XYZ Group
2.12 Virulence Dissociation and Stabilizing Selection
2.13 Stabilizing Selection in Vertical Resistance
2.14 Stabilizing Selection and the Horizontal Resistance Equivalent
2.15 Stabilizing Selection Inhibiting Epidemics
2.16 The Second Gene-for-Gene Hypothesis
2.17 Breeding Wheat for Stem Rust Resistance
2.18 Multilines and Mixed Varieties
2.19 Possible Supergenes
2.20 Oat Stem Rust
2.21 Results with Some Other Pathogens
2.22 Some Conclusions
3 Races of Pathogens
3.1 Introduction
3.2 Additive and Multiplicative Increase
3.3 Genes and Taxa
3.4 The Ineptness of Fixed Races
3.5 Change as the Result of Gene Flow
3.6 Computerized Surveys
3.7 Discussion
4 The Influence of the Host
4.1 Introduction
4.2 Virus Diseases
4.3 Bacterial Diseases
4.4 Fungus Diseases
4.5 The Role of Mutations
4.6 Stabilizing Selection
4.7 Associated Virulence and Destabilizing Selection
4.8 An Illustrative Suggestion
4.9 Epistatic Interaction and Mathematical Models
4.10 Variable Mutation Rates
4.11 Genetic, Phenotypic, and Epidemiological Mutation
5 Host and Pathogen in a Two-Variable System
5.1 Introduction
5.2 The Geometric Illustration
5.3 Illustration by Analysis of Variance
5.4 Limitations of the Analysis of Variance Technique
5.5 Degrees of Freedom as a Limitation
5.6 Host and Pathogen Ranges as Limitations
5.7 Glossary
6 The Gene-for-Gene Hypothesis
6.1 Introduction
6.2 Biotrophy and Gene-for-Gene Systems
6.3 Possible Gene Duplication
6.4 Multiple Alleles with the Same Recognition System
6.5 Pseudoalleles with Different Recognition Systems
6.6 The Quadratic Check versus the Minimum Test for the Hypothesis
6.7 Susceptibility Is Specific
6.8 The Numerical and Chemical Implications of the Hypothesis
6.9 The Axenic Culture Fallacy
6.10 DNA
6.11 RNA
6.12 Protein
6.13 The Protein-for-Protein Hypothesis
6.14 Specific and Unspecific Receptors
6.15 Saccharides
6.16 Discussion
6.17 Ockham's Razor
7 Some Thermodynamic Background
7.1 Introduction
7.2 Free Energy, Enthalpy, Temperature, Entropy
7.3 Thermodynamic Clues
7.4 The Solvent Effect
7.5 A Possible Thermodynamic Sink
8 Continuously Variable Resistance to Disease
8.1 Introduction
8.2 The Polygene Model
8.3 Four Other Models
8.4 Polygenic Resistance versus Breeding for Resistance
8.5 The Error of Expecting Safety in Numbers
8.6 Experimental Evidence about Gene Numbers
8.7 The Central Role of Additive Variance
8.8 Additive Variance and Stable Resistance
8.9 Additive Resistance in Gains by Selection
8.10 Transgressive Segregation and Polygenic Resistance
8.11 Different Methods of Analyzing Variance
9 Epidemiology of Resistance to Disease
9.1 Introduction
9.2 Disease Progress Curves and Resistance
9.3 Slow Rusting and Incomplete Vertical Resistance
9.4 Horizontal Resistance That Delays the Start of an Epidemic
9.5 Resistance as Delayed Adult-Plant Susceptibility
9.6 Slow Rusting and Horizontal Resistance
9.7 The Ineptness of Some Infection Rate Averages
9.8 Testing for Resistance as Delayed Susceptibility
9.9 Young-Plant Susceptibility
9.10 Adult-Plant Resistance
10 The Anatomy of Epidemics
10.1 Introduction
10.2 The Logistic Equation Is Not a Model
10.3 The Background to Modeling
10.4 The Progeny/Parent Ratio in Reality
10.5 The Progeny/Parent Ratio in an Equation
10.6 The Effect of Dwindling Inoculum
10.7 The Role of the Latent Period
10.8 Epidemics with High Progeny/Parent Ratios
10.9 Epidemics with Low Progeny/Parent Ratios
10.10 The Threshold Condition for an Epidemic
10.11 A Varying Progeny/Parent Ratio
10.12 Internal Checks of Accuracy
10.13 Analysis versus Synthesis
10.14 Two Models: Plateaus and Peaks
10.15 Appendix about the Tables
11 The Spread of Disease
11.1 Introduction
11.2 Background
11.3 The Spread of Monocyclic Disease
11.4 The Spread of Poly cyclic Disease
11.5 The Rate of Spread of Fast Epidemics
11.6 Monocyclic and Poly cyclic Disease
11.7 The Effect of the Scatter of Disease on the Infection Rate
Bibliography
Index
Host-Pathogen Interactions in Plant Disease available in Hardcover
Host-Pathogen Interactions in Plant Disease
by J. E. Vanderplank
J. E. Vanderplank
- ISBN-10:
- 0127114203
- ISBN-13:
- 9780127114200
- Pub. Date:
- 01/28/1982
- Publisher:
- Elsevier Science
- ISBN-10:
- 0127114203
- ISBN-13:
- 9780127114200
- Pub. Date:
- 01/28/1982
- Publisher:
- Elsevier Science
Host-Pathogen Interactions in Plant Disease
by J. E. Vanderplank
J. E. Vanderplank
Hardcover
Buy New
$72.95
$72.95
72.95
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Overview
This book describes the genetics, biochemistry, and epidemiology of host-pathogen interactions in plant disease, especially as they concern the breeding of crops for disease resistance. It analyzes a wealth of information that has not previously been recorded in other books or reviews. Some of it stems from basic surveys of disease in the field. The analysis of these surveys not only explains a great deal about host-pathogen interactions that was heretofore obscure, but also indicates directions for future research. Other data, from original papers, have now been coordinated for the first time and organized in a way that suggests new areas of research. The book contains more than fifty new tables that integrate data and relate them to general principles of host-pathogen interactions.For plant pathologists and plant breeders concerned with the control of plant disease, the book shows how to manipulate the host and, indirectly, the pathogen in order to control disease. It analyzes records of resistance against disease that time has shown to be stable in an effort to determine what has kept this resistance stable. It also analyzes the structure of virulence in populations of a pathogen, and demonstrates how virulence can be deliberately restricted. The author updates information on the gene-for-gene hypothesis and discusses the numerical and biological implications of the hypothesis. He analyzes the structure of epidemics based on three fundamental variables: the initial inoculum, the progeny/parent ratio of the pathogen, and the latent period. The author concentrates on the progeny/parent ratio - a subject not hitherto probed in detail in the literature - and shows how to determine the type of epidemic that can occur.
Product Details
| ISBN-13: | 9780127114200 |
|---|---|
| Publisher: | Elsevier Science |
| Publication date: | 01/28/1982 |
| Pages: | 207 |
| Product dimensions: | 6.00(w) x 9.00(h) x (d) |
Table of Contents
ContentsPreface
1 Introduction
Text
2 Virulence Structure of Puccinia graminis Populations
2.1 Introduction
2.2 The Dissociation of Virulence for Genes Sr6 and Sr9d in Canada
2.3 The Association of Virulence for Genes Sr6 and Sr9d in the United States and Mexico
2.4 The Association and Dissociation of Virulence for Gene Sr9d, on the One Hand, and Genes Sr9a, Sr9b, or Sri5, on the Other
2.5 The Involvement of Dates and Temperature
2.6 Loss of Virulence Associations in Race 15B-1
2.7 The Dissociation of Virulence for Genes Sr6 and Sr9e
2.8 The Concept of Fitness
2.9 The Dissociation of Virulence for Gene Sr9e from Virulence for Genes Sr9a, Sr9b, and Sri15
2.10 Matching Virulence and the ABC-XYZ System
2.11 Genes Sr7b, SrlO, Srll, and SrTtl in the XYZ Group
2.12 Virulence Dissociation and Stabilizing Selection
2.13 Stabilizing Selection in Vertical Resistance
2.14 Stabilizing Selection and the Horizontal Resistance Equivalent
2.15 Stabilizing Selection Inhibiting Epidemics
2.16 The Second Gene-for-Gene Hypothesis
2.17 Breeding Wheat for Stem Rust Resistance
2.18 Multilines and Mixed Varieties
2.19 Possible Supergenes
2.20 Oat Stem Rust
2.21 Results with Some Other Pathogens
2.22 Some Conclusions
3 Races of Pathogens
3.1 Introduction
3.2 Additive and Multiplicative Increase
3.3 Genes and Taxa
3.4 The Ineptness of Fixed Races
3.5 Change as the Result of Gene Flow
3.6 Computerized Surveys
3.7 Discussion
4 The Influence of the Host
4.1 Introduction
4.2 Virus Diseases
4.3 Bacterial Diseases
4.4 Fungus Diseases
4.5 The Role of Mutations
4.6 Stabilizing Selection
4.7 Associated Virulence and Destabilizing Selection
4.8 An Illustrative Suggestion
4.9 Epistatic Interaction and Mathematical Models
4.10 Variable Mutation Rates
4.11 Genetic, Phenotypic, and Epidemiological Mutation
5 Host and Pathogen in a Two-Variable System
5.1 Introduction
5.2 The Geometric Illustration
5.3 Illustration by Analysis of Variance
5.4 Limitations of the Analysis of Variance Technique
5.5 Degrees of Freedom as a Limitation
5.6 Host and Pathogen Ranges as Limitations
5.7 Glossary
6 The Gene-for-Gene Hypothesis
6.1 Introduction
6.2 Biotrophy and Gene-for-Gene Systems
6.3 Possible Gene Duplication
6.4 Multiple Alleles with the Same Recognition System
6.5 Pseudoalleles with Different Recognition Systems
6.6 The Quadratic Check versus the Minimum Test for the Hypothesis
6.7 Susceptibility Is Specific
6.8 The Numerical and Chemical Implications of the Hypothesis
6.9 The Axenic Culture Fallacy
6.10 DNA
6.11 RNA
6.12 Protein
6.13 The Protein-for-Protein Hypothesis
6.14 Specific and Unspecific Receptors
6.15 Saccharides
6.16 Discussion
6.17 Ockham's Razor
7 Some Thermodynamic Background
7.1 Introduction
7.2 Free Energy, Enthalpy, Temperature, Entropy
7.3 Thermodynamic Clues
7.4 The Solvent Effect
7.5 A Possible Thermodynamic Sink
8 Continuously Variable Resistance to Disease
8.1 Introduction
8.2 The Polygene Model
8.3 Four Other Models
8.4 Polygenic Resistance versus Breeding for Resistance
8.5 The Error of Expecting Safety in Numbers
8.6 Experimental Evidence about Gene Numbers
8.7 The Central Role of Additive Variance
8.8 Additive Variance and Stable Resistance
8.9 Additive Resistance in Gains by Selection
8.10 Transgressive Segregation and Polygenic Resistance
8.11 Different Methods of Analyzing Variance
9 Epidemiology of Resistance to Disease
9.1 Introduction
9.2 Disease Progress Curves and Resistance
9.3 Slow Rusting and Incomplete Vertical Resistance
9.4 Horizontal Resistance That Delays the Start of an Epidemic
9.5 Resistance as Delayed Adult-Plant Susceptibility
9.6 Slow Rusting and Horizontal Resistance
9.7 The Ineptness of Some Infection Rate Averages
9.8 Testing for Resistance as Delayed Susceptibility
9.9 Young-Plant Susceptibility
9.10 Adult-Plant Resistance
10 The Anatomy of Epidemics
10.1 Introduction
10.2 The Logistic Equation Is Not a Model
10.3 The Background to Modeling
10.4 The Progeny/Parent Ratio in Reality
10.5 The Progeny/Parent Ratio in an Equation
10.6 The Effect of Dwindling Inoculum
10.7 The Role of the Latent Period
10.8 Epidemics with High Progeny/Parent Ratios
10.9 Epidemics with Low Progeny/Parent Ratios
10.10 The Threshold Condition for an Epidemic
10.11 A Varying Progeny/Parent Ratio
10.12 Internal Checks of Accuracy
10.13 Analysis versus Synthesis
10.14 Two Models: Plateaus and Peaks
10.15 Appendix about the Tables
11 The Spread of Disease
11.1 Introduction
11.2 Background
11.3 The Spread of Monocyclic Disease
11.4 The Spread of Poly cyclic Disease
11.5 The Rate of Spread of Fast Epidemics
11.6 Monocyclic and Poly cyclic Disease
11.7 The Effect of the Scatter of Disease on the Infection Rate
Bibliography
Index
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