1;Preface;5 2;List of Contents;7 3;List of Contributors;9 4;The Regulation of Chromatin and DNA-Methylation Patterns in Blood Cell Development;10 4.1;1 Cell-fate Decisions in the Haematopoietic System;10 4.2;2 Transcription Factors Co-operate with Chromatin Components and Reorganise Chromatin Structure Prior to the Activation of Gene Expression;12 4.3;3 The Role of Transcription Factors and Chromatin Components in the Regulation of Cell- fate Decisions;16 4.4;4 Outlook: Epigenetic Plasticity and Reprogramming;18 4.5;References;19 5;Methylation Dynamics in the Early Mammalian Embryo: Implications of Genome Reprogramming Defects for Development;22 5.1;1 Methylation Reprogramming in Early Mouse Embryos;23 5.2;2 Species Differences in Methylation Reprogramming;26 5.3;3 Methylation Reprogramming Defects;27 5.4;References;29 6;Epigenetic Regulation in Drosophila;32 6.1;1 DNA Methylation in Drosophila;33 6.2;2 The Dnmt2 Methyltransferase;34 6.3;3 DNA Methylation-Dependent Chromatin Structures;35 6.4;4 The Methyl-DNA Binding Protein MBD2/3;36 6.5;5 A Functional DNA Methylation System in Drosophila;38 6.6;6 Chromatin-Based Maintenance of Gene Expression;40 6.7;7 Characterization of PcG/TrxG Complexes;41 6.8;8 PC-Containing PcG Complexes and the Compaction of Chromatin;42 6.9;9 ESC/E(Z)-Containing Complexes and Histone Deacetylation/Methylation;44 6.10;10 The Complexity of PcG/TrxG-Regulated Chromatin;45 6.11;References;47 7;Epimutations in Human Disease;54 7.1;1 Epigenetic Inheritance;54 7.2;2 Classification of Epimutations;56 7.3;3 Causes of Primary Epimutations;62 7.4;4 Epigenetic Candidate Diseases;64 7.5;References;65 8;Epigenotypes of Latent Herpesvirus Genomes;70 8.1;1 Cellular and Viral Epigenotypes;71 8.2;2 Epigenetic Modifications of a-Herpesvirus Genomes;73 8.3;3 Epigenetic Modifications Regulate the Activity of a ß-Herpesvirus Promoter;75 8.4;4 Epigenetic Modifications of Latent .-Herpesvirus Genomes;76 8.5;References;83 9;Epigenetics of Complex Diseases: From General Theory to Laboratory Experiments;90 9.1;1 Introduction;91 9.2;2 Epigenetics and Complex Disease;92 9.3;3 Strategies for Detection of Epigenetic Differences in Complex Genomes;100 9.4;4 Study of the Epigenetic Norm;115 9.5;References;116 10;MSL Proteins and the Regulation of Gene Expression;126 10.1;1 Introduction;127 10.2;2 The DCC of Drosophila melanogaster;128 10.3;3 Initiation of Dosage Compensation;129 10.4;4 Assembly of the DCC;129 10.5;5 Targeting and Distribution of the DCC;130 10.6;6 MSL Binding Sites;135 10.7;7 Modification of Chromatin by the DCC;137 10.8;8 Interpreting the Histone Modifications Placed by the DCC;138 10.9;9 Molecular Mechanism of Dosage Compensation;140 10.10;10 The Inverse Effect Hypothesis;142 10.11;References;143 11;DNA Methylation Profiles of Female Steroid Hormone- Driven Human Malignancies;150 11.1;1 Introduction;151 11.2;2 Normal and Aberrant DNA Methylation Profiles;153 11.3;3 Gender-Specific Gene Methylation Profiles in Four Hormone- Driven Cancers;156 11.4;4 Conclusions;176 11.5;References;178 12;Genome-wide Analysis of DNA Methylation Changes in Human Malignancies;188 12.1;1 Introduction;189 12.2;2 DNA Methylation and the Genome;189 12.3;3 The DNA Methylation Machinery;190 12.4;4 DNA Methylation and Gene Silencing;191 12.5;5 Aberrant DNA Methylation in Cancer;192 12.6;6 Loss of DNA Methylation in Cancer;192 12.7;7 Gain of DNA Methylation in Cancer;194 12.8;8 Number of Methylated CpG Islands in the Tumor Genome;195 12.9;9 Targets for Promoter Hypermethylation;198 12.10;10 The Establishment of Tumor Type-Specific and Non-random Aberrant DNA Methylation;198 12.11;References;202 13;Decreased Fidelity in Replicating DNA Methylation Patterns in Cancer Cells Leads to Dense Methylation of a CpG Island;208 13.1;1 Introduction;209 13.2;2 Fidelity in Normal Mammary Epithelial Cells;210 13.3;3 Decreased Fidelity in Gastric Cancer Cells;213 13.4;4 Decreased Fidelity and Induction of Dense Methylation;213 13.5;5 Molecular Basis for CIMP,