Intro -- Preface -- Acknowledgments -- Contents -- 1: Biology of Chromatin -- 1.1 Introduction: Epigenetic Regulation in the Context of the Genome -- 1.1.1 Background: Gene Expression and Chromatin -- 1.1.2 Discovery of the Nucleosomal Structure of the Genome -- 1.2 The Structure of the Nucleosome -- 1.2.1 Histone Variants -- 1.3 Histone Modifications -- 1.3.1 Nomenclature for Histone Modifications -- 1.3.2 Combinatorial Modifications at Pericentric Heterochromatin -- 1.3.3 Histone Modifications at High Resolution -- 1.3.4 Chromatin Modifications Associated with Transcription Units -- 1.3.5 A Concept of Writers, Readers, and Erasers of Histone Modifications -- Method Box 1.1: Chromatin Immunoprecipitation -- 1.4 DNA Modifications -- 1.4.1 DNA Cytosine Methylation -- 1.4.2 DNA Cytosine Hydroxymethylation -- 1.4.3 Interaction of DNA and Histone Modifications -- Method Box 1.2: Analysis of DNA Modifications -- 1.5 Chromatin Organization and Compartmentalization in the Cell Nucleus -- 1.5.1 Replication of Pericentric Heterochromatin Domains -- 1.5.2 Topologically Associating Domains -- 1.5.3 Structural Maintenance of Chromosomes Complexes -- Method Box 1.3: Chromatin Conformation Capture (. Box Fig. 1.3) -- References -- 2: Chromatin Dynamics -- 2.1 Basic Nuclear Activities -- 2.2 Connecting Nucleosomes to DNA Sequence -- 2.3 Nucleosome Remodeling -- 2.3.1 A Template for Transcription -- 2.3.2 Chromatin Remodeling Complexes -- Methods Box 2.1: Determining DNA Accessibility in a Chromatin Template -- 2.4 Nucleosome Assembly -- 2.4.1 Histone Variants and Histone Chaperones -- 2.4.2 The Replication Fork: Still the Major Enigma in Epigenetics -- References -- 3: Cellular Memory -- 3.1 Maintaining Cellular Fates -- 3.2 PcG/TrxG System Maintaining Cellular Memory.

3.3 Biochemical Characterization and Molecular Function of PcG/TrxG Proteins -- 3.4 Targeting and Propagation of PcG/TrxG-Controlled Chromatin Domains -- 3.5 Switching Memory and the Role of Non-coding RNAs -- 3.6 Losing Memory -- References -- 4: Dosage Compensation Systems -- 4.1 Introduction: Evolution of Chromosome-Wide Dosage Compensation -- 4.1.1 Consequences of Gene Dosage Differences Arising from Sex Chromosome Erosion -- 4.2 The Dosage Compensation Complex of the Fruit Fly Drosophila melanogaster -- 4.3 X Chromosome Inactivation in Mammals -- 4.3.1 The Mammalian Dosage Compensation Mechanism -- 4.3.2 Regulation of XCI in Different Mammals -- 4.4 X Chromosome Dosage Compensation in Caenorhabditis elegans -- References -- 5: Genomic Imprinting -- 5.1 Discovery of the Non-equivalence of Maternal and Paternal Genomes -- 5.1.1 Genome-Wide Imprinting in Insects -- 5.1.2 Discovery of Genomic Imprinting at an Individual Locus in Maize -- 5.1.3 Demonstrating the Non-equivalence of Parental Genomes in Mammals -- 5.2 Characteristics of Imprinted Genes in Mammals -- 5.2.1 Molecular Characteristics of Imprinted Gene Clusters -- 5.2.2 Molecular Mechanisms Leading to Imprinted Expression -- 5.2.3 The Life Cycle of a Genomic Imprint -- 5.3 Genomic Imprinting and Human Disease -- 5.4 Genomic Imprinting in Flowering Plants -- 5.4.1 Genomic Imprinting Occurs Predominantly in the Endosperm But Also Exists in the Embryo -- 5.4.2 Mechanisms Underlying Imprinting Show Similarities Between Mammals and Plants -- 5.5 Evolution of Genomic Imprinting -- References -- 6: RNA-Based Mechanisms of Gene Silencing -- 6.1 The Unusual Behavior of Transgenes Led to the Discovery of Novel RNA-Based Silencing Mechanisms -- 6.1.1 Conserved Components of RNA-Based Silencing Mechanisms -- 6.2 Post-Transcriptional Gene Silencing (PTGS).

6.2.1 The Biogenesis and Function of microRNAs -- 6.2.2 Genome Defense by siRNA-Mediated Silencing -- 6.3 Transcriptional Gene Silencing (TGS) -- 6.4 Paramutation -- 6.4.1 The cis-Regulatory Elements Controlling Paramutation and trans-Acting Factors Link Paramutation to RdDM -- References -- 7: Regeneration and Reprogramming -- 7.1 Types of Regenerative Phenomena -- 7.1.1 Regenerating from a Blastema -- 7.1.2 Changing Potency by Transdifferentiation -- 7.1.3 Signaling in the Blastema -- 7.2 Stem Cells in the Adult -- 7.3 Sources of Pluripotent Stem Cells -- 7.4 Chromatin Dynamics During Reprogramming -- 7.5 Regenerative Therapies -- References -- 8: Epigenetics and Cancer -- 8.1 Epigenetics and Cancer -- 8.2 DNA Methylation and Cancer -- 8.2.1 DNA Hypermethylation in Cancer -- 8.2.2 DNA Hypomethylation in Cancer -- 8.2.3 Loss of Imprinting Through Alterations of DNA Methylation -- 8.2.4 Mutations in the DNA Methylation Machinery in Cancers -- 8.2.4.1 Mutations of de novo DNA Methyltransferase 3a -- 8.2.4.2 Mutations of Ten-Eleven Translocation 2 (TET2) -- 8.2.5 Epigenetic Inhibitors of DNA Methyltransferases in Cancer Therapy -- 8.3 Polycomb Group Proteins and Cancer -- 8.3.1 Alterations of PcG Activity in Cancer -- 8.3.2 Mutations of Affecting Lysine 27 of Histone H3 Occur in Multiple Cancers -- 8.3.3 EZH2 Inhibitors in Cancer Therapy -- 8.4 Histone Acetylation and Deacetylation in Cancers -- 8.4.1 Alterations of Histone Acetyltransferases in Cancer -- 8.4.2 Acetyl-Lysine Recognition Proteins and Cancer -- 8.4.3 Alterations of Histone Deacetylases in Cancer -- 8.4.4 HAT and HDAC Inhibitors in Cancer Therapy -- 8.5 Chromatin Remodeling Factors and Cancer -- 8.5.1 SWI/SNF Complexes and Cancer -- 8.5.2 ISWI Complexes and Cancer -- 8.5.3 The NuRD Complex and Cancer -- 8.5.4 The INO80 Complex and Cancer -- References.

9: Epigenetics and Metabolism -- 9.1 Epigenetics and Metabolism -- 9.2 Acetyl-Coenzyme A (Acetyl-CoA) -- 9.2.1 Biosynthesis of Acetyl-CoA -- 9.2.2 Acetyl-CoA as Cofactor of Histone Acetyltransferases -- 9.3 Nicotinamide Adenine Dinucleotide (NAD) -- 9.3.1 Biosynthesis of NAD -- 9.3.2 NAD as Cofactor of Sirtuins and PARPs -- 9.3.2.1 Sirtuins -- 9.3.2.2 PARPs -- 9.4 S-adenosylmethionine (SAM) -- 9.4.1 Biosynthesis of SAM -- 9.4.2 SAM as Cofactor of DNA and Histone Methyltransferases -- 9.5 Flavin Adenine Dinucleotide (FAD) -- 9.5.1 Biosynthesis of FAD -- 9.5.2 FAD as Cofactor of Lysine Demethylase 1 (LSD1) -- 9.6 (Sa(B-Ketoglutarate ((Sa(BKG) -- 9.6.1 Biosynthesis of (Sa(B-Ketoglutarate -- 9.6.2 (Sa(BKG as Cofactor of TET-Family DNA Demethylases and Jumonji C-Family Histone Demethylases -- References -- Glossary -- Index.

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