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2014英文新书：女性乃是马赛克
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Females Are Mosaics by BARBARA R. MIGEON © Oxford University Press 2014，S E C O N D E D I T I O N 328P Contents Acknowledgments xi Introduction xiii PART ONE Background 1 1. Sex Diff erences in Disease 3 1.1. Males More Vulnerable at Every Age 3 1.2. Vulnerability of Males Leads to Sex-Specifi c Disease 7 1.3. Summary and Speculations 10 2. Evolution of the Human Sex Chromosomes and a Portrait of the Human X 11 2.1. Chromosomal Basis of Sex Determination 11 2.2. Th e Human Sex Chromosomes Evolved from Avian Autosomes 13 2.3. Degeneration of the Y Chromosome 16 2.4. Ohno’s Law and the Conservation of the Original X 17 2.5. Residual Homology and the Pseudoautosomal Regions 18 2.6. Genetic Portrait of the Human X 20 2.7. Summary and Speculations 25 3. X Chromosome Dosage Compensation: An Overview 27 3.1. X Chromosome Dosage Compensation 28 3.2. Heterochromatin and Chromosome Silencing 30 3.3. Role in Sex Determination 32 3.4. Mechanisms of Dosage Compensation in Other Organisms 32 3.5. Mechanisms of Dosage Compensation in Mammals 36 3.6. Summary and Speculations 38 4. Th e Discovery of X Chromosome Inactivation 39 4.1. Th e Lyon Hypothesis 43 4.2. General Scheme of Mammalian Dosage Compensation 45 4.3. Summary and Speculations 47 5. Experimental Models for X Inactivation Studies 48 5.1. Spontaneous Human Mutations Th at Interfere with Inactivation 48 5.2. X-Linked Protein Variants Distinguish Parental Origin of X Chromosomes 52 5.3. Characterizing the Inactive X in Human Cell Cultures and Clones 53 5.4. Mouse–Human Hybrids Separate Inactive from Active X 56 5.5. Mouse Embryonic Stem Cells for Manipulating the Early Steps in X Inactivation 57 5.6. Transgenic Mice as a Functional Assay 59 5.7. Assays for X Inactivation Patterns in Heterozygotes 60 5.8. Summary and Speculations 61 PART TWO Th emes and Variations of X Inactivation 63 6. Th eme 1: Th e Initial Steps—Creating the Active and Inactive X 65 6.1. Characteristics of the Inactive X Chromosome 65 6.2. Time of Initiation in the Embryo 69 6.3. C is Inactivation 72 6.4. Th e Master Control Region: XIC and Xist 74 6.5. Silencing the Inactive X Chromosome 78 6.6. Single Active X versus X Inactivation 83 6.7. Choosing the Active X Chromosome 85 6.8. Summary and Speculations 91 7. Th eme 2: Subsequent Steps—Spreading and Maintaining Inactivation 92 7.1. Spreading Inactivation by Modifying Chromatin 93 7.2. Maintaining Inactivation by DNA Methylation of CpG Islands 100 7.3. Escape from Inactivation 104 7.4. Transient X Inactivation in Germ Cells 107 7.5. Induced X Reactivation in Placental Cells 109 7.6. Role of DNA Replication in X Inactivation 110 7.7. Summary and Speculations 111 8. Variations 1: Th e X Inactivation Center 112 8.1. Variations on the Th emes of X Inactivation 112 8.2. Divergence in the Physical Map 113 8.3. Th e Eff ect of Map Changes on X Inactivation in Mouse and Human 116 8.4. Summary and Speculations 120 9. Variations 2: Stability of Inactive X 121 9.1. Stability of Inactivation and DNA Methylation 122 9.2. Genes Th at Escape Inactivation 122 9.3. Summary and Speculations 125 10. Variations 3: Choice of Active X 126 10.1. Primary Nonrandom X Inactivation 126 10.2. Paternal X Inactivation 129 10.3. Relationship of Paternal X Inactivation to Genomic Imprinting 131 10.4. Th e Paternal X Imprint in X Inactivation 132 10.5. Does Antisense Transcription Have a Role? 135 10.6. Evolution and Tinkering 139 10.7. Eff ect of Inactivation Timing 139 10.8. Summary and Speculations 142 PART THREE Medical Consequences of X Inactivation 143 11. Th e Single Active X 145 11.1. Coping with a Monosomy X 145 11.2. Dosage Compensation of the Active X 146 11.3. Sex Diff erences in Susceptibility to Disease 148 11.4. Viability of Turner Syndrome, Klinefelter Syndrome, and X Chromosome Aneuploidy 149 11.5. X Deletions, Ring X Chromosomes, X Duplications, and Functional Disomy 155 11.6. X/Autosome Translocations and Spreading of Inactivation 157 11.7. Polyploidy and the Choice of Active X 159 11.8. Summary and Speculations 162 12. Mosaicism 163 12.1. Th e X-Linked Phenotype Is Dominant at the Cellular Level 163 12.2. Females are Mosaics 164 12.3. Interaction between Mosaic Cell Populations 167 12.4. Skewing of X Inactivation Patterns 175 12.5. Eff ect of X Inactivation on Clinical Phenotype 183 12.6. “Manifesting” Heterozygotes 202 12.7. Summary and Speculations 206 13. Epimutations, Chromatin Disorders, and Sex Diff erences in Phenotype 209 13.1. Epimutations Usually Cause Somatic Diseases 210 13.2. Epimutations in Parental Imprinting Disorders 211 13.3. Epigenetic Regulation of Autosomal Gene Expression by Sex Chromosomes 213 13.4. Disorders of the Epigenetic Machinery 213 13.5. Sex Diff erences in Manifestations of Chromatin Disorders 216 13.6. Treatment of Chromatin Disorders 219 13.7. Summary and Speculations 219 14. Determinants of Female Phenotypes 221 14.1. Th e Dynamic Eff ect of Interacting Cell Populations on the Health of Females 222 14.2. Th e Eff ect of X Inactivation on Normal Female Phenotype and Cell Diversity 225 14.3. Epilogue 226 Appendix A: Descriptions of Model X-linked and Relevant Diseases 229 Appendix B: Sex Chromosome Aneuploidy, Polyploidy, and Parthenogenetic Conceptuses 246 Appendix C: Eff ect of X Inactivation on Phenotype and Cell Selection in X-linked Disorders 251 Glossary 263 References 271 Index 295 - - c.png  Untitled.png |
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