Homology Effects
Regular price
70.250 KD
inc. VAT
Couldn't load pickup availability
Table of contents
- Copyright Pageiv
- Contentsv
- Contributorsxiii
- Preface: Homology Effects: The Difference between 1 and 2xvii
- Chapter 1. Sex and the Single Chromosome1
- I. The Evolution of Sex Chromosomes2
- II. Selective Pressure Has Led to a Variety of Dosage-Compensation Mechanisms6
- III. Dosage Compensation in Drosophila by the MSL Complex7
- IV. A Series of Binary Switches Regulates the Sex Specificity of Dosage Compensation in Drosophila11
- V. Sex lethal Communicates the X:A Ratio to the Dosage-Compensation Pathway through Repression of ms13
- VI. Evidence for the Coexistence of a Female-Specific Dosage-Compensation Pathway in Drosophila14
- VII. MSL-Mediated Dosage Compensation Spreads from Special Entry Sites in cis15
- VIII. The Behavior of MSL Complexes on Paired Chromosomes16
- IX. Noncoding RNAs, Epigenetic Regulation, and Chromatin Structure17
- References18
- Chapter 2. Is X-Chromosome Inactivation a Homology Effect?25
- I. The Phenomenon of X Inactivation26
- II. Control Elements29
- III. Current Models of Xist Regulation36
- IV. Evidence for Additional Control Elements in Random X Inactivation41
- V. Is X Inactivation a Homology Effect?43
- VI. Conclusions44
- References44
- Chapter 3. Homologous Chromosome Associations and Nuclear Order in Meiotic and Mitotically Dividing49
- I. Introduction51
- II. The Global Arrangement of Chromosomes in the Nucleus52
- III. Homology Recognition during DNA Double-Strand Break Repair59
- IV. Pairing and Synapsis of Homologous Chromosomes during Meiosis64
- V. Homolog Interactions in Mitotically Dividing Cells (Vegetative Pairing)74
- VI. Concluding Remarks81
- References81
- Chapter 4. The Role of Sequence Homology in the Repair of DNA Double-Strand Breaks in Drosophila91
- I. Introduction92
- II. The Effect of Sequence Identity on Gene Conversion96
- III. The Effect of the Extent of Donor Homology on Double-Strand Break Repair97
- IV. The Effect of the Extent of Recipient Homology on Double-Strand Break Repair101
- V. The Effect of Donor Location on Double-Strand Break Repair105
- VI. The Effect of Chromosome Pairing on Double-Strand Break Repair107
- VII. Summary109
- References113
- Chapter 5. The Origins of Genomic Imprinting in Mammals119
- I. Introduction120
- II. Definition of Genomic Imprinting120
- III. Evolution and Function of Imprinting121
- IV. Origins of Genomic Imprinting126
- V. Predictions for an Imprinting Mechanism129
- VI. Organization and Epigenetic Modification of Imprinted Genes130
- VII. DNA Methylation and Genomic Imprints139
- VIII. The Function of Methylation Imprints: Model C143
- IX. Innocent Bystanders, Future Challenges147
- X. Concluding Remarks151
- References154
- Chapter 6. Genomic Imprinting during Seed Development165
- I. Introduction166
- II. Historical Overview172
- III. Genome-Wide Imprinting179
- IV. Gene-Specific Imprinting and the Control of Seed Development190
- V. Conclusion204
- References208
- Chapter 7. Long-Distance Cis and Trans Interactions Mediate Paramutation215
- I. Introduction215
- II. Background and Defnitions216
- III. Paramutation at b1 and p1218
- VI. Models for Paramutation226
- V. Implications and Possible Functions230
- References231
- Chapter 8. Homology-Dependent Gene Silencing and Host Defense in Plants235
- I. Introduction236
- II. RNA Silencing238
- III. DNA–DNA Pairing249
- IV. Homology-Dependent Gene Silencing (HDGS) in Genomic Imprinting and X-Chromosome Inactivation in254
- V. HDGS and the Host Genome Defense: Evolutionary Aspects257
- VI. Summary and Conclusions268
- References269
- Chapter 9. Quelling in Neurospora crassa277
- I. Introduction278
- II. The Discovery of Quelling in Neurospora279
- III. The Quest for quelling-defective (qde) Mutants283
- IV. Isolation of the Genes Involved in Quelling in Neurospora284
- V. A Unified Model for Quelling, Co-suppression, and RNA Interference291
- VI. Supporting Evidence for the Proposed Model294
- VII. The Search for Additional PTGS Components296
- VIII. Conclusions297
- References298
- Chapter 10. Non-Mendelian Inheritance and Homology-Dependent Effects in Ciliates305
- I. Introduction306
- II. Regulation of IES Excision by Homology-Dependent Maternal Effects315
- III. Regulation of Zygotic Genome Amplification and Chromosome Fragmentation by Homology-Dependent M323
- IV. Conclusions333
- References335
- Chapter 11. RNAi (Nematodes: Caenorhabditis elegans)339
- I. Introduction/History340
- II. RNAi and Other Silencing Mechanisms in C. elegans342
- III. Spreading and Persistence of RNAi345
- IV. Molecular Mechanism of RNAi348
- V. Components of the RNAi Pathway351
- VI. RNAi and Development354
- References355
- Chapter 12. Antisense RNAs in Bacteria and Their Genetic Elements361
- I. Introduction„Antisense Principle and Gene Regulation362
- II. Naturally Occurring Antisense RNA Control Systems363
- III. Antisense RNA Mechanisms and Biological Context366
- IV. Antisense Structure and Kinetics of Binding378
- V. Matching Antisense RNA Properties with Biological Roles384
- VI. Concluding Remarks387
- References388
- Chapter 13. Transvection in Drosophila399
- I. Introduction400
- II. Historical Background to Bithorax-Complex Transvection400
- III. Transvection, trans Sensing, and Homology Effects406
- IV. Trans-Acting zeste Proteins and Transvection412
- V. Critical RegionsŽ for Transvection413
- References414
- Chapter 14. Pairing-Sensitive Silencing, Polycomb Group Response Elements, and Transposon Homing in421
- I. Introduction422
- II. Three Types of mini-white Silencing423
- III. mini-white Silencing by PREs426
- IV. Effect of Mutations in Polycomb Group Genes on mini-white Silencing428
- V. mini-white Silencing by Other Elements429
- VI. Is the engrailed PS Fragment a PRE?429
- VII. Pleiohomeotic, PREs and PS Sites430
- VIII. Not All PS Sites Are PREs and Vice Versa431
- IX. Pairing-Sensitive Silencing Has Not Been Demonstrated in the Embryo431
- X. Transposon Homing432
- XI. Preferential Insertion of PRE-Containing Transposons Near Endogenous PREs433
- XII. Conclusions433
- References435
- Chapter 15. Repeat-Induced Gene Silencing in Fungi439
- I. Introduction439
- II. Discovery and Basic Features of RIP and MIP440
- III. De Novo and Maintenance Methylation Associated with MIP and RIP442
- IV. Consequences of RIP and MIP445
- V. Concluding Remarks446
- References446
- Chapter 16. The Evolution of Gene Duplicates451
- I. Introduction452
- II. Evolutionary Forces Affecting Gene Copy Number457
- III. Discussion470
- IV. Appendix: Modeling the Invasion of a Duplicate Gene472
- References479
- Chapter 17. Prions of Yeast as Epigenetic Phenomena: High Protein Copy NumberŽ Inducing Protein485
- I. Introduction487
- II. Three Genetic Criteria for Prions489
- III. [URE3] as a Prion of the Ure2 Protein491
- IV. Self-Propagating Ure2p Amyloid Is the [URE3] Prion497
- V. MKS1 Is Necessary for de Novo Generation of the [URE3] Prion501
- VI. Chaperones Affecting [URE3] Propagation503
- VII. [PSI] as a Prion of the SUP35 Protein504
- VIII. Chaperones and [PSI+]506
- IX. Portable Prion Domains and Synthetic Prions508
- X. Curing of [URE3] and [PSI+]510
- XI. [Het-s], a Prion with a Normal Cellular Function511
- XII. Are Yeast Prions Adaptive, a Cellular Stress, or Both?512
- XIII. [PIN+] Is Required for Inducibility of [PSI+]514
- XIV. [KIL-d] Is an Epigenetic Phenomenon: Is It a Prion?515
- XV. Are Transmissible Spongiform Encephalopathies of Mammals Due to Prions?516
- XVI. Conclusions518
- References519
- Index527
Homology Effects offers contributions from an international panel of researchers whose aim has been both to introduce newcomers to the field of homology effects, and to bring colleagues up to date. Topic coverage includes dosage compensation, X-inactivation, imprinting, paramutation, homology-dependent gene silencing, transvection, pairing-sensitive silencing, nuclear organization of chromosomes, DNA repair, quelling, RIP, RNAi and antisense biology, homology effects in ciliates, prion biology, and a discourse on the evolution of gene duplications.
Advances in Genetics presents an eclectic mix of articles of use to all human and molecular geneticists. They are written and edited by recognized leaders in the field and make this an essential series of books for anyone in the genetics field.
Homology, the examination of similarity due to shared common ancestry, encompasses a fascinating class of phenomena in mammals, plants, insects, ciliates, nematodes, fungi, and bacteria. Homology effects concern processes that recognize homology at the level of DNA and/or RNA, as well as at the level of protein. Their collective history begins at the turn of the century and includes some of the most puzzling and extraordinary observations in biology. The volume covers phenomena that have often been considered unusual, exceptional to the rule, and "out of the ordinary" and, therefore, not for general study. However, it is now becoming clear that taken together, these phenomena represent a class of regulatory mechanisms that are widespread, as well as exceptionally powerful.
Advances in Genetics presents an eclectic mix of articles of use to all human and molecular geneticists. They are written and edited by recognized leaders in the field and make this an essential series of books for anyone in the genetics field.
Homology, the examination of similarity due to shared common ancestry, encompasses a fascinating class of phenomena in mammals, plants, insects, ciliates, nematodes, fungi, and bacteria. Homology effects concern processes that recognize homology at the level of DNA and/or RNA, as well as at the level of protein. Their collective history begins at the turn of the century and includes some of the most puzzling and extraordinary observations in biology. The volume covers phenomena that have often been considered unusual, exceptional to the rule, and "out of the ordinary" and, therefore, not for general study. However, it is now becoming clear that taken together, these phenomena represent a class of regulatory mechanisms that are widespread, as well as exceptionally powerful.