Yamamoto Epigenetic Shaping of Sociosexual Interactions: From Plants to Humans

1. Auflage 2014
ISBN: 978-0-12-800333-6
Verlag: Elsevier Science & Techn.
Format: EPUB
Kopierschutz: 6 - ePub Watermark

E-Book, Englisch, Band Volume 86, 326 Seiten

Reihe: Advances in Genetics

Epigenetic Shaping of Sociosexual Interactions: From Plants to Humans is the first attempt to interpret the higher social functions of organisms. This volume covers an extraordinarily wide range of biological research and provides a novel framework for understanding human-specific brain functions. - Covers an extraordinarily wide range of biological research - Provides a novel framework for understanding human-specific brain functions.

Autoren/Hrsg.

Yamamoto, Daisuke

Inhaltsverzeichnis

1;Front Cover;1
2;ADVANCES IN GENETICS, VOLUME 86;3
3;Advances in Genetics;4
4;Copyright;5
5;CONTENTS;6
6;CONTRIBUTORS;10
7;PREFACE;12
8;Chapter One - Genomic Imprinting in Plants: What Makes the Functions of Paternal and Maternal Genes Different in Endosperm Formation?;14
8.1;1. INTRODUCTION;15
8.2;2. WHEN DOES GENOMIC IMPRINTING OCCUR?;17
8.3;3. WHY DOES GENOMIC IMPRINTING OCCUR?;19
8.4;4. HOW DOES GENOMIC IMPRINTING OCCUR? MECHANISMS OF GENOMIC IMPRINTING;20
8.5;5. THE ROLE OF GENOMIC IMPRINTING IN PLANTS: FUNCTION AS A REPRODUCTIVE BARRIER;29
8.6;6. PERSPECTIVES;32
8.7;ACKNOWLEDGMENTS;33
8.8;REFERENCES;33
9;Chapter Two - MicroRNAs and Epigenetics in Adult Neurogenesis;40
9.1;1. EFFECTS OF MICRORNAS ON NEUROGENESIS;41
9.2;2. NEUROGENESIS REGULATION BY SPECIFIC MIRNAS;43
9.3;3. OLIGODENDROCYTE DIFFERENTIATION AND MIRNAS;46
9.4;4. ASTROCYTE DIFFERENTIATION AND MIRNAS;47
9.5;5. IMPACT OF ENVIRONMENTAL FACTORS ON ADULT NEUROGENESIS;48
9.6;6. MIRNAS AND NEURONAL DISORDERS;50
9.7;REFERENCES;52
10;Chapter Three - An Epigenetic Switch of the Brain Sex as a Basis of Gendered Behavior in Drosophila;58
10.1;1. COURTSHIP BEHAVIOR OF DROSOPHILA MELANOGASTER;59
10.2;2. FRU IS A SEX-DETERMINATION GENE;61
10.3;3. FRU PROTEINS AS PUTATIVE TRANSCRIPTION FACTORS;63
10.4;4. FRU AND DSX PROTEINS SPECIFY SEX TYPES OF SINGLE NEURONS;64
10.5;5. THE MAL NEURAL CLUSTER AS A MODEL TO STUDY SINGLE-CELL SEX DIFFERENCES;66
10.6;6. CHROMATIN MODIFICATION AS A PLAUSIBLE MECHANISTIC BASIS FOR THE ACTIONS OF FRUM;67
10.7;7. FRUM PLAYS A ROLE IN THE ALL-OR-NONE SEX SWITCHING OF SINGLE NEURONS;69
10.8;8. ARE THE TWO STABLE STATES ATTAINED BY GRADED CHANGES IN FRUM ACTIVITY?;69
10.9;9. PROSPECTS;71
10.10;ACKNOWLEDGMENTS;72
10.11;REFERENCES;73
11;Chapter Four - Neural Transposition in the Drosophila Brain: Is It All Bad News?;78
11.1;1. INTRODUCTION;78
11.2;2. FRUIT FLY TRANSPOSONS;80
11.3;3. METHODS TO STUDY MOBILE ELEMENT ACTIVITY;84
11.4;4. HOST CELL DEFENSE MECHANISMS;87
11.5;5. IMPACT OF TRANSPOSONS ON THE HOST CELL;90
11.6;6. TIMING OF TRANSPOSON ACTIVITY;92
11.7;7. TRANSPOSONS IN NEUROLOGICAL DISEASE AND DECLINE;94
11.8;8. CELLULAR MOSAICISM AND BEHAVIORAL INDIVIDUALITY;96
11.9;9. IS THERE ANYTHING GOOD TO SAY?;97
11.10;ACKNOWLEDGMENTS;98
11.11;REFERENCES;98
12;Chapter Five - Fine-Tuning Notes in the Behavioral Symphony: Parent-of-Origin Allelic Gene Expression in the Brain;106
12.1;1. EPIGENETICS: SHAPING BEHAVIOR;107
12.2;2. DIO3: A CASE STUDY;109
12.3;3. EVOLUTIONARY SIGNIFICANCE OF VARIED ALLELIC EXPRESSION IN BRAIN;114
12.4;REFERENCES;117
13;Chapter Six - Influencing the Social Group: The Role of Imprinted Genes;120
13.1;1. INTRODUCTION;120
13.2;2. REGULATION;122
13.3;3. IMPRINTED GENES IMPLICATED IN SOCIAL BEHAVIORS;124
13.4;4. IMPRINTED GENES: ACTION OR REACTION?;131
13.5;5. SUMMARY AND CONCLUSIONS;138
13.6;ACKNOWLEDGMENTS;139
13.7;REFERENCES;139
14;Chapter Seven - The Potential Role of SRY in Epigenetic Gene Regulation During Brain Sexual Differentiation in Mammals;148
14.1;1. INTRODUCTION;149
14.2;2. SRY AND SEX DETERMINATION;151
14.3;3. SEXUAL DIFFERENTIATION IN THE BRAIN;152
14.4;4. EPIGENETICS OF BRAIN SEXUAL DIFFERENTIATION;157
14.5;5. DISCUSSION;166
14.6;6. PERSPECTIVES;169
14.7;REFERENCES;170
15;Chapter Eight - The Biological Basis of Human Sexual Orientation: Is There a Role for Epigenetics?;180
15.1;1. INTRODUCTION;181
15.2;2. THE GENETICS OF SEXUAL ORIENTATION;182
15.3;3. EPIGENETICS AND SEXUAL ORIENTATION IN HUMANS;185
15.4;4. MOLECULAR MECHANISMS UNDERLYING THE LONG-TERM EFFECTS OF HORMONES;189
15.5;5. CONCLUSION;191
15.6;REFERENCES;193
16;Chapter Nine - Repetitive Elements and Epigenetic Marks in Behavior and Psychiatric Disease;198
16.1;1. REPETITIVE ELEMENTS;202
16.2;2. PATHOLOGY OF TRANSPOSITION;210
16.3;3. BENEFITS OF TRANSPOSITION;212
16.4;4. FUNCTION OF REPEAT ELEMENTS IN THE NORMAL BRAIN AND BEHAVIOR;216
16.5;5. EPIGENETICS;218
16.6;6. SUMMARY AND CONCLUSIONS;249
16.7;REFERENCES;251
17;Chapter Ten - Epigenetic Modifications Underlying Symbiont–Host Interactions;266
17.1;1. INTRODUCTION;267
17.2;2. UNICELLULAR SYMBIOTIC ASSOCIATIONS;268
17.3;3. PLANT–SYMBIONT ASSOCIATIONS;269
17.4;4. CORAL–ALGAE INTERACTION;270
17.5;5. INSECTS;271
17.6;6. VERTEBRATE GUT MICROBIOTA;277
17.7;7. MICRORNAS AS EPIGENETIC REGULATORS OF SYMBIOTIC ASSOCIATIONS;278
17.8;8. CONCLUSIONS;282
17.9;ACKNOWLEDGMENTS;284
17.10;REFERENCES;284
18;Chapter Eleven - Integrating Early Life Experience, Gene Expression, Brain Development, and Emergent Phenotypes: Unraveling the Thread of Nature ...;290
18.1;1. EARLY LIFE DEVELOPMENT AND TRANSMISSION OF PHENOTYPE;291
18.2;2. EPIGENETIC CONTROL OF GENE EXPRESSION: MOLECULES OF CELLULAR PROGRAMMING AND INHERITANCE;293
18.3;3. THE PRIMARY EPIGENETIC MARK: GENE SILENCING BY DNA METHYLATION;294
18.4;4. DNA METHYLATION REVERSED: ACTIVE DNA DEMETHYLATION IN THE NERVOUS SYSTEM;296
18.5;5. HISTONE MODIFICATIONS: REGULATION OF CHROMATIN STRUCTURE AND FINE-TUNING OF GENE FUNCTION;297
18.6;6. INTERPRETATION OF EPIGENETIC MODIFICATIONS: TOWARD CRACKING THE CODE;298
18.7;7. EPIGENETIC MARKS: LINKING MATERNAL NUTRITION AND CHILD HEALTH AND BEYOND;299
18.8;8. MATERNAL CARE AND EPIGENETIC PROGRAMMING OF PHENOTYPIC DIFFERENCES IN BEHAVIOR;301
18.9;9. CONSERVED EPIGENETIC SENSITIVITY TO EARLY LIFE EXPERIENCE IN HUMANS: IT IS IN YOUR BLOOD;304
18.10;10. REGULATION OF SYNAPTIC TRANSMISSION, NEURONAL PLASTICITY, AND COGNITIVE FUNCTION;306
18.11;11. INFLUENCE OF CHROMATIN PLASTICITY ON MAJOR NEUROPSYCHIATRIC DISEASE;308
18.12;12. CONCLUDING REMARKS;310
18.13;ACKNOWLEDGMENTS;311
18.14;COMPETING INTERESTS STATEMENT;311
18.15;REFERENCES;311
19;INDEX;322
20;COLOR PLATE;328

Leseproben

Chapter One

Genomic Imprinting in Plants

What Makes the Functions of Paternal and Maternal Genes Different in Endosperm Formation?

Takayuki Ohnishi?,1, Daisuke Sekine† and Tetsu Kinoshita?,1     ?Kihara Institute for Biological Research, Yokohama City University, Kanagawa, Japan     †Division of Life Sciences, Graduate School of Natural Science and Technology, Kanazawa University, Ishikawa, Japan
1 Corresponding author: e-mail address: [e-mail], [e-mail] 

Abstract

Genomic imprinting refers to the unequal expression of maternal and paternal alleles according to the parent of origin. This phenomenon is regulated by epigenetic controls and has been reported in placental mammals and flowering plants. Although conserved characteristics can be identified across a wide variety of taxa, it is believed that genomic imprinting evolved independently in animal and plant lineages. Plant genomic imprinting occurs most obviously in the endosperm, a terminally differentiated embryo-nourishing tissue that is required for seed development. Recent studies have demonstrated a close relationship between genomic imprinting and the development of elaborate defense mechanisms against parasitic elements during plant sexual reproduction. In this chapter, we provide an introductory description of genomic imprinting in plants, and focus on recent advances in our understanding of its role in endosperm development, the frontline of maternal and paternal epigenomes.

Keywords

DNA methylation; Endosperm; Epigenetics; Plant genomic imprinting; Polycomb repressive complex 2(PRC2); Sexual reproduction; Transposable elements (transposons)

1. Introduction

Genomic imprinting results in two alleles at the same locus being functionally nonequivalent and is caused by different epigenetic modifications depending on whether the allele is inherited from the mother or the father. The phenotypic differences between heterozygotes are referred to as parent-of-origin effects.

The term genomic imprinting was first used to describe the elimination of paternal chromosomes during spermatogenesis in sciarid flies (Crouse, 1960; Goday & Esteban, 2001; Stern, 1958). The term was later applied to both mammals (McGrath & Solter, 1984; Surani, Barton, & Norris, 1984) and flowering plants (Kermicle, 1970; Kermicle & Alleman, 1990; Kinoshita, Yadegari, Harada, Goldberg, & Fischer, 1999; Vielle-Calzada et al., 1999). These early studies focused on functional differences between parental genomes. In mammals, gynogenetic or androgenetic mice, which contain only a maternally or paternally derived chromosome set, respectively, show contrasting developmental outcomes; gynogenones characteristically have a poorly developed placenta and thin membrane layers surrounding the embryo (extraembryonic membranes), but produce a reasonably well-developed embryo proper; however, androgenones are characterized by retarded embryos that are enveloped by well-developed placenta and extraembryonic membranes (McGrath & Solter, 1984; Surani et al., 1984).

In higher plants, the parent-of-origin gene dosage effects can enhance or repress seed development. Such effects are particularly evident following interploidy crosses. Reproductive barriers can prevent intercrosses between different groups within a species, reducing gene flow between the groups and promoting speciation. The evolution of a reproductive barrier is important for the establishment or fixing of a new species. In angiosperms, it has been estimated that about 15–30% of speciation events within genera are accompanied by polyploidy formation (Mayrose et al., 2011; Wood et al., 2009). An increased dosage of maternal chromosomes enhances endosperm development, while a paternal genome excess results in repressed endosperm development. This suggests that maternally and paternally derived chromosomes are unable to complement one another to play the same roles in development.

In both mammals and flowering plants, the phenotypic characteristics produced by the unequal functions of parental chromosomes have much in common. First, both the placenta and endosperm, which are essential to support embryo development, are very sensitive to parent-of-origin effects on gene expression. Second, maternal and paternal parent-of-origin effects generate a similar directional phenotypic change in the target tissue in both animals and plants, namely, the maternal effect enhances development, while the paternal effects represses development (Figure 1.1).

The endosperm is the product of double fertilization (Figure 1.2). During double fertilization, one of the sperm cells fertilizes the haploid egg cell to give rise to the diploid embryo. The other sperm cell fuses with the diploid central cell to form the triploid endosperm, the tissue that will surround the embryo after fertilization. The endosperm is a triploid tissue composed of two maternal sets of chromosomes and one paternal set. Therefore, although the endosperm contains both maternally and paternally derived chromosomes, its genetic composition is totally different from that of the mammalian placenta.

Figure 1.1 Parent-of-origin effects generate a similar directional phenotypic change. Schematic illustration highlighting the phenotypic characteristics produced by the parent-of-origin effect to the placenta in mammals and to the endosperm in plants. (See the color plate.)

Figure 1.2 Double fertilization in angiosperms. Angiosperm seeds are produced by a double fertilization event. During double fertilization, one of the sperm cells fertilizes the haploid egg cell to give rise to the diploid embryo. The other sperm cell fuses with the diploid central cell to form the triploid endosperm, the tissue that will surround and nourish the embryo after fertilization. A seed coat derived from maternal tissues develops from the integuments of the ovule after fertilization. (See the color plate.)

The plant endosperm nourishes and supports both embryo development and the subsequent growth of the seedling. The endosperm is responsive to problems in interspecific compatibility and in ploidy level differences (Haig & Westoby, 1991). If endosperm development fails, then embryo development will also eventually get arrested (Hehenberger, Kradolfer, & Kohler, 2012). Abnormal development of the endosperm in response to hybridization causes an effective reproductive barrier in angiosperms. The production of endosperm by double fertilization is a specific characteristic of angiosperms and does not occur in other land plant groups; consequently, plant genomic imprinting has only been observed in angiosperms.

2. When Does Genomic Imprinting Occur?

2.1. Taxonomic Distribution of Genomic Imprinting

In mammals, evidence of genomic imprinting has been found in a wide range of both eutherian and marsupial species. These two mammalian groups diverged about 160million years ago (Ma) (Luo, Yuan, Meng, & Ji, 2011). Comprehensive comparative genomic studies have shown that some imprinted regions are conserved in both groups, indicating that genomic imprinting likely evolved in an ancestral species of the two lineages (Renfree, Suzuki, & Kaneko-Ishino, 2013). No imprinted genes have been found in monotremes, birds, and reptiles (Figure 1.3) (Renfree, Hore, Shaw, Graves, & Pask, 2009).

Figure 1.3 The occurrence of genomic imprinting in animals and plants. The timing of genomic imprinting acquisition and of the divergence of animals and plants. The vertical axes represent the time line from 400 Ma to the present. The colored boxes represent the evolution of the groups with and without genomic imprinting. In animals, genomic imprinting is widespread in eutherian and marsupial mammals, although it is not observed in monotremes or in birds. In plants, genomic imprinting occurs in eudicots (Arabidopsis) and monocots (rice, maize). Currently, there is no information whether the phenomenon also occurs in basal angiosperms and in gymnosperms. (See the color plate.)

Recent studies in plants using genomewide detection of differential gene expression patterns in parental alleles have provided new insights into the evolution of plant genomic imprinting. Roughly 150 Ma, flowering plants diverged to form the two dominant extant lineages, monocots, and eudicots (Hedges, Dudley, & Kumar, 2006). Comparison of the genes showing an imprinted expression pattern in Oryza sativa (rice), a monocot species, with those in the model eudicots Arabidopsis thaliana (Arabidopsis), revealed a low degree of overlap between monocots and eudicots, suggesting that genomic imprinting has evolved independently in the two plant clades (Luo, Taylor, et al., 2011). Further analyses and filtering of transcriptome databases have identified some genes that are imprinted in both monocots and eudicots (Kohler, Wolff, & Spillane, 2012). It is possible that genomic imprinting arose at many different time points in plant evolution as an adaptation to various selection pressures in different environments. Possibly, natural selection may result in the replacement of one pattern of genomic imprinting by another that is better adapted to the survival of the...