The chromatin remodeling enzyme Chd4 regulates genome architecture in the mouse brain

The development and function of the brain require tight control of gene expression. Genome architecture is thought to play a critical regulatory role in gene expression, but the mechanisms governing genome architecture in the brain in vivo remain poorly understood. Here, we report that conditional k...

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Published inNature communications Vol. 11; no. 1; pp. 3419 - 14
Main Authors Goodman, Jared V., Yamada, Tomoko, Yang, Yue, Kong, Lingchun, Wu, Dennis Y., Zhao, Guoyan, Gabel, Harrison W., Bonni, Azad
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 09.07.2020
Nature Publishing Group
Nature Portfolio
Subjects
38
38/1
38/15
38/22
38/39
38/91
45
45/90
49
631/136
631/208/200
631/337/100/101
631/337/100/102
631/378
Accessibility
Animals
Architecture
Brain
Brain - metabolism
Brain architecture
Cell Cycle Proteins - metabolism
Cerebellum
Chromatin - metabolism
Chromatin Assembly and Disassembly
Chromatin remodeling
Chromosomal Proteins, Non-Histone - metabolism
Chromosomes, Mammalian - metabolism
Cohesin
Cohesins
DNA Helicases - genetics
DNA Helicases - metabolism
Enhancer Elements, Genetic - genetics
Enhancers
Enzymes
Epigenesis, Genetic
Gene expression
Gene regulation
Genome
Genomes
Granular materials
Granule cells
Humanities and Social Sciences
Mice, Knockout
Models, Genetic
multidisciplinary
Neurons
Occupancy
Protein Binding
Science
Science (multidisciplinary)
Online AccessGet full text
ISSN2041-1723
2041-1723
DOI10.1038/s41467-020-17065-z

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Abstract The development and function of the brain require tight control of gene expression. Genome architecture is thought to play a critical regulatory role in gene expression, but the mechanisms governing genome architecture in the brain in vivo remain poorly understood. Here, we report that conditional knockout of the chromatin remodeling enzyme Chd4 in granule neurons of the mouse cerebellum increases accessibility of gene regulatory sites genome-wide in vivo. Conditional knockout of Chd4 promotes recruitment of the architectural protein complex cohesin preferentially to gene enhancers in granule neurons in vivo. Importantly, in vivo profiling of genome architecture reveals that conditional knockout of Chd4 strengthens interactions among developmentally repressed contact domains as well as genomic loops in a manner that tightly correlates with increased accessibility, enhancer activity, and cohesin occupancy at these sites. Collectively, our findings define a role for chromatin remodeling in the control of genome architecture organization in the mammalian brain. The mechanisms underlying gene regulation and genome architecture remain poorly understood. Here, the authors investigate the role of chromatin remodelling enzyme Chd4 in granule neurons of the mouse cerebellum and find that conditional knockout of Chd4 preferentially activates enhancers and modulates genome architecture at a genome-wide level.
AbstractList The development and function of the brain require tight control of gene expression. Genome architecture is thought to play a critical regulatory role in gene expression, but the mechanisms governing genome architecture in the brain in vivo remain poorly understood. Here, we report that conditional knockout of the chromatin remodeling enzyme Chd4 in granule neurons of the mouse cerebellum increases accessibility of gene regulatory sites genome-wide in vivo. Conditional knockout of Chd4 promotes recruitment of the architectural protein complex cohesin preferentially to gene enhancers in granule neurons in vivo. Importantly, in vivo profiling of genome architecture reveals that conditional knockout of Chd4 strengthens interactions among developmentally repressed contact domains as well as genomic loops in a manner that tightly correlates with increased accessibility, enhancer activity, and cohesin occupancy at these sites. Collectively, our findings define a role for chromatin remodeling in the control of genome architecture organization in the mammalian brain. The mechanisms underlying gene regulation and genome architecture remain poorly understood. Here, the authors investigate the role of chromatin remodelling enzyme Chd4 in granule neurons of the mouse cerebellum and find that conditional knockout of Chd4 preferentially activates enhancers and modulates genome architecture at a genome-wide level.
The mechanisms underlying gene regulation and genome architecture remain poorly understood. Here, the authors investigate the role of chromatin remodelling enzyme Chd4 in granule neurons of the mouse cerebellum and find that conditional knockout of Chd4 preferentially activates enhancers and modulates genome architecture at a genome-wide level.
The development and function of the brain require tight control of gene expression. Genome architecture is thought to play a critical regulatory role in gene expression, but the mechanisms governing genome architecture in the brain in vivo remain poorly understood. Here, we report that conditional knockout of the chromatin remodeling enzyme Chd4 in granule neurons of the mouse cerebellum increases accessibility of gene regulatory sites genome-wide in vivo. Conditional knockout of Chd4 promotes recruitment of the architectural protein complex cohesin preferentially to gene enhancers in granule neurons in vivo. Importantly, in vivo profiling of genome architecture reveals that conditional knockout of Chd4 strengthens interactions among developmentally repressed contact domains as well as genomic loops in a manner that tightly correlates with increased accessibility, enhancer activity, and cohesin occupancy at these sites. Collectively, our findings define a role for chromatin remodeling in the control of genome architecture organization in the mammalian brain.
The development and function of the brain require tight control of gene expression. Genome architecture is thought to play a critical regulatory role in gene expression, but the mechanisms governing genome architecture in the brain in vivo remain poorly understood. Here, we report that conditional knockout of the chromatin remodeling enzyme Chd4 in granule neurons of the mouse cerebellum increases accessibility of gene regulatory sites genome-wide in vivo. Conditional knockout of Chd4 promotes recruitment of the architectural protein complex cohesin preferentially to gene enhancers in granule neurons in vivo. Importantly, in vivo profiling of genome architecture reveals that conditional knockout of Chd4 strengthens interactions among developmentally repressed contact domains as well as genomic loops in a manner that tightly correlates with increased accessibility, enhancer activity, and cohesin occupancy at these sites. Collectively, our findings define a role for chromatin remodeling in the control of genome architecture organization in the mammalian brain.The development and function of the brain require tight control of gene expression. Genome architecture is thought to play a critical regulatory role in gene expression, but the mechanisms governing genome architecture in the brain in vivo remain poorly understood. Here, we report that conditional knockout of the chromatin remodeling enzyme Chd4 in granule neurons of the mouse cerebellum increases accessibility of gene regulatory sites genome-wide in vivo. Conditional knockout of Chd4 promotes recruitment of the architectural protein complex cohesin preferentially to gene enhancers in granule neurons in vivo. Importantly, in vivo profiling of genome architecture reveals that conditional knockout of Chd4 strengthens interactions among developmentally repressed contact domains as well as genomic loops in a manner that tightly correlates with increased accessibility, enhancer activity, and cohesin occupancy at these sites. Collectively, our findings define a role for chromatin remodeling in the control of genome architecture organization in the mammalian brain.
The development and function of the brain require tight control of gene expression. Genome architecture is thought to play a critical regulatory role in gene expression, but the mechanisms governing genome architecture in the brain in vivo remain poorly understood. Here, we report that conditional knockout of the chromatin remodeling enzyme Chd4 in granule neurons of the mouse cerebellum increases accessibility of gene regulatory sites genome-wide in vivo. Conditional knockout of Chd4 promotes recruitment of the architectural protein complex cohesin preferentially to gene enhancers in granule neurons in vivo. Importantly, in vivo profiling of genome architecture reveals that conditional knockout of Chd4 strengthens interactions among developmentally repressed contact domains as well as genomic loops in a manner that tightly correlates with increased accessibility, enhancer activity, and cohesin occupancy at these sites. Collectively, our findings define a role for chromatin remodeling in the control of genome architecture organization in the mammalian brain. The mechanisms underlying gene regulation and genome architecture remain poorly understood. Here, the authors investigate the role of chromatin remodelling enzyme Chd4 in granule neurons of the mouse cerebellum and find that conditional knockout of Chd4 preferentially activates enhancers and modulates genome architecture at a genome-wide level.
The development and function of the brain require tight control of gene expression. Genome architecture is thought to play a critical regulatory role in gene expression, but the mechanisms governing genome architecture in the brain in vivo remain poorly understood. Here, we report that conditional knockout of the chromatin remodeling enzyme Chd4 in granule neurons of the mouse cerebellum increases accessibility of gene regulatory sites genome-wide in vivo. Conditional knockout of Chd4 promotes recruitment of the architectural protein complex cohesin preferentially to gene enhancers in granule neurons in vivo. Importantly, in vivo profiling of genome architecture reveals that conditional knockout of Chd4 strengthens interactions among developmentally repressed contact domains as well as genomic loops in a manner that tightly correlates with increased accessibility, enhancer activity, and cohesin occupancy at these sites. Collectively, our findings define a role for chromatin remodeling in the control of genome architecture organization in the mammalian brain.The mechanisms underlying gene regulation and genome architecture remain poorly understood. Here, the authors investigate the role of chromatin remodelling enzyme Chd4 in granule neurons of the mouse cerebellum and find that conditional knockout of Chd4 preferentially activates enhancers and modulates genome architecture at a genome-wide level.
ArticleNumber 3419
Author Bonni, Azad
Zhao, Guoyan
Kong, Lingchun
Yamada, Tomoko
Gabel, Harrison W.
Goodman, Jared V.
Yang, Yue
Wu, Dennis Y.
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SSID ssj0000391844
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Snippet The development and function of the brain require tight control of gene expression. Genome architecture is thought to play a critical regulatory role in gene...
The mechanisms underlying gene regulation and genome architecture remain poorly understood. Here, the authors investigate the role of chromatin remodelling...
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SubjectTerms 38
38/1
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631/136
631/208/200
631/337/100/101
631/337/100/102
631/378
Accessibility
Animals
Architecture
Brain
Brain - metabolism
Brain architecture
Cell Cycle Proteins - metabolism
Cerebellum
Chromatin - metabolism
Chromatin Assembly and Disassembly
Chromatin remodeling
Chromosomal Proteins, Non-Histone - metabolism
Chromosomes, Mammalian - metabolism
Cohesin
Cohesins
DNA Helicases - genetics
DNA Helicases - metabolism
Enhancer Elements, Genetic - genetics
Enhancers
Enzymes
Epigenesis, Genetic
Gene expression
Gene regulation
Genome
Genomes
Granular materials
Granule cells
Humanities and Social Sciences
Mice, Knockout
Models, Genetic
multidisciplinary
Neurons
Occupancy
Protein Binding
Science
Science (multidisciplinary)
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Title The chromatin remodeling enzyme Chd4 regulates genome architecture in the mouse brain
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