Non-CG methylation and multiple histone profiles associate child abuse with immune and small GTPase dysregulation

Early-life adversity (ELA) is a major predictor of psychopathology, and is thought to increase lifetime risk by epigenetically regulating the genome. Here, focusing on the lateral amygdala, a major brain site for emotional homeostasis, we describe molecular cross-talk among multiple mechanisms of ge...

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Published inNature communications Vol. 12; no. 1; pp. 1132 - 16
Main Authors Lutz, Pierre-Eric, Chay, Marc-Aurèle, Pacis, Alain, Chen, Gary G., Aouabed, Zahia, Maffioletti, Elisabetta, Théroux, Jean-François, Grenier, Jean-Christophe, Yang, Jennie, Aguirre, Maria, Ernst, Carl, Redensek, Adriana, van Kempen, Léon C., Yalcin, Ipek, Kwan, Tony, Mechawar, Naguib, Pastinen, Tomi, Turecki, Gustavo
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 18.02.2021
Nature Publishing Group
Nature Portfolio
Subjects
45/15
45/23
45/91
631/1647/2210/2211
631/337/100/2286
631/337/176/1988
631/378/1689
631/378/2584
Amygdala
Amygdala - pathology
Brain
Child
Child Abuse
Child abuse & neglect
Chromatin
Chromatin - metabolism
Context
Crosstalk
Deoxyribonucleic acid
DNA
DNA methylation
DNA Methylation - genetics
Early experience
Epigenetics
Epigenome - genetics
Gene expression
Gene Expression Profiling
Gene Ontology
Genome, Human
Genomes
Genomics
Histone Code
Histones
Histones - metabolism
Homeostasis
Humanities and Social Sciences
Humans
Life Sciences
Monomeric GTP-Binding Proteins - metabolism
multidisciplinary
Protein Processing, Post-Translational
Psychopathology
Science
Science (multidisciplinary)
Transcriptomes
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Abstract Early-life adversity (ELA) is a major predictor of psychopathology, and is thought to increase lifetime risk by epigenetically regulating the genome. Here, focusing on the lateral amygdala, a major brain site for emotional homeostasis, we describe molecular cross-talk among multiple mechanisms of genomic regulation, including 6 histone marks and DNA methylation, and the transcriptome, in subjects with a history of ELA and controls. In the healthy brain tissue, we first uncover interactions between different histone marks and non-CG methylation in the CAC context. Additionally, we find that ELA associates with methylomic changes that are as frequent in the CAC as in the canonical CG context, while these two forms of plasticity occur in sharply distinct genomic regions, features, and chromatin states. Combining these multiple data indicates that immune-related and small GTPase signaling pathways are most consistently impaired in the amygdala of ELA individuals. Overall, this work provides insights into genomic brain regulation as a function of early-life experience. Early-life adversity is thought to increase the risk of psychopathology through epigenetic mechanisms. Here, the authors profile 6 histone marks, chromatin states and DNA methylation in the lateral amygdala in subjects with a history of early-life adversity.
AbstractList Early-life adversity is thought to increase the risk of psychopathology through epigenetic mechanisms. Here, the authors profile 6 histone marks, chromatin states and DNA methylation in the lateral amygdala in subjects with a history of early-life adversity.
Abstract Early-life adversity (ELA) is a major predictor of psychopathology, and is thought to increase lifetime risk by epigenetically regulating the genome. Here, focusing on the lateral amygdala, a major brain site for emotional homeostasis, we describe molecular cross-talk among multiple mechanisms of genomic regulation, including 6 histone marks and DNA methylation, and the transcriptome, in subjects with a history of ELA and controls. In the healthy brain tissue, we first uncover interactions between different histone marks and non-CG methylation in the CAC context. Additionally, we find that ELA associates with methylomic changes that are as frequent in the CAC as in the canonical CG context, while these two forms of plasticity occur in sharply distinct genomic regions, features, and chromatin states. Combining these multiple data indicates that immune-related and small GTPase signaling pathways are most consistently impaired in the amygdala of ELA individuals. Overall, this work provides insights into genomic brain regulation as a function of early-life experience.
Early-life adversity (ELA) is a major predictor of psychopathology, and is thought to increase lifetime risk by epigenetically regulating the genome. Here, focusing on the lateral amygdala, a major brain site for emotional homeostasis, we describe molecular cross-talk among multiple mechanisms of genomic regulation, including 6 histone marks and DNA methylation, and the transcriptome, in subjects with a history of ELA and controls. In the healthy brain tissue, we first uncover interactions between different histone marks and non-CG methylation in the CAC context. Additionally, we find that ELA associates with methylomic changes that are as frequent in the CAC as in the canonical CG context, while these two forms of plasticity occur in sharply distinct genomic regions, features, and chromatin states. Combining these multiple data indicates that immune-related and small GTPase signaling pathways are most consistently impaired in the amygdala of ELA individuals. Overall, this work provides insights into genomic brain regulation as a function of early-life experience.Early-life adversity (ELA) is a major predictor of psychopathology, and is thought to increase lifetime risk by epigenetically regulating the genome. Here, focusing on the lateral amygdala, a major brain site for emotional homeostasis, we describe molecular cross-talk among multiple mechanisms of genomic regulation, including 6 histone marks and DNA methylation, and the transcriptome, in subjects with a history of ELA and controls. In the healthy brain tissue, we first uncover interactions between different histone marks and non-CG methylation in the CAC context. Additionally, we find that ELA associates with methylomic changes that are as frequent in the CAC as in the canonical CG context, while these two forms of plasticity occur in sharply distinct genomic regions, features, and chromatin states. Combining these multiple data indicates that immune-related and small GTPase signaling pathways are most consistently impaired in the amygdala of ELA individuals. Overall, this work provides insights into genomic brain regulation as a function of early-life experience.
Early-life adversity (ELA) is a major predictor of psychopathology, and is thought to increase lifetime risk by epigenetically regulating the genome. Here, focusing on the lateral amygdala, a major brain site for emotional homeostasis, we describe molecular cross-talk among multiple mechanisms of genomic regulation, including 6 histone marks and DNA methylation, and the transcriptome, in subjects with a history of ELA and controls. In the healthy brain tissue, we first uncover interactions between different histone marks and non-CG methylation in the CAC context. Additionally, we find that ELA associates with methylomic changes that are as frequent in the CAC as in the canonical CG context, while these two forms of plasticity occur in sharply distinct genomic regions, features, and chromatin states. Combining these multiple data indicates that immune-related and small GTPase signaling pathways are most consistently impaired in the amygdala of ELA individuals. Overall, this work provides insights into genomic brain regulation as a function of early-life experience.
Early-life adversity (ELA) is a major predictor of psychopathology, and is thought to increase lifetime risk by epigenetically regulating the genome. Here, focusing on the lateral amygdala, a major brain site for emotional homeostasis, we describe molecular cross-talk among multiple mechanisms of genomic regulation, including 6 histone marks and DNA methylation, and the transcriptome, in subjects with a history of ELA and controls. In the healthy brain tissue, we first uncover interactions between different histone marks and non-CG methylation in the CAC context. Additionally, we find that ELA associates with methylomic changes that are as frequent in the CAC as in the canonical CG context, while these two forms of plasticity occur in sharply distinct genomic regions, features, and chromatin states. Combining these multiple data indicates that immune-related and small GTPase signaling pathways are most consistently impaired in the amygdala of ELA individuals. Overall, this work provides insights into genomic brain regulation as a function of early-life experience. Early-life adversity is thought to increase the risk of psychopathology through epigenetic mechanisms. Here, the authors profile 6 histone marks, chromatin states and DNA methylation in the lateral amygdala in subjects with a history of early-life adversity.
Early-life adversity (ELA) is a major predictor of psychopathology, and is thought to increase lifetime risk by epigenetically regulating the genome. Here, focusing on the lateral amygdala, a major brain site for emotional homeostasis, we describe molecular cross-talk among multiple mechanisms of genomic regulation, including 6 histone marks and DNA methylation, and the transcriptome, in subjects with a history of ELA and controls. In the healthy brain tissue, we first uncover interactions between different histone marks and non-CG methylation in the CAC context. Additionally, we find that ELA associates with methylomic changes that are as frequent in the CAC as in the canonical CG context, while these two forms of plasticity occur in sharply distinct genomic regions, features, and chromatin states. Combining these multiple data indicates that immune-related and small GTPase signaling pathways are most consistently impaired in the amygdala of ELA individuals. Overall, this work provides insights into genomic brain regulation as a function of early-life experience.Early-life adversity is thought to increase the risk of psychopathology through epigenetic mechanisms. Here, the authors profile 6 histone marks, chromatin states and DNA methylation in the lateral amygdala in subjects with a history of early-life adversity.
ArticleNumber 1132
Author Kwan, Tony
Chen, Gary G.
Grenier, Jean-Christophe
Aouabed, Zahia
Chay, Marc-Aurèle
Yalcin, Ipek
Pastinen, Tomi
Théroux, Jean-François
Maffioletti, Elisabetta
Yang, Jennie
Mechawar, Naguib
Redensek, Adriana
Lutz, Pierre-Eric
Pacis, Alain
Aguirre, Maria
Ernst, Carl
Turecki, Gustavo
van Kempen, Léon C.
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Issue 1
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Snippet Early-life adversity (ELA) is a major predictor of psychopathology, and is thought to increase lifetime risk by epigenetically regulating the genome. Here,...
Abstract Early-life adversity (ELA) is a major predictor of psychopathology, and is thought to increase lifetime risk by epigenetically regulating the genome....
Early-life adversity is thought to increase the risk of psychopathology through epigenetic mechanisms. Here, the authors profile 6 histone marks, chromatin...
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StartPage 1132
SubjectTerms 45/15
45/23
45/91
631/1647/2210/2211
631/337/100/2286
631/337/176/1988
631/378/1689
631/378/2584
Amygdala
Amygdala - pathology
Brain
Child
Child Abuse
Child abuse & neglect
Chromatin
Chromatin - metabolism
Context
Crosstalk
Deoxyribonucleic acid
DNA
DNA methylation
DNA Methylation - genetics
Early experience
Epigenetics
Epigenome - genetics
Gene expression
Gene Expression Profiling
Gene Ontology
Genome, Human
Genomes
Genomics
Histone Code
Histones
Histones - metabolism
Homeostasis
Humanities and Social Sciences
Humans
Life Sciences
Monomeric GTP-Binding Proteins - metabolism
multidisciplinary
Protein Processing, Post-Translational
Psychopathology
Science
Science (multidisciplinary)
Transcriptomes
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Title Non-CG methylation and multiple histone profiles associate child abuse with immune and small GTPase dysregulation
URI https://link.springer.com/article/10.1038/s41467-021-21365-3
https://www.ncbi.nlm.nih.gov/pubmed/33602921
https://www.proquest.com/docview/2490848598
https://www.proquest.com/docview/2491941782
https://hal.science/hal-03407809
https://pubmed.ncbi.nlm.nih.gov/PMC7892573
https://doaj.org/article/8c5757658d8b418787c5d3069801d997
Volume 12
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