ArticleScience signaling2018
Learning-dependent chromatin remodeling highlights noncoding regulatory regions linked to autism.
Article in Science signaling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Disintegration of the NuRD Complex in Primary Human Muscle Stem Cells in Critical Illness Myopathy.International journal of molecular sciences · 2023Article
- Chromatin accessibility in neuropsychiatric disorders.Neurobiology of learning and memory · 2021Review
- The Engram's Dark Horse: How Interneurons Regulate State-Dependent Memory Processing and Plasticity.Frontiers in neural circuits · 2021Review
- Environmental Enrichment Induces Epigenomic and Genome Organization Changes Relevant for Cognition.Frontiers in molecular neuroscience · 2021Article
- Myosin XVI in the Nervous System.Cells · 2020Review
- Resolving the Synaptic versus Developmental Dichotomy of Autism Risk Genes.Trends in neurosciences · 2020Review
- Recent developments in transcriptional and translational regulation underlying long-term synaptic plasticity and memory.Learning & memory (Cold Spring Harbor, N.Y.) · 2019Review
- Myosin XVI Regulates Actin Cytoskeleton Dynamics in Dendritic Spines of Purkinje Cells and Affects Presynaptic Organization.Frontiers in cellular neuroscience · 2019Article
- Coalitional Game Theory Facilitates Identification of Non-Coding Variants Associated With Autism.Biomedical informatics insights · 2019Article
- Article
Corrections and comments
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Authors and funding
12 authors at 8 institutions in 1 country.
Funding
Abstract
Autism spectrum disorder (ASD) is a prevalent neurodevelopmental disorder that is associated with genetic risk factors. Most human disease-associated single-nucleotide polymorphisms (SNPs) are not located in genes but rather are in regulatory regions that control gene expression. The function of regulatory regions is determined through epigenetic mechanisms. Parallels between the cellular basis of development and the formation of long-term memory have long been recognized, particularly the role of epigenetic mechanisms in both processes. We analyzed how learning alters chromatin accessibility in the mouse hippocampus using a new high-throughput sequencing bioinformatics strategy we call DEScan (differential enrichment scan). DEScan, which enabled the analysis of data from epigenomic experiments containing multiple replicates, revealed changes in chromatin accessibility at 2365 regulatory regions-most of which were promoters. Learning-regulated promoters were active during forebrain development in mice and were enriched in epigenetic modifications indicative of bivalent promoters. These promoters were disproportionally intronic, showed a complex relationship with gene expression and alternative splicing during memory consolidation and retrieval, and were enriched in the data set relative to known ASD risk genes. Genotyping in a clinical cohort within one of these promoters (
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.