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Dual Requirement of CHD8 for Chromatin Landscape Establishment and Histone Methyltransferase Recruitment to Promote CNS Myelination and Repair.

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TLDR
The data indicate that CHD8 exhibits a dual function through inducing a cascade of chromatin reprogramming and recruiting H3K4 histone methyltransferases to establish oligodendrocyte identity, suggesting potential strategies of therapeutic intervention forCHD8-associated white matter defects.
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This article is published in Developmental Cell.The article was published on 2018-06-18 and is currently open access. It has received 90 citations till now. The article focuses on the topics: Oligodendrocyte differentiation & Chromatin remodeling.

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In vivo Perturb-Seq reveals neuronal and glial abnormalities associated with autism risk genes.

TL;DR: In vivo Perturb-Seq can serve as a scalable tool for systems genetic studies of large gene panels to reveal their cell-intrinsic functions at single-cell resolution in complex tissues and allow simultaneous assessment of the individual phenotypes of a panel of such risk genes in the context of the developing mouse brain.
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Molecular Control of Oligodendrocyte Development

TL;DR: The characterization of several recently identified regulatory factors that govern these processes have greatly increased understanding of oligodendrocyte development and function and are critical to facilitate efforts to enhance OPC differentiation in neurological disorders that disrupt CNS myelin.
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Oligodendrocyte precursor survival and differentiation requires chromatin remodeling by Chd7 and Chd8.

TL;DR: It is shown that Chd 7 protects OPCs from apoptosis by chromatin closing and gene repression of p53, while Chd7 induces chromatin opening and gene activation of OPC-differentiation regulators, which offer new avenues to understand and modulate the CHD7 and CHD8 functions in normal development and disease.
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Autism-associated CHD8 deficiency impairs axon development and migration of cortical neurons

TL;DR: Findings indicate an important role for CHD8 in dendritic and axon development and neuronal migration and thus offer novel insights to further dissect the underlying molecular and circuit mechanisms of ASD caused by CHd8 deficiency.
References
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Journal ArticleDOI

The language of covalent histone modifications.

TL;DR: It is proposed that distinct histone modifications, on one or more tails, act sequentially or in combination to form a ‘histone code’ that is, read by other proteins to bring about distinct downstream events.
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Transposition of native chromatin for fast and sensitive epigenomic profiling of open chromatin, DNA-binding proteins and nucleosome position

TL;DR: The feasibility of analyzing an individual's epigenome on a timescale compatible with clinical decision-making is demonstrated and classes of DNA-binding factors that strictly avoided, could tolerate or tended to overlap with nucleosomes are discovered.
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Axonal transection in the lesions of multiple sclerosis.

TL;DR: Transected axons are common in the lesions of multiple sclerosis, and axonal transection may be the pathologic correlate of the irreversible neurologic impairment in this disease.
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ATAC-seq: A Method for Assaying Chromatin Accessibility Genome-Wide

TL;DR: This method probes DNA accessibility with hyperactive Tn5 transposase, which inserts sequencing adapters into accessible regions of chromatin, which can be used to infer regions of increased accessibility, as well as to map regions of transcription‐factor binding and nucleosome position.
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Active genes are tri-methylated at K4 of histone H3

TL;DR: It is shown that the Saccharomyces cerevisiae Set1 protein can catalyse di- and tri-methylation of K4 and stimulate the activity of many genes, establishing the concept of methyl status as a determinant for gene activity and extending considerably the complexity of histone modifications.
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