In vivo targeted DamID identifies CHD8 genomic targets in fetal mouse brain.

Autor:	Wade AA; Department of Psychiatry and Behavioral Sciences, University of California, Davis, Davis, CA 95616, USA.; Department of Neurobiology, Physiology and Behavior, University of California, Davis, Davis, CA 95616, USA., van den Ameele J; The Gurdon Institute and Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, CB2 1TN, UK., Cheetham SW; The Gurdon Institute and Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, CB2 1TN, UK., Yakob R; The Gurdon Institute and Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, CB2 1TN, UK., Brand AH; The Gurdon Institute and Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, CB2 1TN, UK., Nord AS; Department of Psychiatry and Behavioral Sciences, University of California, Davis, Davis, CA 95616, USA.; Department of Neurobiology, Physiology and Behavior, University of California, Davis, Davis, CA 95616, USA.
Jazyk:	angličtina
Zdroj:	IScience [iScience] 2021 Oct 07; Vol. 24 (11), pp. 103234. Date of Electronic Publication: 2021 Oct 07 (Print Publication: 2021).
DOI:	10.1016/j.isci.2021.103234
Abstrakt:	Genetic studies of autism have revealed causal roles for chromatin remodeling gene mutations. Chromodomain helicase DNA binding protein 8 ( CHD8 ) encodes a chromatin remodeler with significant de novo mutation rates in sporadic autism. However, relationships between CHD8 genomic function and autism-relevant biology remain poorly elucidated. Published studies utilizing ChIP-seq to map CHD8 protein-DNA interactions have high variability, consistent with technical challenges and limitations associated with this method. Thus, complementary approaches are needed to establish CHD8 genomic targets and regulatory functions in developing brain. We used in utero CHD8 Targeted DamID followed by sequencing (TaDa-seq) to characterize CHD8 binding in embryonic mouse cortex. CHD8 TaDa-seq reproduced interaction patterns observed from ChIP-seq and further highlighted CHD8 distal interactions associated with neuronal loci. This study establishes TaDa-seq as a useful alternative for mapping protein-DNA interactions in vivo and provides insights into the regulatory targets of CHD8 and autism-relevant pathophysiology associated with CHD8 mutations. Competing Interests: The authors declare no competing interests. (© 2021 The Author(s).)
Databáze:	MEDLINE
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