000176932 001__ 176932
000176932 005__ 20240229133725.0
000176932 0247_ $$2doi$$a10.1038/s41467-021-25846-3
000176932 0247_ $$2pmid$$apmid:34588434
000176932 0247_ $$2altmetric$$aaltmetric:114213485
000176932 037__ $$aDKFZ-2021-02172
000176932 041__ $$aEnglish
000176932 082__ $$a500
000176932 1001_ $$aReddy, Naveen C$$b0
000176932 245__ $$aCHARGE syndrome protein CHD7 regulates epigenomic activation of enhancers in granule cell precursors and gyrification of the cerebellum.
000176932 260__ $$a[London]$$bNature Publishing Group UK$$c2021
000176932 3367_ $$2DRIVER$$aarticle
000176932 3367_ $$2DataCite$$aOutput Types/Journal article
000176932 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1634034800_10605
000176932 3367_ $$2BibTeX$$aARTICLE
000176932 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000176932 3367_ $$00$$2EndNote$$aJournal Article
000176932 500__ $$aDKFZ-ZMBH Alliance
000176932 520__ $$aRegulation of chromatin plays fundamental roles in the development of the brain. Haploinsufficiency of the chromatin remodeling enzyme CHD7 causes CHARGE syndrome, a genetic disorder that affects the development of the cerebellum. However, how CHD7 controls chromatin states in the cerebellum remains incompletely understood. Using conditional knockout of CHD7 in granule cell precursors in the mouse cerebellum, we find that CHD7 robustly promotes chromatin accessibility, active histone modifications, and RNA polymerase recruitment at enhancers. In vivo profiling of genome architecture reveals that CHD7 concordantly regulates epigenomic modifications associated with enhancer activation and gene expression of topologically-interacting genes. Genome and gene ontology studies show that CHD7-regulated enhancers are associated with genes that control brain tissue morphogenesis. Accordingly, conditional knockout of CHD7 triggers a striking phenotype of cerebellar polymicrogyria, which we have also found in a case of CHARGE syndrome. Finally, we uncover a CHD7-dependent switch in the preferred orientation of granule cell precursor division in the developing cerebellum, providing a potential cellular basis for the cerebellar polymicrogyria phenotype upon loss of CHD7. Collectively, our findings define epigenomic regulation by CHD7 in granule cell precursors and identify abnormal cerebellar patterning upon CHD7 depletion, with potential implications for our understanding of CHARGE syndrome.
000176932 536__ $$0G:(DE-HGF)POF4-311$$a311 - Zellbiologie und Tumorbiologie (POF4-311)$$cPOF4-311$$fPOF IV$$x0
000176932 588__ $$aDataset connected to CrossRef, PubMed, , Journals: inrepo01.inet.dkfz-heidelberg.de
000176932 7001_ $$00000-0001-5106-1012$$aMajidi, Shahriyar P$$b1
000176932 7001_ $$aKong, Lingchun$$b2
000176932 7001_ $$aNemera, Mati$$b3
000176932 7001_ $$aFerguson, Cole J$$b4
000176932 7001_ $$aMoore, Michael$$b5
000176932 7001_ $$aGoncalves, Tassia M$$b6
000176932 7001_ $$0P:(DE-He78)76aeb2431f7458c9261e69c5420390c6$$aLiu, Hai-Kun$$b7$$udkfz
000176932 7001_ $$00000-0002-7907-3602$$aFitzpatrick, James A J$$b8
000176932 7001_ $$00000-0001-5615-6774$$aZhao, Guoyan$$b9
000176932 7001_ $$aYamada, Tomoko$$b10
000176932 7001_ $$00000-0003-1391-1500$$aBonni, Azad$$b11
000176932 7001_ $$00000-0001-6894-5113$$aGabel, Harrison W$$b12
000176932 773__ $$0PERI:(DE-600)2553671-0$$a10.1038/s41467-021-25846-3$$gVol. 12, no. 1, p. 5702$$n1$$p5702$$tNature Communications$$v12$$x2041-1723$$y2021
000176932 909CO $$ooai:inrepo02.dkfz.de:176932$$pVDB
000176932 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)76aeb2431f7458c9261e69c5420390c6$$aDeutsches Krebsforschungszentrum$$b7$$kDKFZ
000176932 9131_ $$0G:(DE-HGF)POF4-311$$1G:(DE-HGF)POF4-310$$2G:(DE-HGF)POF4-300$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lKrebsforschung$$vZellbiologie und Tumorbiologie$$x0
000176932 9141_ $$y2021
000176932 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bNAT COMMUN : 2019$$d2021-02-02
000176932 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS$$d2021-02-02
000176932 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline$$d2021-02-02
000176932 915__ $$0StatID:(DE-HGF)0320$$2StatID$$aDBCoverage$$bPubMed Central$$d2021-02-02
000176932 915__ $$0StatID:(DE-HGF)0501$$2StatID$$aDBCoverage$$bDOAJ Seal$$d2021-02-02
000176932 915__ $$0StatID:(DE-HGF)0500$$2StatID$$aDBCoverage$$bDOAJ$$d2021-02-02
000176932 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bDOAJ : Peer review$$d2021-02-02
000176932 915__ $$0LIC:(DE-HGF)CCBYNV$$2V:(DE-HGF)$$aCreative Commons Attribution CC BY (No Version)$$bDOAJ$$d2021-02-02
000176932 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List$$d2021-02-02
000176932 915__ $$0StatID:(DE-HGF)1030$$2StatID$$aDBCoverage$$bCurrent Contents - Life Sciences$$d2021-02-02
000176932 915__ $$0StatID:(DE-HGF)0160$$2StatID$$aDBCoverage$$bEssential Science Indicators$$d2021-02-02
000176932 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews$$d2021-02-02
000176932 915__ $$0StatID:(DE-HGF)1150$$2StatID$$aDBCoverage$$bCurrent Contents - Physical, Chemical and Earth Sciences$$d2021-02-02
000176932 915__ $$0StatID:(DE-HGF)1060$$2StatID$$aDBCoverage$$bCurrent Contents - Agriculture, Biology and Environmental Sciences$$d2021-02-02
000176932 915__ $$0StatID:(DE-HGF)1040$$2StatID$$aDBCoverage$$bZoological Record$$d2021-02-02
000176932 915__ $$0StatID:(DE-HGF)1190$$2StatID$$aDBCoverage$$bBiological Abstracts$$d2021-02-02
000176932 915__ $$0StatID:(DE-HGF)0113$$2StatID$$aWoS$$bScience Citation Index Expanded$$d2021-02-02
000176932 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection$$d2021-02-02
000176932 915__ $$0StatID:(DE-HGF)9910$$2StatID$$aIF >= 10$$bNAT COMMUN : 2019$$d2021-02-02
000176932 915__ $$0StatID:(DE-HGF)0561$$2StatID$$aArticle Processing Charges$$d2021-02-02
000176932 915__ $$0StatID:(DE-HGF)0700$$2StatID$$aFees$$d2021-02-02
000176932 9201_ $$0I:(DE-He78)A240-20160331$$kA240$$lA240 Molekulare Neurogenetik$$x0
000176932 980__ $$ajournal
000176932 980__ $$aVDB
000176932 980__ $$aI:(DE-He78)A240-20160331
000176932 980__ $$aUNRESTRICTED