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Hanseul, Kweon
시냅스 뇌질환 연구단
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Age-differential sexual dimorphism in CHD8-S62X-mutant mouse behaviors

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dc.contributor.authorLee, Soo Yeon-
dc.contributor.authorHanseul Kweon-
dc.contributor.authorKang, Hyojin-
dc.contributor.authorEunjoon Kim-
dc.date.accessioned2023-01-26T02:36:35Z-
dc.date.available2023-01-26T02:36:35Z-
dc.date.created2022-11-29-
dc.date.issued2022-10-
dc.identifier.issn1662-5099-
dc.identifier.urihttps://pr.ibs.re.kr/handle/8788114/12626-
dc.description.abstractAutism spectrum disorders (ASD) are similar to 4-times more common in males than females, and CHD8 (a chromatin remodeler)-related ASD shows a strong male bias (similar to 4:1), although the underlying mechanism remains unclear. Chd8-mutant mice with a C-terminal protein-truncating mutation (N2373K) display male-preponderant behavioral deficits as juveniles and adults, although whether this also applies to other Chd8 mutations remains unknown. In addition, it remains unclear whether sexually dimorphic phenotypes in Chd8-mutant mice are differentially observed in males and females across different ages. We here generated new Chd8-mutant (knock-in) mice carrying a patient-derived mutation causing an N-terminal and stronger protein truncation (Chd8(+/S62X) mice) and characterized the mice by behavioral analyses. Juvenile Chd8(+/S62X) mice displayed male-preponderant autistic-like behaviors; hypoactivity and enhanced mother-seeking/attachment behavior in mates but not in females. Adult male and female Chd8(+/S62X) mice showed largely similar deficits in repetitive and anxiety-like behavioral domains. Therefore, the CHD8-S62X mutation induces ASD-like behaviors in juvenile male mice and adult male and female mice, pointing to an age-differential sexual dimorphism and also distinct sexual dimorphisms in different Chd8 mutations (N2373K and S62X).-
dc.language영어-
dc.publisherFRONTIERS MEDIA SA-
dc.titleAge-differential sexual dimorphism in CHD8-S62X-mutant mouse behaviors-
dc.typeArticle-
dc.type.rimsART-
dc.identifier.wosid000880911200001-
dc.identifier.scopusid2-s2.0-85141388342-
dc.identifier.rimsid79308-
dc.contributor.affiliatedAuthorHanseul Kweon-
dc.contributor.affiliatedAuthorEunjoon Kim-
dc.identifier.doi10.3389/fnmol.2022.1022306-
dc.identifier.bibliographicCitationFRONTIERS IN MOLECULAR NEUROSCIENCE, v.15-
dc.relation.isPartOfFRONTIERS IN MOLECULAR NEUROSCIENCE-
dc.citation.titleFRONTIERS IN MOLECULAR NEUROSCIENCE-
dc.citation.volume15-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalClass1-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaNeurosciences & Neurology-
dc.relation.journalWebOfScienceCategoryNeurosciences-
dc.subject.keywordPlusCHD8-
dc.subject.keywordPlusAUTISM-
dc.subject.keywordPlusCONNECTIVITY-
dc.subject.keywordPlusDISORDER-
dc.subject.keywordPlusGENES-
dc.subject.keywordAuthorautism spectrum disorders-
dc.subject.keywordAuthorCHD8-
dc.subject.keywordAuthormouse model of ASD-
dc.subject.keywordAuthorchromatin remodeling-
dc.subject.keywordAuthorsexual dimorphism-
dc.subject.keywordAuthorage dependence-
Appears in Collections:
Center for Synaptic Brain Dysfunctions(시냅스 뇌질환 연구단) > 1. Journal Papers (저널논문)
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