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Impact of c-JUN deficiency on thalamus development in mice and human neural models [ATACseq, RNAseq, CUT&Tag]

ABSTRACT: Impact of c-JUN deficiency on thalamus development in mice and human neural models [ATACseq, RNAseq, CUT&Tag]

PROVIDER: PRJNA1083042 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28203104_1.fastq.gz	Fastqsanger.gz
	SRR28203104_2.fastq.gz	Fastqsanger.gz
	SRR28203105_1.fastq.gz	Fastqsanger.gz
	SRR28203105_2.fastq.gz	Fastqsanger.gz
	SRR28203106_1.fastq.gz	Fastqsanger.gz

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Impact of c-JUN deficiency on thalamus development in mice and human neural models [ATACseq, RNAseq, CUT&Tag]

Project description:c-Jun is a gene expression regulator. By forming homo- or heterodimer, c-Jun binds to DNA and regulates gene transcription. c-Jun is deeply involved in embryonic development but its effect on nervous system development especially in higher mammal is unclear. In this study, we combined H1ESC derived neural progenitor cells (NPCs), cerebral organoids (COs),Thalamus Organoids(ThOs) and mouse model to study the role of c-Jun in early nervous system development. c-Jun KO promoted NPCs induction and differentiation while weakened NPCs’ adhesion ability. c-Jun KO COs got more robust neural ectoderm and expanded Pax6+/Nestin+ cortex-like layer while less tight junctional core. c-Jun KO mouse embryos on E14.5 showed malformation of thalamus in diencephalon with tight junction loose and cell lose. Taken together, the consistent trend in three models implied that c-Jun deletion promoted neural differentiation while weakened the tight junctions. The thalamus/diencephalon was vulnerable to dysplasia when lose c-Jun in early mouse embryonic development.

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Impact of c-JUN deficiency on thalamus development in mice and human neural models

Project description:c-Jun is a gene expression regulator. By forming homo- or heterodimer, c-Jun binds to DNA and regulates gene transcription. c-Jun is deeply involved in embryonic development but its effect on nervous system development especially in higher mammal is unclear. In this study, we combined H1ESC derived neural progenitor cells (NPCs), cerebral organoids (COs) and mouse model to study the role of c-Jun in early nervous system development. c-Jun KO promoted NPCs induction and differentiation while weakened NPCs’ adhesion ability. c-Jun KO COs got more robust neural ectoderm and expanded Pax6+/Nestin+ cortex-like layer while less tight junctional core. c-Jun KO mouse embryos on E14.5 showed malformation of thalamus in diencephalon with tight junction loose and cell lose. Taken together, the consistent trend in three models implied that c-Jun deletion promoted neural differentiation while weakened the tight junctions. The thalamus/diencephalon was vulnerable to dysplasia when lose c-Jun in early mouse embryonic development.

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Impact of c-JUN deficiency on thalamus development in mice and human neural models

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