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Fetal Exposure of low dose Methylmercury Enhances CREB Activity to Induce Premature Neuronal Differentiation During Embryonic Cortex Development

ABSTRACT: Fetal Exposure of low dose Methylmercury Enhances CREB Activity to Induce Premature Neuronal Differentiation During Embryonic Cortex Development

PROVIDER: PRJNA741513 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14916183_1.fastq.gz	Fastqsanger.gz
	SRR14916183_2.fastq.gz	Fastqsanger.gz
	SRR14916184_1.fastq.gz	Fastqsanger.gz
	SRR14916184_2.fastq.gz	Fastqsanger.gz
	SRR14916185_1.fastq.gz	Fastqsanger.gz

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Fetal Exposure of low dose Methylmercury Enhances CREB Activity to Induce Premature Neuronal Differentiation During Embryonic Cortex Development

Project description:Methylmercury is a bioaccumulated environmental neurotoxicant, however, it remains largely unknown regarding impacts of non-apoptotic low dose methylmercury on embryonic cerebral cortex development. Here, using single cell RNA-seq analysis we show that prenatal exposure of MeHg favors RGP developmental trajectory towards directly producing cortical neurons, omitting intermediate progenitor stage. Our findings reveal the outcomes of low dose MeHg exposure on the fetal brain development and provide insights into its underlying mechanisms and potential therapeutic strategy.

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Project description:Transcription factor CREB regulates lens Epithelial-Mesenchymal Transition（EMT）in both S133 phosphorylation dependent and independent manners. We found that S133A-CREB can activate lens EMT, while R314A-CREB attenuated it. To understand the mechanism by which S133A-CREB and R314A-CREB modulates EMT gene expression. ChIP assay using CREB antibody in the in the mouse lens epithelial cells alpha-TN4 overexpressing Vector, WT-CREB, S133A-CREB, R314A-CREB and S133A/R314A-CREB, and ChIP-seq was conducted on the ChIP DNA. We found that WT-CREB, S133A-CREB as well as R314A-CREB binds to the promoter regions of mesenchymal genes, and S133A-CREB retained canonical CREB binding motif, while R314A-CREB exhibited shifted binding motif preference to ATF1.

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Analyzing CREB binding motif and sites in the mouse lens epithelial cells alpha-TN4 overexpressing Vector, WT-CREB, S133A-CREB, R314A-CREB and S133A/R314A –CREB.

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Zfp189 Mediates Stress Resilience Through a CREB-Regulated Transcriptional Network in Prefrontal Cortex

Project description:Stress resilience involves numerous brain-wide transcriptional changes. Determining the organization and orchestration of these transcriptional events may reveal novel antidepressant targets, but this remains unexplored. Here, we characterize the resilient transcriptome with co-expression analysis and identify a single transcriptionally-active uniquely-resilient gene network. Zfp189, a previously unstudied zinc finger protein, is the top network key driver and its overexpression in prefrontal cortical (PFC) neurons preferentially activates this network, alters neuronal activity and promotes behavioral resilience. CREB, which binds Zfp189, is the top upstream regulator of this network. To probe CREB-Zfp189 interactions as a network regulatory mechanism, we employ CRISPR-mediated locus-specific transcriptional reprogramming to direct CREB selectively to the Zfp189 promoter. This single molecular interaction in PFC neurons recapitulates the pro-resilient Zfp189-dependent downstream effects on gene network activity, electrophysiology and behavior. These findings reveal an essential role for Zfp189 and a CREB-Zfp189 regulatory axis in mediating a central transcriptional network of resilience.

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