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Enhanced hippocampal neurogenesis mediated by PGC-1α-activated OXPHOS after neonatal subclinical dose of Propofol exposure revealed by single-nuclei transcriptomic profiling

ABSTRACT: Enhanced hippocampal neurogenesis mediated by PGC-1α-activated OXPHOS after neonatal subclinical dose of Propofol exposure revealed by single-nuclei transcriptomic profiling

PROVIDER: PRJNA772978 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16497778_1.fastq.gz	Fastqsanger.gz
	SRR16497778_2.fastq.gz	Fastqsanger.gz
	SRR16497779_1.fastq.gz	Fastqsanger.gz
	SRR16497779_2.fastq.gz	Fastqsanger.gz

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Enhanced hippocampal neurogenesis mediated by PGC-1α-activated OXPHOS after neonatal low-dose Propofol exposure

Project description:Enhanced hippocampal neurogenesis mediated by PGC-1α-activated OXPHOS after neonatal low-dose Propofol exposure

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Enhanced hippocampal neurogenesis mediated by PGC-1α-activated OXPHOS after neonatal subclinical dose of Propofol exposure revealed by single-nuclei transcriptomic profiling

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Enhanced hippocampal neurogenesis mediated by PGC-1α-activated OXPHOS after neonatal low-dose Propofol exposure

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A map of the PGC-1α- and NT-PGC-1α-regulated transcriptional network in brown adipose tissue [SAGE]

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Project description:PGC-1α is a transcriptional coactivator that controls expression of metabolic/energetic genes programming cellular responses to nutrient and environmental adaptations such as fasting, cold or exercise. Unlike most other coactivators, PGC-1α contains protein domains involved in RNA binding and processing such as serine/arginine (SR) and RNA Recognition (RRM) motifs. However, little is known regarding the specific RNAs that bind PGC-1α to possibly control specific metabolic and energetic functions. To address this, we have performed single-end enhanced crosslinking and immunoprecipitation (seCLIP)-based transcriptome-wide analysis to identify specific RNA sequences that bind to PGC-1α. Primary hepatocytes were used to perform seCLIP experiments with glucagon-induced endogenous PGC-1α. RNA sequencing reveals that a large fraction of the RNAs bound to PGC-1α were intronic sequences related to genes involved in transcriptional, signaling or metabolic function linked to glucagon and fasting responses, but were not the canonical direct transcriptional targets of PGC-1α, such as OXPHOS or gluconeogenic genes. Validation of this analysis confirmed that among the top scoring RNA sequences bound to PGC-1α were Sik1, Camk1d, Ppard, Klf15, Gfra1 and Slc25a25. PGC-1α depletion decreased a fraction of mRNA transcript levels of these glucagon-induced genes. Importantly, knock-down of these genes affected glucagon-dependent glucose production, a PGC-1α-regulated metabolic pathway. These studies show that PGC-1α largely binds to intronic RNA sequences, some of them controlling transcript levels associated with glucagon action.

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Project description:The peroxisome-proliferator-activated receptor-γ coactivator-1α (PGC-1α) integrates environmental cues by controlling complex transcriptional networks in various metabolically active tissues. However, it is unclear how a transcriptional coregulator coordinates dynamic biological programs in response to multifaceted stimuli such as endurance training or fasting. Here, we discovered a central function of the poorly understood C-terminal domain (CTD) of PGC-1α to bind RNAs and assemble multi-protein complexes. Surprisingly, in addition to controlling the coupling of transcription and processing of target genes, RNA binding is indispensable for the recruitment of PGC-1α to chromatin into liquid-like nuclear condensates, which compartmentalize and regulate active transcription. These results demonstrate a hitherto unsuspected molecular mechanism by which complexity in the regulation of large transcriptional networks by PGC-1α is achieved. These findings are not only essential for the basic understanding of transcriptional coregulator-driven control of biological programs, but will also help to devise new strategies to modulate these processes in pathological contexts in which PGC-1α function is dysregulated, such as type 2 diabetes, cardiovascular diseases or skeletal muscle wasting.

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