Endothelial RNF20 regulates the self-renewal and differentiation of neural precursor cells during embryonic development
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ABSTRACT:
PROVIDER: PRJNA794109 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17424072_1.fastq.gz | Fastqsanger.gz | |||
| SRR17424072_2.fastq.gz | Fastqsanger.gz | |||
| SRR17424073_1.fastq.gz | Fastqsanger.gz | |||
| SRR17424073_2.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: To further explore how endothelial RNF20 regulates embryonic neurogenesis, RNA isolated from the endothelial cells of RNF20fl/fl and RNF20cKO-Tie2 brain cortex at E13 was analyzed by RNA-seq to determine the genome-wide changes. Methods: mRNA from E13 isolated endothelial cells of RNF20fl/fl and RNF20cKO-Tie2 mice was extracted. Specifically, Agilent 2100 Bioanalyze was used to quality controlled and quantified. then, mRNA was converted to cDNA and bound the library. RNA-sequencing analysis was used by the Illumina HiSeq 2500 platform in Annoroad Genomics Results: Approximately one thousand transcripts showed differential expression between the RNF20fl/fl and RNF20cKO-Tie2 mice brain cortex, with a fold change ≥2 and p value <0.05. Gene ontology analysis of downregulated genes showed the genes were enriched in terms related to neuron differentiation, cell communication and secretion by cells.Concomitantly, upregulated genes were enriched in terms related to negative regulation of cytokine production and cell development.The results showed that endothelial RNF20 is critical for neurogenesis. Conclusions: Endothelial RNF20 RNA-seq would provide a overall understanding how endothelial RNF20 regulates the self-renewal and differentiation of neural precursor cells during embryonic development
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Project description:The transition between quiescence and activation in neural stem and progenitor cells (NSPCs) is coupled to reversible changes in energy metabolism with key implications for life-long NSPC self-renewal and neurogenesis. How this metabolic plasticity is ensured between NSPC activity states is unclear. We find that a state-specific rewiring of the mitochondrial proteome by the i-AAA peptidase YME1L is required to preserve NSPC self-renewal. YME1L controls the abundance of numerous mitochondrial substrates in quiescent NSPCs, and its deletion activates a differentiation program characterized by broad metabolic changes causing the irreversible shift away from a fatty acid oxidation-dependent state. Conditional Yme1l deletion in adult NSPCs in vivo results in defective self-renewal and premature differentiation, ultimately leading to NSPC pool depletion. Our results disclose an important role for YME1L in coordinating the switch between metabolic states of NSPCs and suggest that NSPC fate is regulated by compartmentalized changes in protein network dynamics.
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