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Arterialization requires the timely suppression of cell growth

ABSTRACT: Arterialization requires the timely suppression of cell growth

PROVIDER: PRJNA666387 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12739810_1.fastq.gz	Fastqsanger.gz
	SRR12739810_2.fastq.gz	Fastqsanger.gz
	SRR12739811_1.fastq.gz	Fastqsanger.gz
	SRR12739811_2.fastq.gz	Fastqsanger.gz
	SRR12739812_1.fastq.gz	Fastqsanger.gz

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Arterialization requires the timely suppression of cell growth

Project description:Arteries are thought to be formed through the induction of a highly conserved arterial genetic programme in a subset of vessels that will later experience an increase in oxygenated blood flow. The initial steps of arterial specification require both VEGF and Notch signalling. Here, we combined inducible genetic mosaics and transcriptomics to modulate and define the function of these signalling pathways in cell proliferation, arteriovenous (AV) differentiation and mobilization. We observed that endothelial cells (ECs) with high VEGF or Notch signalling are intrinsically biased to mobilize and form arteries; nevertheless, they are not genetically pre-determined, and can also form veins. Mechanistically, we found that higher VEGF and Notch signalling in pre-arterial capillaries suppresses Myc-dependent metabolic and cell-cycle activities, promoting the incorporation of ECs in arteries. Mosaic lineage tracing studies revealed that ECs completely lacking the Notch-Rbpj transcriptional activator complex rarely form arteries; however, these cells regained the ability to form arteries when Myc function was suppressed. Thus, arterial development does not require the direct induction of a Notch-dependent arterial differentiation programme, but rather the timely suppression of endothelial cell-cycle progression and metabolism, a process preceding arterial mobilization and complete differentiation.

2020-09-30 | GSE158731 | GEO

Arterialization requires the timely suppression of cell growth.

Project description:The formation of arteries is thought to occur by the induction of a highly conserved arterial genetic programme in a subset of vessels that will later experience an increase in oxygenated blood flow1,2. The initial steps of arterial specification require both the VEGF and Notch signalling pathways3-5. Here, we combine inducible genetic mosaics and transcriptomics to modulate and define the function of these signalling pathways in cell proliferation, arteriovenous differentiation and mobilization. We show that endothelial cells with high levels of VEGF or Notch signalling are intrinsically biased to mobilize and form arteries; however, they are not genetically pre-determined, and can also form veins. Mechanistically, we found that increased levels of VEGF and Notch signalling in pre-arterial capillaries suppresses MYC-dependent metabolic and cell-cycle activities, and promotes the incorporation of endothelial cells into arteries. Mosaic lineage-tracing studies showed that endothelial cells that lack the Notch-RBPJ transcriptional activator complex rarely form arteries; however, these cells regained the ability to form arteries when the function of MYC was suppressed. Thus, the development of arteries does not require the direct induction of a Notch-dependent arterial differentiation programme, but instead depends on the timely suppression of endothelial cell-cycle progression and metabolism, a process that precedes arterial mobilization and complete differentiation.

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