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Mst1-mediated phosphorylation of FoxO1 and C/EBP-β Stimulates Cell-protective Mechanisms in Cardiomyocytes

ABSTRACT: Mst1-mediated phosphorylation of FoxO1 and C/EBP-β Stimulates Cell-protective Mechanisms in Cardiomyocytes

PROVIDER: PRJNA878773 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21498084.fastq.gz	Fastqsanger.gz
	SRR21498085.fastq.gz	Fastqsanger.gz
	SRR21498086.fastq.gz	Fastqsanger.gz
	SRR21498087.fastq.gz	Fastqsanger.gz
	SRR21498088.fastq.gz	Fastqsanger.gz

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Mst1-mediated phosphorylation of FoxO1 and C/EBP-β Stimulates Cell-protective Mechanisms in Cardiomyocytes

Project description:The molecular mechanisms by which FoxO transcription factors mediate diametrically opposite cellular responses, namely death and survival, remain unknown. Mst1 phosphorylates FoxO1 Ser209/Ser215/Ser218/Thr228/Ser232/Ser243, thereby inducing nuclear translocation of FoxO1 in cardiomyocytes. Mst1 inhibits the FoxO1-mediated transcription of proapoptotic genes but promotes that of prosurvival genes. Mst1 increases FoxO1-C/EBP-β interaction and phosphorylates C/EBP-β at Thr299, thereby promoting transcription of prosurvival genes. Myocardial ischemia/reperfusion (I/R) injury was larger in cardiac-specific FoxO1 knockout (c-FoxO1–/–) mice than in control mice. However, the concurrent presence of C/EBP-β T299E phospho-mimetic mutation reduced infarct size in c-FoxO–/– mice. The C/EBP-β phospho-mimetic mutant exhibited a higher binding to the promoter of prosurvival genes compared to wild-type C/EBP-β. In conclusion, phosphorylation of FoxO1 by Mst1 inhibits the binding of FoxO1 to pro-apoptotic gene promoters but enhances its binding to C/EBP-β, phosphorylation of C/EBP-β, and transcription of prosurvival genes, which stimulate protective mechanisms in the heart.

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Transcriptional profiling of MST1 or FOXO1 depleted human umbilical vein endothelial cells

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Mst1-mediated phosphorylation of FoxO1 and C/EBP-β stimulates cell-protective mechanisms in cardiomyocytes.

Project description:The molecular mechanisms by which FoxO transcription factors mediate diametrically opposite cellular responses, namely death and survival, remain unknown. Here we show that Mst1 phosphorylates FoxO1 Ser209/Ser215/Ser218/Thr228/Ser232/Ser243, thereby inhibiting FoxO1-mediated transcription of proapoptotic genes. On the other hand, Mst1 increases FoxO1-C/EBP-β interaction and activates C/EBP-β by phosphorylating it at Thr299, thereby promoting transcription of prosurvival genes. Myocardial ischemia/reperfusion injury is larger in cardiac-specific FoxO1 knockout mice than in control mice. However, the concurrent presence of a C/EBP-β T299E phospho-mimetic mutation reduces infarct size in cardiac-specific FoxO1 knockout mice. The C/EBP-β phospho-mimetic mutant exhibits greater binding to the promoter of prosurvival genes than wild type C/EBP-β. In conclusion, phosphorylation of FoxO1 by Mst1 inhibits binding of FoxO1 to pro-apoptotic gene promoters but enhances its binding to C/EBP-β, phosphorylation of C/EBP-β, and transcription of prosurvival genes, which stimulate protective mechanisms in the heart.

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