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Mus musculus

ABSTRACT: Transient Hes5 activity instructs mesodermal cells toward a cardiac fate

PROVIDER: PRJNA271275 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1735780.fastq.gz	Fastqsanger.gz
	SRR1735781.fastq.gz	Fastqsanger.gz

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Transient Hes5 activity instructs mesodermal cells toward a cardiac fate

Project description:Notch signaling plays a role in specifying a cardiac fate but the downstream effectors remain unknown. In this study we implicate the Notch downstream effector HES5 in cardiogenesis. We show transient Hes5 expression in early mesoderm of gastrulating embryos and demonstrate, by loss and gain-of-function experiments in mouse embryonic stem cells, that HES5 favors cardiac over primitive erythroid fate. Hes5 overexpression promotes upregulation of the cardiac gene Isl1, while the hematopoietic regulator Scl is downregulated. Moreover, whereas a pulse of Hes5 instructs cardiac commitment, sustained expression after lineage specification impairs progression of differentiation to contracting cardiomyocytes. These findings establish a role for HES5 in cardiogenesis and provide insights into the early cardiac molecular network.

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Persulfidation alters gene regulatory programs and promotes endothelial specification

Project description:Endogenously generated sulfides are conserved among species and tissues and exert multiple effects through diverse mechanisms. Although sulfides have been linked to cell fates, their role in pluripotent stem cell commitment remains unknown. Here we discovered that during directed differentiation of induced pluripotent stem cells, endogenous sulfide levels drop in all three germ layers, with the mesodermal lineage exhibiting the lowest capacity to generate these species at early specification events. Addition of a rapid releasing sulfide donor in iPSCs or mesodermal cells did not affect the redox surveillance mechanisms, however altered persulfidation and transcription of cell fate commitment pathways. In particular, sulfide supplementation in pluripotent stem cells reduced cell differentiation processes by preserving the activity of the stem cell transcription factors OCT4 and KLF4. In contrast, supplementation of sulfide during mesodermal lineage specification promoted persulfidation and activated the WNT signaling as well as enriched the activity of the ETS transcription factor family, resulting in increased transcription of angiogenic and vessel morphogenesis genes. Sulfide addition during the development of vascular organoids enhanced blood vessel morphogenesis. Taken together, these data position protein persulfidation as a timing-dependent regulator that preserves pluripotency prior to commitment but subsequently biases mesoderm toward endothelial specification, thereby emerging as a tractable redox modification for engineering stem cell fate and vascularization.

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The interactomes of RUNX1 and RUNX3 from Mus musculus T cells

Project description:Cellular binary fate decisions require the progeny to silence genes associated with the alternative fate. The major subsets of alpha:beta T cells have been extensively studied as a model system for fate decisions. While the transcription factor RUNX3 is required for the initiation of Cd4 silencing in CD8 T cell progenitors, it is not required to maintain the silencing of Cd4 and other helper T lineage genes. The other runt domain containing protein, RUNX1, silences Cd4 in an earlier T cell progenitor, but this silencing is reversed whereas the gene silencing after RUNX3 expression is not reverse. Therefore, we hypothesized that RUNX3 and not RUNX1 recruits other factors that maintains the silencing of helper T lineage genes in CD8 T cells. To this end, we performed a proteomics screen of RUNX1 and RUNX3 to determine candidate silencing factors.

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