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- W2903766360 abstract "Abstract During development, it is unclear if lineage-fated cells derive from multilineage-primed progenitors and whether active mechanisms operate to restrict cell fate. Here we investigate how mesoderm specifies into blood-fated cells. We document temporally restricted co-expression of blood ( Scl/Tal1 ), cardiac ( Mesp1 ) and paraxial ( Tbx6 ) lineage-affiliated transcription factors in single cells, at the onset of blood specification, supporting the existence of common progenitors. At the same time-restricted stage, absence of SCL results in expansion of cardiac/paraxial cell populations and increased cardiac/paraxial gene expression, suggesting active suppression of alternative fates. Indeed, SCL normally activates expression of co-repressor ETO2 and Polycomb-PRC1 subunits (RYBP, PCGF5) and maintains levels of Polycomb-associated histone marks (H2AK119ub/H3K27me3). Genome-wide analyses reveal ETO2 and RYBP co-occupy most SCL target genes, including cardiac/paraxial loci. Reduction of Eto2 or Rybp expression mimics Scl -null cardiac phenotype. Therefore, SCL-mediated transcriptional repression prevents mis-specification of blood-fated cells, establishing active repression as central to fate determination processes." @default.
- W2903766360 created "2018-12-22" @default.
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- W2903766360 date "2018-12-18" @default.
- W2903766360 modified "2023-10-11" @default.
- W2903766360 title "SCL/TAL1 cooperates with Polycomb RYBP-PRC1 to suppress alternative lineages in blood-fated cells" @default.
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- W2903766360 doi "https://doi.org/10.1038/s41467-018-07787-6" @default.
- W2903766360 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6299140" @default.
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- W2903766360 hasPublicationYear "2018" @default.
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