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MRNA sequencing of the global effect of SET1A on gene expression in mouse ES cells

ABSTRACT: Gene expression profiling reveals that SET1A regulates gene expression, metabolism and development programs in mouse ES Cells

ORGANISM(S): Mus musculus

PROVIDER: GSE66066 | GEO | 2016/02/18

SECONDARY ACCESSION(S): PRJNA275807

REPOSITORIES: GEO

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mRNA sequencing of the global effect of SET1A on gene expression in mouse ES cells

Project description:Gene expression profiling reveals that SET1A regulates gene expression, metabolism and development programs in mouse ES Cells To analyze the global effect of SET1A on gene expression in ES cells, we compared the gene expression profiles in CGR8 cells treated with control and Set1A siRNA by RNA-seq.

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Histone H3K4 methylation-dependent and independent functions of Set1A/COMPASS in embryonic stem cell self-renewal and differentiation

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A Synthetic Lethality Screen Reveals ING5 as a Genetic Dependency of Catalytically Dead Set1A/COMPASS in Mouse Embryonic Stem Cells

Project description:Embryonic stem cells (ESCs) are defined by their ability to self-renew and the potential to differentiate into all tissues of the developing organism. We previously demonstrated that deleting the catalytic SET domain of the Set1A/COMPASS histone methyltransferase in mouse ESCs does not impair their viability or ability to self-renew, however, leads to defects in differentiation. The precise mechanisms by which Set1A executes these functions remain to be elucidated. In this study, we demonstrate that mice lacking the SET domain of Set1A are embryonic lethal at a stage that is unique from null alleles. To gain insight into Set1A function in regulating pluripotency, we conducted a CRISPR/Cas9-mediated dropout screen and identified the MOZ/MORF and HBO1 acetyltransferase complex member ING5 as a synthetic perturbation to Set1A. The loss of Ing5 in Set1AΔSET mESCs decreases the fitness of these cells; and the simultaneous loss of ING5 and in Set1AΔSET leads to upregulation of differentiation-associated genes. Taken together, our results point towards Set1A and ING5 as potential co-regulators of the self-renewal and differentiation status of ESCs.

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