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Dido as a switchboard that regulates self-renewal and differentiation in embryonic stem cells (Affy)

ABSTRACT: Transition from symmetric to asymmetric cell division requires precise coordination of differential gene expression. Embryonic stem cells (ESC) strongly express Dido3, whose C-terminal truncation impedes ESC differentiation while retaining self-renewal. We show that Dido3 binds to its gene locus via H3K4me3 and RNA pol II and, at differentiation onset, induces expression of its splice variant Dido1, which then leads to Dido3 degradation and downregulation of stemness genes. We propose that Dido isoforms act as a switchboard to regulate genetic programs for ESC transition from pluripotency maintenance to promotion of differentiation. We used microarrays to determine how the deletion of exon 16 (C-terminal truncation) of the Dido3 affects gene expression that results in the suppression of ESC differentiation.

ORGANISM(S): Mus musculus

PROVIDER: GSE85006 | GEO | 2017/03/16

SECONDARY ACCESSION(S): PRJNA335984

REPOSITORIES: GEO

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Dido as a switchboard that regulates self-renewal and differentiation in embryonic stem cells (vsmutCT)

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The SPOC proteins DIDO3 and PHF3 co-regulate gene expression and neuronal differentiation - RNAseq

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Project description:Embryonic stem cell (ESC) differentiation and somatic cell reprogramming are biological processes governed by antagonistic expression or repression of a largely common set of genes. Accurate regulation of gene expression is thus essential for both processes, and alterations in RNA processing are predicted to negatively affect both. We show that truncation of the DIDO gene alters RNA splicing and transcription termination in ESC and mouse embryo fibroblasts (MEF), which affects genes involved in both differentiation and reprogramming. We combined transcriptomic, protein interaction, and cellular studies to identify the underlying molecular mechanism. We found that DIDO3 interacts with the helicase DHX9, which is involved in R-loop processing and transcription termination, and that DIDO3-exon16 deletion increases nuclear R-loop content and causes DNA replication stress. Overall, these defects result in failure of ESC to differentiate and of MEF to be reprogrammed. MEF immortalization restored impaired reprogramming capacity. We conclude that DIDO3 has essential functions in ESC differentiation and somatic cell reprogramming by supporting accurate RNA metabolism, with its exon16-encoded domain playing the main role.

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Dido as a switchboard that regulates self-renewal and differentiation in embryonic stem cells

Project description:Dido as a switchboard that regulates self-renewal and differentiation in embryonic stem cells

| PRJNA335995 | ENA

DIDO is necessary for adipogenesis promoting diet-induced obesity [I]

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