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

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. Overall design: Study of HADido3 DNA binding by chipseq technology in mouse embryonic stem cells Dido3deltaCT reconstituted with HADido3