Dido3 PHD modulates cell differentiation and division.

By J. Gatchalian, A. Fütterer, Scott B. Rothbart, Qiong Tong, Héctor Rincón-Arano, Ainhoa Sánchez de Diego, Mark Groudine, Brian D. Strahl, Carlos Martínez-A, K. V. van Wely and 1 more. 2013

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Death Inducer Obliterator 3 (Dido3) is implicated in the maintenance of stem cell genomic stability and tumorigenesis. Here, we show that Dido3 regulates the expression of stemness genes in embryonic stem cells through its plant homeodomain (PHD) finger. Binding of Dido3 PHD to histone H3K4me3 is disrupted by threonine phosphorylation that triggers Dido3 translocation from chromatin to the mitotic spindle. The crystal structure of Dido3 PHD in complex with H3K4me3 reveals an atypical aromatic-cage-like binding site that contains a histidine residue. Biochemical, structural, and mutational analyses of the binding mechanism identified the determinants of specificity and affinity and explained the inability of homologous PHF3 to bind H3K4me3. Together, our findings reveal a link between the transcriptional control in embryonic development and regulation of cell division.

Subfields: Molecular Biology, Plant Science

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Citations in the corpus

Dido3-dependent SFPQ recruitment maintains efficiency in mammalian alternative splicing (2019, background): “The lack of chromatin binding (24) implies that Dido3 is no longer enriched at the 5′ end of active genes in E3+4, but instead resides free in the nucleoplasm (35).”
Structures of RNA polymerase II complexes with Bye1, a chromatin-binding PHF3/DIDO homologue (2013, background): “Specific binding of the DIDO PHD domain to H3K4me3 has been reported recently (41).”
DIDO as a Switchboard that Regulates Self-Renewal and Differentiation in Embryonic Stem Cells (2017, methodology): “All array data are from three biological replicates. previous results, HA-DIDONT EBs recovered downregulation of stemness genes (Gatchalian et al., 2013) and expression of a subset of other genes; GO analysis indicated that these genes are involved in endoderm and mesoderm differentiation (Figures…”
A Unique pH-Dependent Recognition of Methylated Histone H3K4 by PPS and DIDO. (2017, background): “Mitotic chromatin acidification promotes DIDO dissociation We have previously shown that DIDO associates with chromatin in interphase through binding of its PHD finger to H3K4me3 but translocates to the cytosol in mitosis (Gatchalian et al., 2013).”
Interplay between splicing and transcriptional pausing exerts genome-wide control over alternative polyadenylation (2021, background): “DIDO is the vertebrate homolog to yeast BYE1 and insect PPS genes [20,21], and produces a family of transcription factors that bind to histone H3 trimethylated on lysine 4 [22,23].”