ArticleCell death and differentiation2012
Ablation of Dido3 compromises lineage commitment of stem cells in vitro and during early embryonic development.
Article in Cell death and differentiation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- The scramblases VMP1 and TMEM41B are required for primitive endoderm specification by targeting WNT signaling.Cell death and differentiation · 2025Article
- The chromatin reader Dido3 is a regulator of the gene network that controls B cell differentiation.Cell & bioscience · 2025Article
- DIDO is necessary for the adipogenesis that promotes diet-induced obesity.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The SPOC proteins DIDO3 and PHF3 co-regulate gene expression and neuronal differentiation.Nature communications · 2023Article
- SPOC domain proteins in health and disease.Genes & development · 2023Review
- The SPOC domain is a phosphoserine binding module that bridges transcription machinery with co- and post-transcriptional regulators.Nature communications · 2023Article
- Hepatitis, testicular degeneration, and ataxia in DIDO3-deficient mice with altered mRNA processing.Cell & bioscience · 2022Article
- Phosphorylation of H3-Thr3 by Haspin Is Required for Primary Cilia Regulation.International journal of molecular sciences · 2021Article
- Impaired stem cell differentiation and somatic cell reprogramming in DIDO3 mutants with altered RNA processing and increased R-loop levels.Cell death & disease · 2021Article
- Role of DIDO1 in Progression of Esophageal Squamous Cell Carcinoma.Journal of gastrointestinal cancer · 2020Article
- Dido3-dependent SFPQ recruitment maintains efficiency in mammalian alternative splicing.Nucleic acids research · 2019Article
- Whole‑exome sequencing analysis of products of conception identifies novel mutations associated with missed abortion.Molecular medicine reports · 2018Article
- Molecular structures guide the engineering of chromatin.Nucleic acids research · 2017Article
- DIDO as a Switchboard that Regulates Self-Renewal and Differentiation in Embryonic Stem Cells.Stem cell reports · 2017Article
- Dido mutations trigger perinatal death and generate brain abnormalities and behavioral alterations in surviving adult mice.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Dido3-dependent HDAC6 targeting controls cilium size.Nature communications · 2014Article
- The death-inducer obliterator 1 (Dido1) gene regulates embryonic stem cell self-renewal.The Journal of biological chemistry · 2014Article
- Dido3 PHD modulates cell differentiation and division.Cell reports · 2013Article
- Transcriptional dissection of human limbal niche compartments by massive parallel sequencing.PloS one · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
The death inducer obliterator (Dido) locus encodes three protein isoforms, of which Dido3 is the largest and most broadly expressed. Dido3 is a nuclear protein that forms part of the spindle assembly checkpoint (SAC) and is necessary for correct chromosome segregation in somatic and germ cells. Here we report that specific ablation of Dido3 function in mice causes lethal developmental defects at the onset of gastrulation. Although these defects are associated with centrosome amplification, spindle malformation and a DNA damage response, we provide evidence that embryonic lethality of the Dido3 mutation cannot be explained by its impact on chromosome segregation alone. We show that loss of Dido3 expression compromises differentiation of embryonic stem cells in vitro and of epiblast cells in vivo, resulting in early embryonic death at around day 8.5 of gestation. Close analysis of Dido3 mutant embryoid bodies indicates that ablation of Dido3, rather than producing a generalized differentiation blockade, delays the onset of lineage commitment at the primitive endoderm specification stage. The dual role of Dido3 in chromosome segregation and stem cell differentiation supports the implication of SAC components in stem cell fate decisions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.