ArticleNature communications2016
Lack of Diaph3 relaxes the spindle checkpoint causing the loss of neural progenitors.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 37 citations in OpenAlex.
- Loss of DIAPH3 accelerates glioma genesis in mice.Cell death & disease · 2026Article
- Loss of function variants in HPDL impair human cortical development via alterations of mitochondrial function.Cell death & disease · 2026Article
- Identification of a Novel Likely Pathogenic Variant of DIAPH3 Associated With New Phenotype of Sensorineural Hearing Loss.Molecular genetics & genomic medicine · 2026Article
- Thyroid hormone promotes fetal neurogenesis.JCI insight · 2025Article
- Review
- Identification of novel genomic loci for anxiety symptoms and extensive genetic overlap with psychiatric disorders.Psychiatry and clinical neurosciences · 2024Article
- Stub1 promotes degradation of the activated Diaph3: A negative feedback regulatory mechanism of the actin nucleator.The Journal of biological chemistry · 2024Article
- INF2 formin variants linked to human inherited kidney disease reprogram the transcriptome, causing mitotic chaos and cell death.Cellular and molecular life sciences : CMLS · 2024Article
- Parasympathetic neurons derived from human pluripotent stem cells model human diseases and development.Cell stem cell · 2024Article
- Identification of Novel Genomic Loci for Anxiety and Extensive Genetic Overlap with Psychiatric Disorders.medRxiv : the preprint server for health sciences · 2024Article
- DIAPH3 predicts survival of patients withFrontiers in oncology · 2024Article
- mDia formins form hetero-oligomers and cooperatively maintain murine hematopoiesis.PLoS genetics · 2023Article
- Investigating Mammalian Formins with SMIFH2 Fifteen Years in: Novel Targets and Unexpected Biology.International journal of molecular sciences · 2023Review
- Executable Network Models of Integrated Multiomics Data.Journal of proteome research · 2023Article
- Short-Term Effects of Human versus Bovine Sialylated Milk Oligosaccharide Microinjection on Zebrafish Larvae Survival, Locomotor Behavior and Gene Expression.International journal of molecular sciences · 2023Article
- Review
- Article
- Formins in Human Disease.Cells · 2021Review
- DIAPH3 deficiency links microtubules to mitotic errors, defective neurogenesis, and brain dysfunction.eLife · 2021Article
- Primary Cilia and Centrosomes in Neocortex Development.Frontiers in neuroscience · 2021Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The diaphanous homologue Diaph3 (aka mDia2) is a major regulator of actin cytoskeleton. Loss of Diaph3 has been constantly associated with cytokinesis failure ascribed to impaired accumulation of actin in the cleavage furrow. Here we report that Diaph3 is required before cell fission, to ensure the accurate segregation of chromosomes. Inactivation of the Diaph3 gene causes a massive loss of cortical progenitor cells, with subsequent depletion of intermediate progenitors and neurons, and results in microcephaly. In embryonic brain extracts, Diaph3 co-immunoprecipitates with BubR1, a key regulator of the spindle assembly checkpoint (SAC). Diaph3-deficient cortical progenitors have decreased levels of BubR1 and fail to properly activate the SAC. Hence, they bypass mitotic arrest and embark on anaphase in spite of incorrect chromosome segregation, generating aneuploidy. Our data identify Diaph3 as a major guard of cortical progenitors, unravel novel functions of Diaphanous formins and add insights into the pathobiology of microcephaly.
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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.