ArticleNature communications2016
Severe NDE1-mediated microcephaly results from neural progenitor cell cycle arrests at multiple specific stages.
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 43 papers.
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Who cites it
43 citing papers in PubMed, 71 citations in OpenAlex.
- Primary cilium disassembly - from mechanisms to roles in physiology and disease.Journal of cell science · 2026Review
- Non-transport functions of motor proteins in corticogenesis.Frontiers in cell and developmental biology · 2026Review
- Cell division during Xenopus gastrulation influences neuroectoderm patterning.Frontiers in cell and developmental biology · 2026Article
- Bi-allelic deleterious variants in SNAPIN, which encodes a retrograde dynein adaptor, cause a prenatal-onset neurodevelopmental disorder.American journal of human genetics · 2025Article
- Rest Induces a Distinct Transcriptional Program in the Nervous System of the ExercisedInternational journal of molecular sciences · 2025Article
- Genetic variants underlying congenital Zika syndrome and severe microcephaly: a systematic review and meta-analysis.Virusdisease · 2025Article
- Congenital Oropouche in Humans: Clinical Characterization of a Possible New Teratogenic Syndrome.Viruses · 2025Article
- The Role of Nde1 phosphorylation in interkinetic nuclear migration and neural migration during cortical development.Molecular biology of the cell · 2024Article
- Astrocytes control quiescent NSC reactivation via GPCR signaling-mediated F-actin remodeling.Science advances · 2024Article
- Novel lissencephaly-associated NDEL1 variant reveals distinct roles of NDE1 and NDEL1 in nucleokinesis and human cortical malformations.Acta neuropathologica · 2024Article
- oFlowSeq: a quantitative approach to identify protein coding mutations affecting cell type enrichment using mosaic CRISPR-Cas9 edited cerebral organoids.Human genetics · 2023Article
- MeCP2 dysfunction prevents proper BMP signaling and neural progenitor expansion in brain organoid.Annals of clinical and translational neurology · 2023Article
- BICD2 phosphorylation regulates dynein function and centrosome separation in G2 and M.Nature communications · 2023Article
- Gcap14 is a microtubule plus-end-tracking protein coordinating microtubule-actin crosstalk during neurodevelopment.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Cerebral organoids containing an AUTS2 missense variant model microcephaly.Brain : a journal of neurology · 2023Article
- Deficiency ofiScience · 2022Article
- Nde1 and Ndel1: Outstanding Mysteries in Dynein-Mediated Transport.Frontiers in cell and developmental biology · 2022Review
- FBW7 couples structural integrity with functional output of primary cilia.Communications biology · 2021Article
- Hedgehog signaling and the primary cilium: implications for spatial and temporal constraints on signaling.Development (Cambridge, England) · 2021Review
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Microcephaly is a cortical malformation disorder characterized by an abnormally small brain. Recent studies have revealed severe cases of microcephaly resulting from human mutations in the NDE1 gene, which is involved in the regulation of cytoplasmic dynein. Here using in utero electroporation of NDE1 short hairpin RNA (shRNA) in embryonic rat brains, we observe cell cycle arrest of proliferating neural progenitors at three distinct stages: during apical interkinetic nuclear migration, at the G2-to-M transition and in regulation of primary cilia at the G1-to-S transition. RNAi against the NDE1 paralogue NDEL1 has no such effects. However, NDEL1 overexpression can functionally compensate for NDE1, except at the G2-to-M transition, revealing a unique NDE1 role. In contrast, NDE1 and NDEL1 RNAi have comparable effects on postmitotic neuronal migration. These results reveal that the severity of NDE1-associated microcephaly results not from defects in mitosis, but rather the inability of neural progenitors to ever reach this stage.
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