ArticleDevelopmental biology2014
Geminin loss causes neural tube defects through disrupted progenitor specification and neuronal differentiation.
Article in Developmental biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Optical coherence tomography-guided Brillouin microscopy highlights regional tissue stiffness differences during anterior neural tube closure in the Mthfd1l murine mutant.Development (Cambridge, England) · 2024Article
- Distinct H3K27me3 and H3K27ac Modifications in Neural Tube Defects Induced by Benzo[a]pyrene.Brain sciences · 2023Article
- Intrinsic neural stem cell properties define brain hypersensitivity to genotoxic stress.Stem cell reports · 2022Article
- Geminin is required for Hox gene regulation to pattern the developing limb.Developmental biology · 2020Article
- Reduced H3K27me3 leads to abnormal Hox gene expression in neural tube defects.Epigenetics & chromatin · 2019Article
- Controlling centriole numbers: Geminin family members as master regulators of centriole amplification and multiciliogenesis.Chromosoma · 2018Review
- High Glucose Inhibits Neural Stem Cell Differentiation Through Oxidative Stress and Endoplasmic Reticulum Stress.Stem cells and development · 2018Article
- Geminin deletion in pre-meiotic DNA replication stage causes spermatogenesis defect and infertility.The Journal of reproduction and development · 2017Article
- Geminin deficiency enhances survival in a murine medulloblastoma model by inducing apoptosis of preneoplastic granule neuron precursors.Genes & cancer · 2017Article
- Geminin facilitates FoxO3 deacetylation to promote breast cancer cell metastasis.The Journal of clinical investigation · 2017Article
- Foxd4 is essential for establishing neural cell fate and for neuronal differentiation.Genesis (New York, N.Y. : 2000) · 2017Article
- Lacking of palladin leads to multiple cellular events changes which contribute to NTD.Neural development · 2017Article
- Geminin Is Essential for Pluripotent Cell Viability During Teratoma Formation, but Not for Differentiated Cell Viability During Teratoma Expansion.Stem cells and development · 2017Article
- Review
- Gene regulatory networks in neural cell fate acquisition from genome-wide chromatin association of Geminin and Zic1.Scientific reports · 2016Article
- Genome Duplication: The Heartbeat of Developing Organisms.Current topics in developmental biology · 2016Review
- High proliferation index, as determined by immunohistochemical expression of Aurora kinase B and geminin, indicates poor prognosis in neuroblastomas.Virchows Archiv : an international journal of pathology · 2015Article
- DNA Replication Inhibitor Geminin and Retinoic Acid Signaling Participate in Complex Interactions Associated With Pluripotency.Cancer genomics & proteomicsArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Geminin is a nucleoprotein that can directly bind chromatin regulatory complexes to modulate gene expression during development. Geminin knockout mouse embryos are preimplantation lethal by the 32-cell stage, precluding in vivo study of Geminin's role in neural development. Therefore, here we used a conditional Geminin allele in combination with several Cre-driver lines to define an essential role for Geminin during mammalian neural tube (NT) formation and patterning. Geminin was required in the NT within a critical developmental time window (embryonic day 8.5-10.5), when NT patterning and closure occurs. Geminin excision at these stages resulted in strongly diminished expression of genes that mark and promote dorsal NT identities and decreased differentiation of ventral motor neurons, resulting in completely penetrant NT defects, while excision after embryonic day 10.5 did not result in NT defects. When Geminin was deleted specifically in the spinal NT, both NT defects and axial skeleton defects were observed, but neither defect occurred when Geminin was excised in paraxial mesenchyme, indicating a tissue autonomous requirement for Geminin in developing neuroectoderm. Despite a potential role for Geminin in cell cycle control, we found no evidence of proliferation defects or altered apoptosis. Comparisons of gene expression in the NT of Geminin mutant versus wild-type siblings at embryonic day 10.5 revealed decreased expression of key regulators of neurogenesis, including neurogenic bHLH transcription factors and dorsal interneuron progenitor markers. Together, these data demonstrate a requirement for Geminin for NT patterning and neuronal differentiation during mammalian neurulation in vivo.
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Registered trials
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