nervous system
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• in E14 and E17 embryos
• normal in E12 embryos
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Analysis Tools
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in E14 and E17 embryos
• normal in E12 embryos
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• starting in E9.5 embryos, worsening with age
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• starting in E9.5 embryos, worsening with age
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| N |
• normal outflow tract septation in E12 embryos
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• median lip notches in some E14-E15 embryos
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• in some E14-E15 embryos
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• in some E14-E15 embryos
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• in some E14-E15 embryos
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• median lip notches in some E14-E15 embryos
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• in some E14-E15 embryos
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• in some E14-E15 embryos
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in E12 embryos
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• in newborns, owing to blood pooling
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• in E12 embryos
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• shorter in E10 embryos
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• newborn hearts have only single ventricle
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• in newborns, owing to blood pooling
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in E12 embryos
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• in newborns, owing to blood pooling
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• in E12 embryos
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• shorter in E10 embryos
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• newborn hearts have only single ventricle
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• in newborns, owing to blood pooling
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in E12 embryos
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• in newborns, owing to blood pooling
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• in E12 embryos
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• shorter in E10 embryos
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• newborn hearts have only single ventricle
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• in newborns, owing to blood pooling
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in E11.5 embryos
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• in E12 embryos
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• in E12.5 embryos
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• diffuse vascular leakage in E11.5 embryos
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• in E11.5 embryos
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• starting in E9.5 embryos, worsening with age
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• in E11.5 embryos
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• starting in E9.5 embryos, worsening with age
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in E11.5 embryos
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• in E12 embryos
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• in E12.5 embryos
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• diffuse vascular leakage in E11.5 embryos
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• in E11.5 embryos
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• starting in E9.5 embryos, worsening with age
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• in E11.5 embryos
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• starting in E9.5 embryos, worsening with age
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in E11.5 embryos
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• in E12 embryos
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• in E12.5 embryos
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• diffuse vascular leakage in E11.5 embryos
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• in E11.5 embryos
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• starting in E9.5 embryos, worsening with age
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• in E11.5 embryos
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• starting in E9.5 embryos, worsening with age
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• normal outflow tract septation in E9.5 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• mandibular cleft in E14-E17 embryos
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• in E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• mandibular cleft in E14-E17 embryos
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• in E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• mandibular cleft in E14-E17 embryos
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• in E17 embryos
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• in E16 and E17 embryos
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• normal outflow tract septation in E9.5 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• mandibular cleft in E14-E17 embryos
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• in E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• mandibular cleft in E14-E17 embryos
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• in E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• mandibular cleft in E14-E17 embryos
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• in E17 embryos
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• in E16 and E17 embryos
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• at E12, brightfield images of embryos (tamoxifen-induced at E9.5) show craniofacial malformations
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• at E12.5, embryos (tamoxifen-injected at E9.5) exhibit craniofacial abnormalities
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• at E12.5, in situ hybridization for Sox9 (a master regulator of chondrogenesis) and Sox10 (a marker of developing peripheral nervous system) and immunostaining for SOX9 and TUJ1 (TUBB3A; neuron-specific class III beta-tubulin) indicate a decreased SOX9 signal in the mandibular region, consistent with reduced cartilage development
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• compositional analysis of single cell transcriptomics data from E12.5 embryos (tamoxifen-injected at E9.5) shows a significant reduction of several ectomesenchymal clusters, without affecting neuroglial progeny
• at E12.5, embryos (tamoxifen-injected at E9.5) exhibit reduced facial mesenchymal condensations and impaired cartilage development
• 3D visualizations based on microCT data indicate that while ectomesenchymal chondrogenic condensations are severely reduced at E12.5, trigeminal ganglia are not significantly affected, indicating that facial skeletogenesis is specifically disrupted due to reduced rRNA transcription and ribosome biogenesis
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• at E12.5, embryos (tamoxifen-injected at E9.5) exhibit a disrupted Meckels cartilage, presenting as two discrete non-contiguous proximal and distal elements rather than a continuous structure
• however, the branches of the neural crest-derived trigeminal ganglion are relatively less affected, and the mandibular nerve now traverses the gap between the non-contiguous Meckels cartilage elements
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• at E12.5, embryos (tamoxifen-injected at E9.5) exhibit reduced facial mesenchymal condensations
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• at E12.5, embryos (tamoxifen-injected at E9.5) exhibit reduced facial mesenchymal condensations
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• at E12.5, embryos (tamoxifen-injected at E9.5) exhibit a disrupted Meckels cartilage, presenting as two discrete non-contiguous proximal and distal elements rather than a continuous structure
• however, the branches of the neural crest-derived trigeminal ganglion are relatively less affected, and the mandibular nerve now traverses the gap between the non-contiguous Meckels cartilage elements
|
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• at E12.5, in situ hybridization for Sox9 (a master regulator of chondrogenesis) and Sox10 (a marker of developing peripheral nervous system) and immunostaining for SOX9 and TUJ1 (TUBB3A; neuron-specific class III beta-tubulin) indicate a decreased SOX9 signal in the mandibular region, consistent with reduced cartilage development
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• normal outflow tract septation in E9.5 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
|
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• mandibular cleft in E14-E17 embryos
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• in E17 embryos
|
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• in E16 and E17 embryos
|
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• in E16 and E17 embryos
|
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• in E16 and E17 embryos
|
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• in E16 and E17 embryos
|
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• in E16 and E17 embryos
|
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• mandibular cleft in E14-E17 embryos
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• in E17 embryos
|
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• in E16 and E17 embryos
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• in E16 and E17 embryos
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• in E16 and E17 embryos
|
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• in E16 and E17 embryos
|
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• in E16 and E17 embryos
|
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• in E16 and E17 embryos
|
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• mandibular cleft in E14-E17 embryos
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• in E17 embryos
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• in E16 and E17 embryos
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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 09/08/2026 MGI 6.24 |
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