Phenotypes associated with this allele
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Slit3tm1.1Dor mutation
(1 available);
any
Slit3 mutation
(80 available)
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cardiovascular system
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• vascularization in diaphragmatic tendon is impaired, especially in the anterior tendon regions
• diaphragmatic tendon vessels show diverse diameters and sprout discontinuity and vascular plexus density are reduced
• vascular density and sprouting in diaphragmatic muscle is reduced
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muscle
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• vascular density and sprouting in diaphragmatic muscle is reduced
• microvessels in the diaphragm are dilated and disorganized some vessels terminate with large, distended heads with fewer extending filopodia rather than sprouting and communicating with neighboring vessels
• tip endothelial cells are reduced by 89% in diaphragms
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• vascularization in diaphragmatic tendon is impaired, especially in the anterior tendon regions
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• 86% of mice exhibit central tendon congenital diaphragmatic hernia
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skeleton
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• vascularization in diaphragmatic tendon is impaired, especially in the anterior tendon regions
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Slit3tm1.1Dor mutation
(1 available);
any
Slit3 mutation
(80 available)
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mortality/aging
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• phenotype is stated to be identical to that of Slit3tm1Dor homozygotes; however, no data are presented in J:83292
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growth/size/body
muscle
liver/biliary system
digestive/alimentary system
respiratory system
cardiovascular system
muscle
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• 100% of mice develop central tendon congenital diaphragmatic hernia compared to 57% of conditional Ndst1 homozygotes and 86% of Slit3 homozygotes
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muscle
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• mice develop central tendon congenital diaphragmatic hernia with the same penetrance as seen in single Ndst1 conditional homozygotes
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nervous system
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• at E12.5 commissural axons occasionally recross the floor plate, this is never seen in controls
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• the ventral commissure (bundle of nerve fibers passing from one side to the other in the spinal cord) appears thicker compared to controls
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• the ventral funiculus (white matter tract) appears reduced in mutants compared to controls
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cellular
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• at E12.5 commissural axons occasionally recross the floor plate, this is never seen in controls
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cellular
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• in mammary gland ducts formed by transplanted mammary anlage
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endocrine/exocrine glands
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• in mammary gland ducts formed by transplanted mammary anlage
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• mammary gland ducts formed by transplanted mammary anlage display hyperplasticity and organization defects, including mild to severe defects in ductal lumens and disrupted growth control, 100% penetrant phenotype
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integument
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• in mammary gland ducts formed by transplanted mammary anlage
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• mammary gland ducts formed by transplanted mammary anlage display hyperplasticity and organization defects, including mild to severe defects in ductal lumens and disrupted growth control, 100% penetrant phenotype
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nervous system
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• at E12.5 commissural axons appear disorganized as they exit the floor plate lacking the typical bundled morphology
• at E12.5 more commissural axons stall and fail to exit the floor plate (78% versus 28% in controls) or recross the floor plate (~20% versus 0% in controls; controls in this study were Slit1tm1.1Matl homozygotes)
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• the lateral funiculus (white matter tract) is significantly thinner in triple homozygous mutants compared to controls
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cellular
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• at E12.5 commissural axons appear disorganized as they exit the floor plate lacking the typical bundled morphology
• at E12.5 more commissural axons stall and fail to exit the floor plate (78% versus 28% in controls) or recross the floor plate (~20% versus 0% in controls; controls in this study were Slit1tm1.1Matl homozygotes)
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