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Mice null for sox18 are viable and display a mild coat defect
1Institute for Molecular Bioscience, University of Queensland, Brisbane 4072, Australia.
Molecular and Cellular Biology
|November 30, 2000
Summary
Sox18 knockout mice show mild coat defects, unlike their ragged counterparts. This suggests the ragged mutation
Area of Science:
- Developmental Biology
- Genetics
- Molecular Biology
Background:
- Sox18 is crucial for vascular endothelium and hair follicle development in mice.
- Mutations in Sox18 cause cardiovascular and hair follicle defects in ragged (Ra) mice.
Purpose of the Study:
- To analyze the phenotype of Sox18 knockout mice (Sox18(-/-)).
- To investigate the mechanism behind the semidominant nature of Ra mutations.
Main Methods:
- Gene targeting to produce Sox18(-/-) mice.
- Phenotypic analysis of Sox18(-/-) mice, including cardiovascular and coat characteristics.
Main Results:
- Sox18(-/-) mice exhibit mild coat defects, not severe cardiovascular issues seen in Ra mice.
- Reduced zigzag hairs and altered pheomelanin pigmentation were observed.
- Sox18(-/-) mice are viable, fertile, and show no growth impairment.
Conclusions:
- The semidominant Ra phenotype is likely due to a trans-dominant negative effect of mutant SOX18 proteins.
- Functional redundancy with SOX7 and SOX17 may explain the mild phenotype in Sox18(-/-) mice.