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Molecular and Cellular Biology, December 2000, p. 9331-9336, Vol. 20, No. 24
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Mice Null for Sox18 Are Viable and Display a Mild Coat Defect

David Pennisi,1,dagger Josephine Bowles,1 Andras Nagy,2 George Muscat,1 and Peter Koopman1,*

Institute for Molecular Bioscience, University of Queensland, Brisbane 4072, Australia,1 and Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Canada M5G 1X52

Received 21 June 2000/Returned for modification 21 August 2000/Accepted 11 September 2000

We have previously shown that Sox18 is expressed in developing vascular endothelium and hair follicles during mouse embryogenesis and that point mutations in Sox18 are the underlying cause of cardiovascular and hair follicle defects in ragged (Ra) mice. Here we describe the analysis of Sox18-/- mice produced by gene targeting. Despite the profound defects seen in Ra mice, Sox18-/- mice have no obvious cardiovascular defects and only a mild coat defect with a reduced proportion of zigzag hairs. A reduction in the amount of pheomelanin pigmentation in hair shafts was also observed; later-forming hair follicles showed a reduced subapical pheomelanin band, giving Sox18-/- mice a slightly darker appearance than Sox18+/+ and Sox18+/- siblings. Sox18-/- mice are viable and fertile and show no difference in the ability to thrive relative to littermates. Because of the mild effect of the mutation on the phenotype of Sox18-/- mice, we conclude that the semidominant nature of the Ra mutations is due to a trans-dominant negative effect mediated by the mutant SOX18 proteins rather than haploinsufficiency as has been observed for other SOX genes. Due to the similarity of SOX18 to other subgroup F SOX proteins, SOX7 and -17, and the overlap in expression of these genes, functional redundancy amongst these SOX proteins could also account for the mild phenotype of Sox18-/- mice.

* Corresponding author. Mailing address: Institute for Molecular Bioscience, University of Queensland, Brisbane 4072, Australia. Phone: 61 7 3365 4491. Fax: 61 7 3365 4388. E-mail: p.koopman{at}cmcb.uq.edu.au.

dagger Present address: Department of Cell Biology and Anatomy, Cornell University Weill Medical College, New York, NY 10021.

Molecular and Cellular Biology, December 2000, p. 9331-9336, Vol. 20, No. 24
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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