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Development 129, 3009-3019 (2002)
© 2002 The Company of Biologists Limited

DEVELOPMENT AND DISEASE

Disruption of acvrl1 increases endothelial cell number in zebrafish cranial vessels

Beth L. Roman1, Van N. Pham1, Nathan D. Lawson1, Magdalena Kulik2,*, Sarah Childs3,{dagger}, Arne C. Lekven4,{ddagger}, Deborah M. Garrity3, Randall T. Moon4, Mark C. Fishman3, Robert J. Lechleider2,* and Brant M. Weinstein1,§

1 Laboratory of Molecular Genetics, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA
2 Department of Pharmacology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA
3 Cardiovascular Research Center, Massachusetts General Hospital East, Charlestown, MA 02129, USA
4 Howard Hughes Medical Institute and Department of Pharmacology, University of Washington School of Medicine, Seattle, WA 98185 USA
* Present address: Department of Cell Biology, Georgetown University Medical School, Washington, DC 20007, USA
{dagger} Present address: Department of Biochemistry and Molecular Biology, University of Calgary, Calgary, AB T2N 4N1, Canada
{ddagger} Present address: Biology Department, Texas A&M University, College Station, TX 77843, USA

§Author for correspondence (e-mail: flyingfish{at}nih.gov)

Accepted 1 April 2002

The zebrafish mutant violet beauregarde (vbg) can be identified at two days post-fertilization by an abnormal circulation pattern in which most blood cells flow through a limited number of dilated cranial vessels and fail to perfuse the trunk and tail. This phenotype cannot be explained by caudal vessel abnormalities or by a defect in cranial vessel patterning, but instead stems from an increase in endothelial cell number in specific cranial vessels. We show that vbg encodes activin receptor-like kinase 1 (Acvrl1; also known as Alk1), a TGFß type I receptor that is expressed predominantly in the endothelium of the vessels that become dilated in vbg mutants. Thus, vbg provides a model for the human autosomal dominant disorder, hereditary hemorrhagic telangiectasia type 2, in which disruption of ACVRL1 causes vessel malformations that may result in hemorrhage or stroke.

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Key words: Acvrl1, Hereditary hemorrhagic telangiectasia, Endothelium, Angiogenesis, Zebrafish, violet beauregarde




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© The Company of Biologists Ltd 2002