QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

This Article Figures Only Full Text Full Text (PDF) DEV14536 Movies Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Roman, B. L. Articles by Weinstein, B. M. Search for Related Content PubMed PubMed Citation Articles by Roman, B. L. Articles by Weinstein, B. M. Social Bookmarking                         What's this?

Disruption of acvrl1 increases endothelial cell number in zebrafish cranial vessels

Beth L. Roman¹, Van N. Pham¹, Nathan D. Lawson¹, Magdalena Kulik^2,*, Sarah Childs^3,, Arne C. Lekven^4,, Deborah M. Garrity³, Randall T. Moon⁴, Mark C. Fishman³, Robert J. Lechleider^2,* and Brant M. Weinstein^1,

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
Present address: Department of Biochemistry and Molecular Biology, University of Calgary, Calgary, AB T2N 4N1, Canada
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.

Movies available on-line

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

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				S. Lamouille, C. Mallet, J.-J. Feige, and S. Bailly Activin receptor-like kinase 1 is implicated in the maturation phase of angiogenesis Blood, December 15, 2002; 100(13): 4495 - 4501. [Abstract] [Full Text] [PDF]