Disruption ofacvrl1increases endothelial cell number in zebrafish cranial vessels-Reference-Cited by-同舟云学术

Disruption ofacvrl1increases endothelial cell number in zebrafish cranial vessels

Published:2002-06-15 Issue:12 Volume:129 Page:3009-3019
ISSN:1477-9129
Container-title:Development
language:en
Short-container-title:

Author:

Roman Beth L.¹,Pham Van N.¹,Lawson Nathan D.¹,Kulik Magdalena²³,Childs Sarah⁴⁵,Lekven Arne C.⁶⁷,Garrity Deborah M.⁴,Moon Randall T.⁶,Fishman Mark C.⁴,Lechleider Robert J.²³,Weinstein Brant M.¹

Affiliation:

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. Present address: Department of Cell Biology, Georgetown University Medical School, Washington, DC 20007, USA

4. Cardiovascular Research Center, Massachusetts General Hospital East, Charlestown, MA 02129, USA

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

6. Howard Hughes Medical Institute and Department of Pharmacology, University of Washington School of Medicine, Seattle, WA 98185 USA

7. Present address: Biology Department, Texas A&M University, College Station, TX 77843, USA

Abstract

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 TGFβ 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

Publisher

The Company of Biologists

Subject

Developmental Biology,Molecular Biology

Link

http://journals.biologists.com/dev/article-pdf/129/12/3009/1205432/3009.pdf

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