PUBLICATION
Vertebrate MAX-1 is required for vascular patterning in zebrafish
- Authors
- Zhong, H., Wu, X., Huang, H., Fan, Q., Zhu, Z., and Lin, S.
- ID
- ZDB-PUB-061031-13
- Date
- 2006
- Source
- Proceedings of the National Academy of Sciences of the United States of America 103(45): 16800-16805 (Journal)
- Registered Authors
- Huang, Haigen, Lin, Shuo, Zhong, Hanbing
- Keywords
- ephrin
- MeSH Terms
-
- Animals
- Animals, Genetically Modified
- Base Sequence
- Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/genetics*
- Blood Vessels/embryology*
- Caenorhabditis elegans/embryology
- Caenorhabditis elegans/genetics
- Ephrin-B3/genetics
- Gene Expression Regulation, Developmental
- Gene Targeting
- In Situ Hybridization
- Molecular Sequence Data
- Oligoribonucleotides, Antisense/genetics
- RNA, Messenger/genetics
- Zebrafish/embryology*
- Zebrafish/genetics*
- Zebrafish Proteins/genetics*
- PubMed
- 17065323 Full text @ Proc. Natl. Acad. Sci. USA
Citation
Zhong, H., Wu, X., Huang, H., Fan, Q., Zhu, Z., and Lin, S. (2006) Vertebrate MAX-1 is required for vascular patterning in zebrafish. Proceedings of the National Academy of Sciences of the United States of America. 103(45):16800-16805.
Abstract
During embryogenesis, stereotypic vascular patterning requires guidance cues from neighboring tissues. However, key molecules involved in this process still remain largely elusive. Here, we report molecular cloning, expression, and functional studies of zebrafish max-1, a homolog of Caenorhabditis elegans max-1 that has been implicated in motor neuron axon guidance. During early embryonic development, zebrafish max-1 is specifically expressed in subsets of neuronal tissues, epithelial cells, and developing somites through which vascular endothelial cells migrate from large ventral axial vessels to form stereotypic intersegmental blood vessels (ISV). Blocking zebrafish max-1 mRNA splicing by morpholino injection led to aberrant ISV patterning, which could be rescued by injection of either C. elegans or zebrafish max-1 mRNA. Analysis of motor neurons in the same region showed normal neuronal axon pathfinding. Further studies suggested that the ISV defect caused by max-1 knockdown could be partially rescued by overexpression of ephrinb3 and that max-1 was involved in mediating membrane localization of ephrin proteins, which have been shown to provide guidance cues for endothelial cell migration. Our findings therefore suggest that max-1, acting upstream of the ephrin pathway, is critically required in vascular patterning in vertebrate species.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping