PUBLICATION
Retinoic acid-metabolizing enzyme Cyp26a1 is essential for determining territories of hindbrain and spinal cord in zebrafish
- Authors
- Emoto, Y., Wada, H., Okamoto, H., Kudo, A., and Imai, Y.
- ID
- ZDB-PUB-050202-3
- Date
- 2005
- Source
- Developmental Biology 278(2): 415-427 (Journal)
- Registered Authors
- Imai, Yoshiyuki, Okamoto, Hitoshi, Wada, Hironori
- Keywords
- giraffe; neckless; cyp26a1; raldh2; hox; Retinoic acid; Common cardinal vein; Hindbrain; Spinal cord; Zebrafish
- MeSH Terms
-
- Animals
- Base Sequence
- Body Patterning/genetics
- Chromosome Mapping
- Cytochrome P-450 Enzyme System/metabolism*
- DNA Primers
- In Situ Hybridization
- Morphogenesis
- Mutation
- Phenotype
- Rhombencephalon/embryology*
- Rhombencephalon/enzymology
- Spinal Cord/embryology*
- Spinal Cord/enzymology
- Tretinoin/metabolism*
- Zebrafish/embryology
- Zebrafish/genetics
- PubMed
- 15680360 Full text @ Dev. Biol.
Citation
Emoto, Y., Wada, H., Okamoto, H., Kudo, A., and Imai, Y. (2005) Retinoic acid-metabolizing enzyme Cyp26a1 is essential for determining territories of hindbrain and spinal cord in zebrafish. Developmental Biology. 278(2):415-427.
Abstract
Retinoic acid (RA) plays a critical role in neural patterning and organogenesis in the vertebrate embryo. Here we characterize a mutant of the zebrafish named giraffe (gir) in which the gene for the RA-degrading enzyme Cyp26a1 is mutated. The gir mutant displayed patterning defects in multiple organs including the common cardinal vein, pectoral fin, tail, hindbrain, and spinal cord. Analyses of molecular markers suggested that the lateral plate mesoderm is posteriorized in the gir mutant, which is likely to cause the defects of the common cardinal vein and pectoral fin. The cyp26a1 expression in the rostral spinal cord was strongly upregulated in the gir mutant, suggesting a strong feedback control of its expression by RA signaling. We also found that the rostral spinal cord territory was expanded at the expense of the hindbrain territory in the gir mutant. Such a phenotype is the opposite of that of the mutant for Raldh2, an enzyme that synthesizes RA. We propose a model in which Cyp26a1 attenuates RA signaling in the prospective rostral spinal cord to limit the expression of hox genes and to determine the hindbrain-spinal cord boundary.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping