PUBLICATION
Independent roles for retinoic acid in segmentation and neuronal differentiation in the zebrafish hindbrain
- Authors
- Linville, A., Gumusaneli, E., Chandraratna, R.A., and Schilling, T.F.
- ID
- ZDB-PUB-040514-9
- Date
- 2004
- Source
- Developmental Biology 270(1): 186-199 (Journal)
- Registered Authors
- Schilling, Tom
- Keywords
- Danio rerio, RAR, Islet-1, Rhombomere, Cranial nerve, Hox, Motor neuron
- MeSH Terms
-
- Aldehyde Oxidoreductases/genetics
- Aldehyde Oxidoreductases/metabolism
- Animals
- Body Patterning*
- Branchial Region/cytology
- Branchial Region/embryology
- Cell Differentiation/physiology*
- Cell Movement/physiology
- Neurons/cytology
- Neurons/physiology*
- Receptors, Retinoic Acid/antagonists & inhibitors
- Retinal Dehydrogenase
- Rhombencephalon/cytology
- Rhombencephalon/embryology*
- Rhombencephalon/metabolism
- Signal Transduction/physiology
- Tretinoin/metabolism*
- Zebrafish/anatomy & histology
- Zebrafish/embryology*
- Zebrafish/genetics
- PubMed
- 15136149 Full text @ Dev. Biol.
Citation
Linville, A., Gumusaneli, E., Chandraratna, R.A., and Schilling, T.F. (2004) Independent roles for retinoic acid in segmentation and neuronal differentiation in the zebrafish hindbrain. Developmental Biology. 270(1):186-199.
Abstract
Segmentation of the vertebrate hindbrain into rhombomeres is essential for the anterior-posterior patterning of cranial motor nuclei and their associated nerves. The vitamin A derivative, retinoic acid (RA), is an early embryonic signal that specifies rhombomeres, but its roles in neuronal differentiation within the hindbrain remain unclear. Here we have analyzed the formation of primary and secondary hindbrain neurons in the zebrafish mutant neckless (nls), which disrupts retinaldehyde dehydrogenase 2 (raldh2), and in embryos treated with retinoid receptor (RAR) antagonists. Mutation of nls disrupts secondary, branchiomotor neurons of the facial and vagal nerves, but not the segmental pattern of primary, reticulospinal neurons, suggesting that RA acts on branchiomotor neurons independent of its role in hindbrain segmentation. Very few vagal motor neurons form in nls mutants and many facial motor neurons do not migrate out of rhombomere 4 into more posterior segments. When embryos are treated with RAR antagonists during gastrulation, we observe more severe patterning defects than seen in nls. These include duplicated reticulospinal neurons and posterior expansions of rhombomere 4, as well as defects in branchiomotor neurons. However, later antagonist treatments after rhombomeres are established still disrupt branchiomotor development, suggesting that requirements for RARs in these neurons occur later and independent of segmental patterning. We also show that RA produced by the paraxial mesoderm controls branchiomotor differentiation, since we can rescue the entire motor innervation pattern by transplanting wild-type cells into the somites of nls mutants. Thus, in addition to its role in determining rhombomere identities, RA plays a more direct role in the differentiation of subsets of branchiomotor neurons within the hindbrain.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping