PUBLICATION
Nkx6 proteins specify one zebrafish primary motoneuron subtype by regulating late islet1 expression
- Authors
- Hutchinson, S.A., Cheesman, S.E., Hale, L.A., Boone, J.Q., and Eisen, J.S.
- ID
- ZDB-PUB-070330-34
- Date
- 2007
- Source
- Development (Cambridge, England) 134(9): 1671-1677 (Journal)
- Registered Authors
- Cheesman, Sarah, Eisen, Judith S., Hale, Laura
- Keywords
- Zebrafish, Motoneuron, Islet1, Nkx6, Interneuron
- MeSH Terms
-
- Animals
- Homeodomain Proteins/genetics*
- Homeodomain Proteins/metabolism*
- Interneurons/cytology
- Interneurons/metabolism
- LIM-Homeodomain Proteins
- Motor Neurons/cytology*
- Motor Neurons/metabolism
- Transcription Factors/genetics
- Transcription Factors/metabolism*
- Zebrafish
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- PubMed
- 17376808 Full text @ Development
Citation
Hutchinson, S.A., Cheesman, S.E., Hale, L.A., Boone, J.Q., and Eisen, J.S. (2007) Nkx6 proteins specify one zebrafish primary motoneuron subtype by regulating late islet1 expression. Development (Cambridge, England). 134(9):1671-1677.
Abstract
The ability of animals to carry out their normal behavioral repertoires requires exquisitely precise matching between specific motoneuron subtypes and the muscles they innervate. However, the molecular mechanisms that regulate motoneuron subtype specification remain unclear. Here, we use individually identified zebrafish primary motoneurons to describe a novel role for Nkx6 and Islet1 proteins in the specification of vertebrate motoneuron subtypes. We show that zebrafish primary motoneurons express two related Nkx6 transcription factors. In the absence of both Nkx6 proteins, the CaP motoneuron subtype develops normally, whereas the MiP motoneuron subtype develops a more interneuron-like morphology. In the absence of Nkx6 function, MiPs exhibit normal early expression of islet1, which is required for motoneuron formation; however, they fail to maintain islet1 expression. Misexpression of islet1 RNA can compensate for loss of Nkx6 function, providing evidence that Islet1 acts downstream of Nkx6. We suggest that Nkx6 proteins regulate MiP development at least in part by maintaining the islet1 expression that is required both to promote the MiP subtype and to suppress interneuron development.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping