PUBLICATION
Autonomous expression of the nic1 acetylcholine receptor mutation in zebrafish muscle cells
- Authors
- Sepich, D.S., Ho, R.K., and Westerfield, M.
- ID
- ZDB-PUB-961014-1023
- Date
- 1994
- Source
- Developmental Biology 161: 84-90 (Journal)
- Registered Authors
- Ho, Robert K., Sepich, Diane, Westerfield, Monte
- Keywords
- none
- MeSH Terms
-
- Animals
- Cell Differentiation
- Cells, Cultured
- Female
- Motor Neurons/physiology
- Muscles/metabolism*
- Mutation
- Receptors, Cholinergic/biosynthesis
- Receptors, Cholinergic/genetics*
- Zebrafish/embryology
- PubMed
- 8293888 Full text @ Dev. Biol.
Citation
Sepich, D.S., Ho, R.K., and Westerfield, M. (1994) Autonomous expression of the nic1 acetylcholine receptor mutation in zebrafish muscle cells. Developmental Biology. 161:84-90.
Abstract
The nic1b107 (nic1) mutation blocks expression of both functional and clustered acetylcholine receptors (AChRs) in zebrafish muscle. Normally, signaling between motoneurons and muscles regulates AChR clustering. To learn if signaling is affected and to identify the primary cellular target of the nic1 mutation, we made mosaic embryos by transplanting motoneurons and muscle precursors from wild-type to mutant embryos. Genotypically mutant muscle cells fail to cluster AChRs even when contacted by wild-type motoneurons, whereas genotypically mutant motoneurons induce AChR clustering on wild-type muscle cells. Moreover, mutant muscle cells fail to cluster AChRs under culture conditions that induce AChR clustering on wild-type cells. We conclude that the nic1 mutation acts autonomously in muscle cells rather than by affecting signaling between motoneurons and muscle. The wild- type nic1 gene is necessary in muscle for expression and clustering of AChRs.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping