Acetylcholinesterase is required for neuronal and muscular development in the zebrafish embryo
- Behra, M., Cousin, X., Bertrand, C., Vonesch, J.L., Biellmann, D., Chatonnet, A., and Strähle, U.
- Nature Neuroscience 5(2): 111-118 (Journal)
- Registered Authors
- Behra, Martine, Bertrand, Christelle, Biellmann, Dominique, Chatonnet, Arnaud, Cousin, Xavier, Strähle, Uwe
- MeSH Terms
- Amino Acid Sequence/genetics
- Base Sequence/genetics
- Cell Death
- Embryo, Nonmammalian/physiology
- Molecular Sequence Data
- Muscle, Skeletal/embryology*
- Muscular Diseases/genetics
- Nervous System/embryology*
- Neuromuscular Junction/embryology
- Neurons, Afferent/physiology
- Receptors, Nicotinic/physiology
- 11753420 Full text @ Nat. Neurosci.
Behra, M., Cousin, X., Bertrand, C., Vonesch, J.L., Biellmann, D., Chatonnet, A., and Strähle, U. (2002) Acetylcholinesterase is required for neuronal and muscular development in the zebrafish embryo. Nature Neuroscience. 5(2):111-118.
The neurotransmitter acetylcholine (ACh) has a crucial role in central and neuromuscular synapses of the cholinergic system. After release into the synaptic cleft, ACh is rapidly degraded by acetylcholinesterase (AChE). We have identified a mutation in the ache gene of the zebrafish, which abolishes ACh hydrolysis in homozygous animals completely. Embryos are initially motile but subsequently develop paralysis. Mutant embryos show defects in muscle fiber formation and innervation, and primary sensory neurons die prematurely. The neuromuscular phenotype in ache mutants is suppressed by a homozygous loss-of-function allele of the alpha-subunit of the nicotinic acetylcholine receptor (nAChR), indicating that the impairment of neuromuscular development is mediated by activation of nAChR in the mutant. Here we provide genetic evidence for non-classical functions of AChE in vertebrate development.
Genes / Markers
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Engineered Foreign Genes
Errata and Notes