TY - JOUR
T1 - Synaptic function is impaired but not eliminated in C. elegans mutants lacking synaptotagmin
AU - Nonet, Michael L.
AU - Grundahl, Kiely
AU - Meyer, Barbara J.
AU - Rand, James B.
N1 - Funding Information:
We thank Aixa Alfonso, Janet Duerr, Gian Garrigaand the members of the Meyer lab for their comments; Erik Jorgensen for help in identifying DVB; Leon Avery, Erik Jorgensen, and Bob Horvitz for providing mutants prior to publication; 6. Wendland and R. Scheller for providing antibodies; A. Coulson and J. Sulston for cosmid and YAC clones; and Alex Karu and Ted Pelman for assistance in the production of antibodies. Some of the nematode strains used in this study were provided bytheCaenorhabditisGeneticsCenter (St. Paul, Minnesota), which is funded by the National Center for Research Resources. This work was supported by a grant to B. J. M. from the Muscular Dystrophy Association and grants to J. B. R. from the Oklahoma Center for the Advancement of Science and Technology and the Muscular Dystrophy Association. M. L. N. was previously supported by the Helen Hay Whitney Foundation and is presently supported by the National Institutes of Health.
PY - 1993/7/2
Y1 - 1993/7/2
N2 - Synaptotagmin is an abundant synaptic vesicle-associated protein proposed to be involved in calcium-mediated neurotransmitter release. Our molecular and genetic results demonstrate that, although synaptotagmin is required for the proper function of the presynaptic nerve terminal in C. elegans, some neurotransmitter release persists in synaptogamin mutants. In C. elegans neurons, synaptotagmin is localized to regions known to be rich in synapses and appears to be associated with synaptic vesicles. Mutants defective in the synaptotagmin gene, called snt-1, exhibit severe behavioral abnormalities that are characteristic of deficiencies in synaptic function, including severe locomotion, feeding, and defecation defects. The mutants are defective in exocytosis, since they accumulate acetylcholine, and are resistant to cholinesterase inhibitors, but they nevertheless remain sensitive to cholinergic receptor agonists. In spite of these exocytic defects, snt-1 mutants are capable of coordinated motor movements, indicating that the mutants do not have a complete block of neurotransmitter release.
AB - Synaptotagmin is an abundant synaptic vesicle-associated protein proposed to be involved in calcium-mediated neurotransmitter release. Our molecular and genetic results demonstrate that, although synaptotagmin is required for the proper function of the presynaptic nerve terminal in C. elegans, some neurotransmitter release persists in synaptogamin mutants. In C. elegans neurons, synaptotagmin is localized to regions known to be rich in synapses and appears to be associated with synaptic vesicles. Mutants defective in the synaptotagmin gene, called snt-1, exhibit severe behavioral abnormalities that are characteristic of deficiencies in synaptic function, including severe locomotion, feeding, and defecation defects. The mutants are defective in exocytosis, since they accumulate acetylcholine, and are resistant to cholinesterase inhibitors, but they nevertheless remain sensitive to cholinergic receptor agonists. In spite of these exocytic defects, snt-1 mutants are capable of coordinated motor movements, indicating that the mutants do not have a complete block of neurotransmitter release.
UR - http://www.scopus.com/inward/record.url?scp=0027319325&partnerID=8YFLogxK
U2 - 10.1016/0092-8674(93)90357-V
DO - 10.1016/0092-8674(93)90357-V
M3 - Article
C2 - 8391930
AN - SCOPUS:0027319325
VL - 73
SP - 1291
EP - 1305
JO - Cell
JF - Cell
SN - 0092-8674
IS - 7
ER -