TY - JOUR
T1 - aex-3 encodes a novel regulator of presynaptic activity in C. elegans
AU - Iwasaki, Kouichi
AU - Staunton, Jane
AU - Saifee, Owais
AU - Nonet, Michael
AU - Thomas, James H.
N1 - Funding Information:
We thank E. Hankins and P. Colacurcio for technical assistance; E. Jorgensen for the n2166 allele and information about ox3; A. Fire for pPD95.69; L. Huang and P. Sternberg for pbHL98; A. Loewy and L. Salkoff for providing recording equipment; A. Coulson for cosmids; R. Barstead for the C. elegans cDNA library; D. Birnby for C. elegans RNA; the C. elegans Genome Sequencing Consortium for C. elegans genome sequences; C. Manoil for advice on protein structure; and M. Ailion, S. Bajjalieh, T. Inoue, D. Johnstone, E. Jorgensen, E. Malone, P. Swoboda, and K. Yook for comments on the manuscript. This work was supported by Public Health Service Grant R01NS30187 and R01NS32057 to J. H. T., NS09937 to J. S., and R01NS33535 to M. N. Some strains were obtained from the Caenorhabditis Genetics Center, which is funded by the National Institutes of Health National Center for Research Resources.
PY - 1997/4
Y1 - 1997/4
N2 - C. elegans aex-3 mutations cause pleiotropic behavioral defects that are suggestive of reduced synaptic transmission. aex-3 mutations also show strong genetic interactions with mutations in unc-31 and unc-64, two other genes implicated in synaptic transmission. Physiological and pharmacological studies indicate that aex-3 defects are presynaptic. In aex-3 mutants, the synaptic vesicle-associated RAB-3 protein aberrantly accumulates in neuronal cell bodies and is reduced in synapse-rich axons. This localization defect is specific to RAB-3, since other synaptic proteins are localized normally in aex-3 mutants. aex-3 encodes a 1409 amino acid protein with strong homology to DENN, a human protein of unknown function. In C. elegans, aex-3 is expressed in all or nearly all neurons. These results suggest that AEX-3 is a novel regulator of presynaptic activity that interacts with RAB-3 to regulate synaptic vesicle release.
AB - C. elegans aex-3 mutations cause pleiotropic behavioral defects that are suggestive of reduced synaptic transmission. aex-3 mutations also show strong genetic interactions with mutations in unc-31 and unc-64, two other genes implicated in synaptic transmission. Physiological and pharmacological studies indicate that aex-3 defects are presynaptic. In aex-3 mutants, the synaptic vesicle-associated RAB-3 protein aberrantly accumulates in neuronal cell bodies and is reduced in synapse-rich axons. This localization defect is specific to RAB-3, since other synaptic proteins are localized normally in aex-3 mutants. aex-3 encodes a 1409 amino acid protein with strong homology to DENN, a human protein of unknown function. In C. elegans, aex-3 is expressed in all or nearly all neurons. These results suggest that AEX-3 is a novel regulator of presynaptic activity that interacts with RAB-3 to regulate synaptic vesicle release.
UR - http://www.scopus.com/inward/record.url?scp=0030989110&partnerID=8YFLogxK
U2 - 10.1016/S0896-6273(00)80302-5
DO - 10.1016/S0896-6273(00)80302-5
M3 - Article
C2 - 9136770
AN - SCOPUS:0030989110
SN - 0896-6273
VL - 18
SP - 613
EP - 622
JO - Neuron
JF - Neuron
IS - 4
ER -