aex-3 encodes a novel regulator of presynaptic activity in C. elegans.

Abstract:

: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.

journal_name

Neuron

journal_title

Neuron

authors

Iwasaki K,Staunton J,Saifee O,Nonet M,Thomas JH

doi

10.1016/s0896-6273(00)80302-5

subject

Has Abstract

pub_date

1997-04-01 00:00:00

pages

613-22

issue

4

eissn

0896-6273

issn

1097-4199

pii

S0896-6273(00)80302-5

journal_volume

18

pub_type

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