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The evolutionarily conserved gene LNP‐1 is required for synaptic vesicle trafficking and synaptic transmission
Author(s) -
Ghila Luiza,
Gomez Marie
Publication year - 2008
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2008.06049.x
Subject(s) - neurotransmission , synaptic vesicle , biology , microbiology and biotechnology , synaptobrevin , synaptogenesis , caenorhabditis elegans , synapse , postsynaptic potential , neuroscience , gene , genetics , vesicle , receptor , membrane
The control of vesicle‐mediated transport in nerve cells is of great importance in the function, development and maintenance of synapse. In this paper, we characterize the new Caenorhabditis elegans gene, lnp‐1 . The lnp‐1 gene is broadly distributed in many neuronal structures and its localization is dependent of the UNC‐104/kinesin protein. Deletion mutations in lnp‐1 result in increased resistance to aldicarb, an acetylcholinesterase inhibitor, and in locomotor defects. However, sensitivity to levamisole, a nicotinic agonist which, unlike aldicarb, only affects postsynaptic function, was similar to that of wild‐type animals, suggesting a presynaptic function for LNP‐1 in neurotransmission. The mislocalization of presynaptic proteins, such as synaptobrevin‐1 or RAB‐3, in lnp‐1 mutants further supports this hypothesis. In summary, our studies suggest that LNP‐1 plays a role in synaptogenesis by regulating vesicular transport or localization.