Genetics, Vol. 162, 259-271, September 2002, Copyright © 2002

A Drosophila SNAP-25 Null Mutant Reveals Context-Dependent Redundancy With SNAP-24 in Neurotransmission

Ilya Vilinskya, Bryan A. Stewartb, James Drummondc, Iain Robinsonc, and David L. Deitchera
a Department of Neurobiology and Behavior, Cornell University, Ithaca, New York 14853,
b Division of Life Sciences, University of Toronto at Scarborough, Ontario M1C 1A4, Canada
c Department of Genetics, Cambridge, CB2 3EH, England

Corresponding author: David L. Deitcher, Department of Neurobiology and Behavior, Cornell University, Ithaca, NY 14853., dld14{at}cornell.edu (E-mail)

Communicating editor: R. S. HAWLEY

The synaptic protein SNAP-25 is an important component of the neurotransmitter release machinery, although its precise function is still unknown. Genetic analysis of other synaptic proteins has yielded valuable information on their role in synaptic transmission. In this study, we performed a mutagenesis screen to identify new SNAP-25 alleles that fail to complement our previously isolated recessive temperature-sensitive allele of SNAP-25, SNAP-25ts. In a screen of 100,000 flies, 26 F1 progeny failed to complement SNAP-25ts and 21 of these were found to be null alleles of SNAP-25. These null alleles die at the pharate adult stage and electroretinogram recordings of these animals reveal that synaptic transmission is blocked. At the third instar larval stage, SNAP-25 nulls exhibit nearly normal neurotransmitter release at the neuromuscular junction. This is surprising since SNAP-25ts larvae exhibit a much stronger synaptic phenotype. Our evidence indicates that a related protein, SNAP-24, can substitute for SNAP-25 at the larval stage in SNAP-25 nulls. However, if a wild-type or mutant form of SNAP-25 is present, then SNAP-24 does not appear to take part in neurotransmitter release at the larval NMJ. These results suggest that the apparent redundancy between SNAP-25 and SNAP-24 is due to inappropriate genetic substitution.




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