MUTATIONS IN SHAKING-B PREVENT ELECTRICAL SYNAPSE FORMATION IN THE DROSOPHILA GIANT FIBER SYSTEM

Citation
P. Phelan et al., MUTATIONS IN SHAKING-B PREVENT ELECTRICAL SYNAPSE FORMATION IN THE DROSOPHILA GIANT FIBER SYSTEM, The Journal of neuroscience, 16(3), 1996, pp. 1101-1113
Citations number
43
Categorie Soggetti
Neurosciences,Neurosciences
Journal title
ISSN journal
02706474
Volume
16
Issue
3
Year of publication
1996
Pages
1101 - 1113
Database
ISI
SICI code
0270-6474(1996)16:3<1101:MISPES>2.0.ZU;2-I
Abstract
The giant fiber system (GFS) is a simple network of neurons that media tes visually elicited escape behavior in Drosophila. The giant fiber ( GF), the major component of the system, is a large, descending interne uron that relays visual stimuli to the motoneurons that innervate the tergotrochanteral jump muscle (TTM) and dorsal longitudinal flight mus cles (DLMs). Mutations in the neural transcript from the shaking-B loc us abolish the behavioral response by disrupting transmission at some electrical synapses in the GFS. This study focuses on the role of the gene in the development of the synaptic connections. Using an enhancer -trap line that expresses lacZ in the GFs, we show that the neurons de velop during the first 30 hr of metamorphosis. Within the next 15 hr, they begin to form electrical synapses, as indicated by the transfer o f intracellularly injected Lucifer yellow. The GFs dye-couple to the T TM motoneuron between 30 and 45 hr of metamorphosis, to the peripheral ly synapsing interneuron that drives the DLM motoneurons at similar to 48 hr, and to giant commissural interneurons in the brain at similar to 55 hr. Immunocytochemistry with shaking-B peptide antisera demonstr ates that the expression of shaking-B protein in the region of GFS syn apses coincides temporally with the onset of synaptogenesis; expressio n persists thereafter. The mutation shak-B-2, which eliminates protein expression, prevents the establishment of dye coupling. shaking-B, th erefore, is essential for the assembly and/or maintenance of functiona l gap junctions al electrical synapses in the GFS.