Worm Breeder's Gazette 14(3): 46 (June 1, 1996)
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
Department of Physiology, The Hebrew University-Hadassah Medical School, P.O.B 12272, 91120 Jerusalem, Israel.
DEG-3 is an acetylcholine receptor alpha subunit that can mutate to
cause neuronal degeneration. Molecular and pharmacological analysis
suggest that deregulation of channel activity is the cause of the
deg-3(u662) induced neuronal degeneration. However a more precise
understanding of the degeneration causing changes requires
electrophysiological analysis. As expression of deg-3 cDNA in Xenopus
oocytes did not produce acetylcholine gated currents, additional
subunits are probably needed for channel activity (1).
Candidates for DEG-3 channel subunits where identified from genetic
and molecular analysis. Extragenic suppressors of the deg-3(u662)
mutation may code for additional subunits. Another candidate was
obtained from molecular analysis; deg-3 message is trans-spliced to
SL2, suggesting that it is part of a polycistronic transcription unit
(2). Indeed sequencing upstream of deg-3 led us to a nearby gene also
encoding for an acetylcholine receptor alpha subunit (3).
The presence of two acetylcholine receptor subunits in the same
cells, a finding supported by expression analysis, suggested that these
two subunits may interact in forming a channel. Support for this
proposal comes from electrophysiology in Xenopus oocytes. Expression of
both genes produced acetylcholine dependent currents, while alone
neither produce any detectable currents. Thus we have demonstrated a
functional interaction between the two components of the deg-3 operon.
This also provides us with a tool needed for the characterization of the
normal and mutant DEG-3 channel.
1. Treinin and Chalfie (1995). Neuron 14, 871-877.
2. Spieth et al. (1993). Cell 73, 521-532.
3. Garcia-Anoveros et al. (1995) International C. elegans Meeting 75.