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The interference of truncated with normal potassium channel subunits leads to abnormal behaviour in transgenic Drosophila melanogaster.
Author(s) -
Gisselmann G.,
Sewing S.,
Madsen B.W.,
Mallart A.,
AngautPetit D.,
MüllerHoltkamp F.,
Ferrus A.,
Pongs O.
Publication year - 1989
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1989.tb08364.x
Subject(s) - biology , drosophila melanogaster , potassium channel , transgene , interference (communication) , rna interference , genetics , channel (broadcasting) , drosophila (subgenus) , microbiology and biotechnology , melanogaster , potassium , biophysics , gene , rna , telecommunications , chemistry , organic chemistry , computer science
The Shaker locus of Drosophila melanogaster encodes a family of A‐type potassium channel subunits. Shaker mutants behave as antimorphs in gene dosage tests. This behaviour is due to the production of truncated A‐channel subunits. We propose that they interfere with the function of their normal counterpart by forming multimeric A‐channel structures. This hypothesis was tested by constructing transgenic flies carrying a heat‐inducible gene encoding a truncated A‐type potassium channel subunit together with a normal wild type doses of A‐type potassium channel subunits. The altered subunit leads at larval, pupal or adult stages to the transformation of wild type into Shaker flies. The transformed flies exhibited a heat‐inducible abnormal leg shaking behaviour and a heat‐inducible facilitated neurotransmitter release at larval neuromuscular junctions. By the overexpression of an aberrant A‐channel subunit the normal behaviour of transgenic D. melanogaster can be altered in a predictable way.