Courtship and Other Behaviors Affected by a Heat-Sensitive, Molecularly Novel Mutation in the cacophony Calcium-Channel Gene of Drosophila

Corresponding author: Jeffrey C. Hall, Brandeis University, 415 South St., Waltham, MA 02454-9110., hall{at}brandeis.edu (E-mail)

Communicating editor: M. NOOR

The cacophony (cac) locus of Drosophila melanogaster, which encodes a calcium-channel subunit, has been mutated to cause courtship-song defects or abnormal responses to visual stimuli. However, the most recently isolated cac mutant was identified as an enhancer of a comatose mutation's effects on general locomotion. We analyzed the cac^TS2 mutation in terms of its intragenic molecular change and its effects on behaviors more complex than the fly's elementary ability to move. The molecular etiology of this mutation is a nucleotide substitution that causes a proline-to-serine change in a region of the polypeptide near its EF hand. Given that this motif is involved in channel inactivation, it was intriguing that cac^TS2 males generate song pulses containing larger-than-normal numbers of cycles—provided that such males are exposed to an elevated temperature. Similar treatments caused only mild visual-response abnormalities and generic locomotor sluggishness. These results are discussed in the context of calcium-channel functions that subserve certain behaviors and of defects exhibited by the original cacophony mutant. Despite its different kind of amino-acid substitution, compared with that of cac^TS2, cac^S males sing abnormally in a manner that mimics the new mutant's heat-sensitive song anomaly.

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