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Tim Tully

Publications and source records attributed to Tim Tully.

20 records · Page 2Linked to original sources

Isogenic autosomes to be applied in optimal screening for novel mutants with viable phenotypes in Drosophila melanogaster.

Most insertional mutagenesis screens of Drosophila performed to date have not used target chromosomes that have been checked for their suitability for phenotypic screens for viable phenotypes. To address this, we have generated a selection of stocks carrying either isogenized second chromosomes or isogenized third chromosomes, in a genetic background derived from a Canton-S wild-type strain. We have tested these stocks for a range of behavioral and other viable phenotypes. As expected, most lines are statistically indistinguishable from Canton-S in most phenotypes tested. The lines generated are now being used as target chromosomes in mutagenesis screens, and the characterization reported here will facilitate their use in screens of these lines for behavioral and other viable phenotypes.

Anesthetics↗

Conditioning deficits of CaM-kinase transgenic Drosophila melanogaster in a new excitatory courtship assay.

Courtship suppression is an associative conditioning procedure in Drosophila melanogaster that is ethologically based and capable of being tested on individual flies. We have expanded the range of the courtship conditioning by developing an excitatory procedure in which male flies learn to associate a novel odor with the courtship stimulating cues of virgin females. Wild-type males normally court other mature males very little, but following training, the odor alone is able to elicit increased levels of courtship towards an object male. Flies expressing an inhibitor of calcium/calmodulin-dependent protein kinase II (CaMKII) were previously shown to have no retention one hour after training in the courtship suppression task, as manifested in their persistent courting of a virgin female. A possible trivial explanation for this response is that the CaMKII-inhibited fly strains (ala1 and ala2) were merely hyperactive courters. The poor performance of these mutants in the new excitatory conditioning procedure confirms that their conditioning deficit results from a disruption of an associative mechanism per se.

Animals↗