This Program Project grant revolves around the development and function of the nervous system in Drosophila. Many of the approaches involve genetics and molecular biology. In Project I (Rosbash) and II (Hall), circadian rhythms will be investigated. Several such studies will apply existing """"""""clock"""""""" mutations and cloned DNA defined by mutant alleles at a locus called period (per). In addition (Project I), it is proposed to isolate several new circadian rhythm mutants, using chemical and transposon-mobilization mutageneses. It is also proposed to initiate molecular analyses of certain emerging rhythm mutants. In Project II, the neural substrates of Drosophila's circadian rhythms will be delved into. Cyclings of per product levels, known to fluctuate with circadian periodicities, will be dissected molecularly, immunohistochemically, and behaviorally. Searches for interspecific relatives of the per gene will be made. In project III (White), the influence of two genes on Drosophila's embryonic development will be analyzed. One is embryonic-lethal/abnormal-visual-system (elav), whose encoded. protein will be studied with regard to its presumed role in the control of neuronal-specific mRNA processing. Putative targets of ELAV's action will be looked for in genetic and biochemically based screens. Aberrant expression of elav will be analyzed, by molecularly characterizing conditional mutants, and eliciting ectopic expression of the gene's product(s). The other gene, erect-wing (ewg), which is expressed in the nuclei of developing neurons and muscle precursors, will be investigated with regard to possible involvement in transcriptional regulation. Project IV (Lisman) involves the function of Drosophila photoreceptors. The two reactions involved in the first stage of transducing visual stimuli [activation of G-protein by light-activated rhodopsin (M*), and the reaction by which M* is deactivated] will be quantitated. Molecular manipulations of a cloned opsin gene-- to eliminate most of the putative phosphorylation sites-- will be effected in order to: measure the rate of M * deactivation and gain and determine if the reliability of this deactivation is impinged upon. A separate photoreceptor-based subproject will connect with Projects I and II, whose previous studies showed that per expression is prominent in these visual-system cells. Project V (Griffith) will study the role of the multifunctional calcium/calmodulin protein kinase II (CaM kinase) and its relatives in experience-dependent behavior. Gene cloning, biochemical characterization, spatial expression studies, and the identification of other biochemical components that contribute to behavioral plasticity are the goals of this project.
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