Similarities of Drosophila rab GTPases based on expression profiling: completion and analysis of the rab-Gal4 kit.

We recently generated rab-Gal4 lines for 25 of 29 predicted Drosophila rab GTPases. These lines provide tools for the expression of reporters, mutant rab variants or other genes, under control of the regulatory elements of individual rab loci. Here, we report the generation and characterization of the remaining four rab-Gal4 lines. Based on the completed 'rab-Gal4 kit' we performed a comparative analysis of the cellular and subcellular expression of all rab GTPases. This analysis includes the cellular expression patterns in characterized neuronal and non-neuronal cells and tissues, the subcellular localization of wild type, constitutively active and dominant negative rab GTPases and colocalization with known intracellular compartment markers. Our comparative analysis identifies all Rab GTPases that are expressed in the same cells and localize to the same intracellular compartments. Remarkably, similarities based on these criteria are typically not predicted by primary sequence homology. Hence, our findings provide an alternative basis to assess potential roles and redundancies based on expression in developing and adult cell types, compartment identity and subcellular localization.

Speech discrimination after early exposure to pulsed-noise or speech.

Early experience of structured inputs and complex sound features generate lasting changes in tonotopy and receptive field properties of primary auditory cortex (A1). In this study we tested whether these changes are severe enough to alter neural representations and behavioral discrimination of speech. We exposed two groups of rat pups during the critical period of auditory development to pulsed-noise or speech. Both groups of rats were trained to discriminate speech sounds when they were young adults, and anesthetized neural responses were recorded from A1. The representation of speech in A1 and behavioral discrimination of speech remained robust to altered spectral and temporal characteristics of A1 neurons after pulsed-noise exposure. Exposure to passive speech during early development provided no added advantage in speech sound processing. Speech training increased A1 neuronal firing rate for speech stimuli in naïve rats, but did not increase responses in rats that experienced early exposure to pulsed-noise or speech. Our results suggest that speech sound processing is resistant to changes in simple neural response properties caused by manipulating early acoustic environment.