Tau and tan reporters disrupt central projections of sensory neurons in Drosophila

In this paper, the authors report that the expression of tau-based reporter genes causes severe defects in the morphology of sensory neurons in adult Drosophila. Targeted expression of tau-green fluorescent protein (tau-GFP) in sensory neurons, using the galactosidase-4 (GAL4) system, produced a ran ge of characteristic defects in expressing neurons. The defects observed in cluded loss of axons, abnormal axon bundling, reduced sensory arborisations , and axonal swellings (beads). Blind comparisons of adult sensory neurons labelled with tau-GFP or CD8-GFP showed that tau-GFP neurons exhibited many more defects than CD8-GFP-expressing neurons. CD8-GFP was found to induce no significant defects on sensory neuron morphology. Expression of tau-lacZ and human tau in sensory neurons produced defects comparable to those seen with tau-GFP. A developmental study showed that tau-expressing axons grow normally and innervate the correct regions of the neuropil. The absence of these axons later in development suggests that tau-expressing axone are los t after initial ingrowth. Examination of silver-stained sections suggests t hat the absence of axons is due to axon loss rather than failure of the exp ression system to label the neurons. The results suggest that the expressio n of tau-based reporter constructs causes severe defects in sensory neurons , resulting in degeneration. The results also indicate that Drosophila may provide a useful model system for examining the role of tau in neurodegener ative disorders. J. Comp. Neurol. 428: 630-640, 2000. (C) 2000 Wiley-Liss, Inc.