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.