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Shu Kondo

Publications and source records attributed to Shu Kondo.

3 recordsLinked to original sources

Cross-species implementation of an innate courtship behavior by manipulation of the sex-determinant gene.

In accepting a courting male, Drosophila subobscura females require nuptial gift giving in which a male gives regurgitated crop contents to her mouth to mouth. No similar behavior is found in D. melanogaster. By clonal activation of neurons expressing the male-determinant FruM, we identified insulin-like peptide-producing cells (IPCs) and their putative postsynaptic targets, proboscis-innervating motoneurons, as those critical for gift giving. We demonstrate that loss of FruM from D. subobscura IPCs abrogates neurite extension and gift giving, whereas FruM overexpression in their D. melanogaster counterparts induces overgrowth of neurites that harbor functional synapses, culminating in increased regurgitation. We suggest that the acquisition of FruM expression by IPCs was a key event occurring in an ancestral D. subobscura that conferred a latent capability to perform nuptial gift giving.

Animals↗

Local caspase activity directs engulfment of dendrites during pruning.

Pruning is important for sculpting neural circuits, as it removes excessive or inaccurate projections. Here we show that the removal of sensory neuron dendrites during pruning in Drosophila melanogaster is directed by local caspase activity. Suppressing caspase activity prevented dendrite removal, whereas a global activation of caspases within a neuron caused cell death. A new genetically encoded caspase probe revealed that caspase activity is confined to the degenerating dendrites of pruning neurons.

Analysis of Variance↗

DRONC coordinates cell death and compensatory proliferation.

Accidental cell death often leads to compensatory proliferation. In Drosophila imaginal discs, for example, gamma-irradiation induces extensive cell death, which is rapidly compensated by elevated proliferation. Excessive compensatory proliferation can be artificially induced by "undead cells" that are kept alive by inhibition of effector caspases in the presence of apoptotic stimuli. This suggests that compensatory proliferation is induced by dying cells as part of the apoptosis program. Here, we provide genetic evidence that the Drosophila initiator caspase DRONC governs both apoptosis execution and subsequent compensatory proliferation. We examined mutants of five Drosophila caspases and identified the initiator caspase DRONC and the effector caspase DRICE as crucial executioners of apoptosis. Artificial compensatory proliferation induced by coexpression of Reaper and p35 was completely suppressed in dronc mutants. Moreover, compensatory proliferation after gamma-irradiation was enhanced in drice mutants, in which DRONC is activated but the cells remain alive. These results show that the apoptotic pathway bifurcates at DRONC and that DRONC coordinates the execution of cell death and compensatory proliferation.

Animals↗