ftz-f1 and Hr39 opposing roles on EcR expression during Drosophila mushroom body neuron remodeling
Résumé
Developmental axon pruning is a general mechanism required for maturation of neural circuits. During Drosophila metamorphosis, the larval-specific dendrites and axons of early γ neurons of the mushroom bodies are pruned and replaced by adult-specific processes. We show here that the nuclear receptor ftz-f1 is required for this pruning and has two roles: (i) to activate expression of the steroid hormone receptor EcR-B1 whose activity is essential for γ remodeling and (ii) to repress expression of Hr39, a ftz-f1 homologous gene. If inappropriately expressed in the γ neurons, HR39 inhibits normal pruning likely by competing with endogenous FTZ-F1 that results in decreased EcR-B1 expression. EcR-B1 was previously identified as a target of the TGF-β signaling pathway. Here we show that the ftz-f1/Hr39 pathway acts apparently independent from TGF-β signaling, suggesting that EcR-B1 is the target of two parallel molecular pathways acting during γ neuron remodeling.
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