Abstract
Developmental axon pruning is a general mechanism that is 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 found that the nuclear receptor ftz-f1 is required for this pruning, activates expression of the steroid hormone receptor EcR-B1, whose activity is essential for γ remodeling, and represses expression of Hr39, an ftz-f1 homologous gene. If inappropriately expressed in the γ neurons, HR39 inhibits normal pruning, probably by competing with endogenous FTZ-F1, which results in decreased EcR-B1 expression. EcR-B1 was previously identified as a target of the TGFβ signaling pathway. We found that the ftz-f1 and Hr39 pathway apparently acts independently of TGFβ signaling, suggesting that EcR-B1 is the target of two parallel molecular pathways that act during γ neuron remodeling.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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DNA-Binding Proteins / genetics
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DNA-Binding Proteins / metabolism*
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Drosophila
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Drosophila Proteins / genetics
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Drosophila Proteins / metabolism
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Drosophila Proteins / physiology*
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Gene Expression Regulation, Developmental / genetics
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Gene Expression Regulation, Developmental / physiology*
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Metamorphosis, Biological / genetics
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Metamorphosis, Biological / physiology*
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Mushroom Bodies / growth & development
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Mushroom Bodies / metabolism*
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Mutant Proteins / metabolism
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Mutant Proteins / physiology
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Neurons / metabolism*
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Neurons / physiology
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Receptors, Steroid / genetics
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Receptors, Steroid / metabolism*
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Receptors, Steroid / physiology*
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Transcription Factors / genetics
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Transcription Factors / metabolism*
Substances
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DNA-Binding Proteins
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Drosophila Proteins
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Mutant Proteins
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Receptors, Steroid
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Transcription Factors
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ecdysone receptor
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nuclear hormone receptor FTZ-F1 beta, Drosophila
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nuclear hormone receptor FTZ-F1, Drosophila