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Nat Neurosci. 2011 Jan;14(1):37-44. doi: 10.1038/nn.2700. Epub 2010 Dec 5.

ftz-f1 and Hr39 opposing roles on EcR expression during Drosophila mushroom body neuron remodeling.

Author information

1
Institute of Human Genetics, CNRS UPR1142, Montpellier, France.

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.

PMID:
21131955
DOI:
10.1038/nn.2700
[Indexed for MEDLINE]

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