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

Boulanger, A.; Clouet-Redt, C.; Farge, M.; Flandre, A.; Guignard, T.; Fernando, C.; Juge, F.; Dura, J. M.

Nat Neurosci

2011-01 / vol 14 / pages 37-44

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 gamma 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 gamma remodeling, and represses expression of Hr39, an ftz-f1 homologous gene. If inappropriately expressed in the gamma 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 TGFbeta signaling pathway. We found that the ftz-f1 and Hr39 pathway apparently acts independently of TGFbeta signaling, suggesting that EcR-B1 is the target of two parallel molecular pathways that act during gamma neuron remodeling.

Lire sur PubMed

10.1038/nn.2700 nn.2700 [pii]

1546-1726 (Electronic) 1097-6256 (Linking)

IGMM team(s) involved in this publication
Étiquettes

Animals; DNA-Binding Proteins/genetics/*metabolism; Drosophila; Drosophila Proteins/genetics/metabolism/*physiology; Gene Expression Regulation, Developmental/genetics/*physiology; Metamorphosis, Biological/genetics/*physiology; Mushroom Bodies/growth & development/*metabolism; Mutant Proteins/metabolism/physiology; Neurons/*metabolism/physiology; Receptors, Steroid/genetics/*metabolism/*physiology; Transcription Factors/genetics/*metabolism

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