Περίληψη:
Dendrites are subject to subtle modifications as well as extensive
remodeling during the assembly and maturation of neural circuits in a
wide variety of organisms. During metamorphosis Drosophila flight
motoneurons MN1-MN4 undergo dendritic regression, followed by regrowth,
whereas MN5 differentiates de novo (Consoulas et al. [2002] J.
Neurosci. 22:49064917). Many cellular changes during metamorphosis are
triggered and orchestrated by the steroid hormone 20-hydroxyecdysone,
which initiates a cascade of coordinated gene expression. Broad Complex
(BRC), a primary response gene in the ecdysone cascade, encodes a family
of transcription factors (BRC-Z1-Z4) that are essential for metamorphic
reorganization of the central nervous system (CNS). Using neuron-filling
techniques that reveal cellular morphology with very high resolution, we
tested the hypothesis that BRC is required for metamorphic development
of MN1-MN5. Through a combination of loss-of-function mutant analyses,
genetic mapping, and transgenic rescue experiments, we found that 2Bc
function, mediated by BRC-Z3, is required selectively for motoneuron
dendritic regrowth (MN1-MN4) and de novo outgrowth (MN5), as well as for
soma expansion of MN5. In contrast, larval development and dendritic
regression of MN1-MN4 are BRC-independent. Surprisingly, BRC proteins
are not expressed in the motoneurons, suggesting that BRC-Z3 exerts its
effect in a non-cell-autonomous manner. The 2Bc mutants display no gross
defects in overall thoracic CNS structure, or in peripheral structures
such as target muscles or sensory neurons. Candidates for mediating the
effect of BRC-Z3 on dendritic growth of MN1-MN5 include their synaptic
inputs and non-neuronal CNS cells that interact with them through direct
contact or diffusible factors. (c) 2005 Wiley-Liss, Inc.
Συγγραφείς:
Consoulas, C
Levine, RB
Restifo, LL
