Abstract
Stress-induced changes to the dendritic architecture of neurons have been demonstrated in numerous mammalian and invertebrate systems. Remodeling of dendrites varies tremendously among neuron types. During the stress-induced dauer stage of Caenorhabditis elegans, the IL2 neurons arborize to cover the anterior body wall. In contrast, the FLP neurons arborize to cover an identical receptive field during reproductive development. Using time-course imaging, we show that branching between these two neuron types is highly coordinated. Furthermore, we find that the IL2 and FLP arbors have a similar dendritic architecture and use an identical downstream effector complex to control branching; however, regulation of this complex differs between stress-induced IL2 branching and FLP branching during reproductive development. We demonstrate that the unfolded protein response (UPR) sensor IRE-1, required for localization of the complex in FLP branching, is dispensable for IL2 branching at standard cultivation temperatures. Exposure of ire-1 mutants to elevated temperatures results in defective IL2 branching, thereby demonstrating a previously unknown genotype by environment interaction within the UPR. We find that the FOXO homolog, DAF-16, is required cell-autonomously to control arborization during stress-induced arborization. Likewise, several aspects of the dauer formation pathway are necessary for the neuron to remodel, including the phosphatase PTEN/DAF-18 and Cytochrome P450/DAF-9. Finally, we find that the TOR associated protein, RAPTOR/DAF-15 regulates mutually exclusive branching of the IL2 and FLP dendrites. DAF-15 promotes IL2 branching during dauer and inhibits precocious FLP growth. Together, our results shed light on molecular processes that regulate stress-mediated remodeling of dendrites across neuron classes.
Highlights
Dendrite morphology is crucial for efficient neural signaling
Using forward and reverse genetics, we find that branching in both neuron types is controlled by a similar protein complex, but that regulation of this complex differs between cell types
We found that cbc1 fails to Stress-induced dendritic remodeling in C. elegans complement the deletion mutant dma-1(tm5159) for IL2 branching (11/11 cbc-1/tm5159 dauers defective, S1A Fig)
Summary
Dendrite morphology is crucial for efficient neural signaling. Recent years have seen increased attention given to the molecular basis of dendritic arborization using both cell-culture studies and model organisms. Experience-driven remodeling of a dendrite can contribute to both the size and complexity of dendritic arbors in a diverse range of species. These changes can include both increasing and decreasing dendritic volume [1,2,3]. Dendrites in the basal lateral amygdala undergo hypertrophic growth following chronic stress [4], whereas those of the hippocampus atrophy [5]. Little is known about the molecular mechanisms that cause differential arborization in different neuron classes during normal physiological conditions versus stress-exposed conditions. What, if any, coordination occurs among distinct neuron types is unknown
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