Stress-induced dendritic branching inC. elegansrequires both common arborization effectors and stress-responsive molecular pathways

Abstract

Stress influences the shape of dendritic arbors in neurons. 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 the anterior body wall during non-dauer development.Previous work showed that the membrane-bound receptor DMA-1 regulates FLP branching as part of a larger protein complex. Using forward genetics, we show that the IL2 neurons also use the DMA-1 complex to regulate branching. To understand the coordination of the IL2s and FLPs we conducted a time-course examination of FLPs and found previously undescribed branching patterns indicating a neighborhood effect wherein the FLPs and IL2s in the anterior have differential branching compared to the more posteriorly located PVD arborizing neurons. To determine how the IL2s and FLPs differentially regulate branching, we examined several regulators of DMA-1 localization. We show that the unfolded protein response sensor IRE-1, required for FLP branching, is only required for dauer-specific branching at elevated temperatures. Interestingly, we found that ire-1 mutants have broad, organism-wide temperaturedependent effects on dauer remodeling, suggesting a previously undescribed role for IRE-1 in phenotypic plasticity. We also found that defects in other regulators of dauer remodeling including DAF-16/FOXO, DAF-9/Cytochrome P450, and DAF-18/PTEN are required for proper IL2 arborization, but dispensable for FLP branching. Interestingly, we find that TOR adaptor protein DAF-15/RAPTOR is both required for promoting IL2 branching and inhibiting precocious development of the FLPs. Our results demonstrate specific genotypic by environmental interactions regulating dendrite arborization.

The special unfolded protein response in plasma cells

“…For example, in Drosophila , IRE1’s RIDD activity is essential for differentiation of the photoreceptor cells 31 . In C elegans , IRE1 deficiency prevents normal dendrite branching in touch‐sensing neurons 32 and interferes with dendrite remodeling during developmental adaptation of the worm to harsh environment 33 . Similarly, the anticipatory nature of UPR target induction is not unique to plasma cells.…”

Neurite Branching Regulated by Neuronal Cell Surface Molecules in Caenorhabditis elegans

“…While many of the molecular mechanisms that control PVD neurite branching have been identified, it is unknown whether other highly branched C. elegans neurons are governed by similar mechanisms. However, in addition to PVD neurons, studies have shown that depletion of the DMA-1 receptor complex components and associated proteins, including DMA-1, MNR-1, LECT-2, HPO-30, TIAM-1, and ACT-4/Actin, causes reduced branching phenotypes in FLP neurons, although these neurons have distinct branching architectures during development (Liu and Shen, 2011 ; Salzberg et al, 2013 ; Díaz-Balzac et al, 2016 ; Androwski et al, 2019 ; Tang et al, 2019 ; Figure 1A ). Moreover, a proprotein convertase KPC-1/Furin, originally identified as a negative regulator of the DMA-1 complex pathway, was shown to promote both PVD and FLP branching by adjusting dendritic DMA-1 levels (Salzberg et al, 2014 ; Dong et al, 2016 ).…”

“…KPC-1 is also required for the dendritic arborization of IL2 neurons, specifically induced during dauer stages (Schroeder et al, 2013 ). Recently, it was shown that the DMA-1 complex components are also required for IL2 arborization during dauer stages (Androwski et al, 2019 ). Therefore, it is likely that different neurons utilize similar DMA-1 receptor complexes to modulate dendrite morphogenesis; however, individual ligand-receptor complex components may differ.…”