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Resources » Paper

Laura Moffat et al. (2006) Neuronal Development, Synaptic Function, and Behavior Meeting "PLR-1 Controls Anteroposterior Neuronal Polarity and Downregulates Wnt Signaling"

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    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00028090

    Laura Moffat, Anastasia Bakoulis, & Scott Clark (2006). PLR-1 Controls Anteroposterior Neuronal Polarity and Downregulates Wnt Signaling presented in Neuronal Development, Synaptic Function, and Behavior Meeting. Unpublished information; cite only with author permission.

    Secreted Wnts regulate anteroposterior (AP) cell migrations, axon guidance and neuronal polarity. For example, disruption of Wnt signaling inverts ALM and PLM polarity: the anterior process adopts the length, branching pattern and synaptic properties of the wild-type posterior process and vice versa. The interneuron AVG, which is located in the retrovesicular ganglion, is polarized and has a short anterior process and a long posterior process that extends along the ventral nerve cord to the tail. plr-1 mutations caused AVG AP polarity to be reversed or symmetric, similar to the effect of Wnt mutations on ALM/PLM. In addition, plr-1 mutations altered the long-range AP cell migrations of CAN and HSN. PLR-1 has a protease-associated domain, a transmembrane domain and a RING finger domain. PLR-1 belongs to a family of transmembrane E3 ubiquitin ligases, which includes GRAIL, Goliath and plant vacuolar sorting proteins, implicated in regulating membrane trafficking. We found that PLR-1 was associated with Golgi as well as early and late endosomes, supporting the idea that PLR-1 also functions in membrane trafficking. The cytoplasmic domain, which contains the RING finger motif, was both necessary and sufficient for Golgi and endosomal localization. Both plr-1 mutations affect the RING finger domain, suggesting that ubiquitin ligase activity is required for function. plr-1-gfp was expressed in the excretory canal, tail epidermis and many neurons, including AVG, CAN and HSN. AVG, CAN and HSN expression was transient and coincided with differentiation and/or migration. Using the lin-11 promoter, we showed that PLR-1 acts autonomously to control AVG AP polarity. ALM/PLM polarity was wild-type in plr-1 mutants. Surprisingly, ectopic expression of PLR-1 in the mechanosensory neurons induced highly specific Wnt-related phenotypes, including defects in ALM/PLM polarity, PVM migration and AVM axon growth, indicating that PLR-1 can downregulate Wnt signaling in responding cells. We propose that PLR-1 regulates trafficking of a transmembrane protein, such as a receptor, needed for Wnt signaling and that plr-1 polarity and migration defects result from a misregulation of signaling.


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