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Resources » Paper

Kim Schuske et al. (2006) Neuronal Development, Synaptic Function, and Behavior Meeting "Overexpression of the Type I PIP Kinase in Neurons Causes Progressive Neuron Overgrowth and Degeneration in C. elegans"

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    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00028089

    Kim Schuske, Michael Bastiani, Deepa Joshi, Tamara Chessa, Nullin Divecha, Maelle Jospin, & David Weinkove (2006). Overexpression of the Type I PIP Kinase in Neurons Causes Progressive Neuron Overgrowth and Degeneration in C. elegans presented in Neuronal Development, Synaptic Function, and Behavior Meeting. Unpublished information; cite only with author permission.

    During axon outgrowth, dramatic remodeling of the membrane and actin cytoskeleton of a growth cone enables the neuron to migrate and find its correct target tissue. Phosphatidylinositol 4,5 bisphosphate (PIP2) is an important membrane lipid that is required for multiple cell functions including membrane trafficking and actin polymerization. Therefore, we proposed that misregulation of PIP2 synthesis by overexpressing the type 1 PIP kinase (PPK-1) in Caenorhabditis elegans neurons would disrupt axon outgrowth. We have shown that PIP2 levels in L1 larvae are indeed higher in worms overexpressing PPK-1 than in wild type animals. Surprisingly, we have not detected defects in larval neuronal development. However, neurons in adults form extensive projections extending from cell bodies, nerve cord, and commissural axons. As adult animals age, some neurons become progressively overgrown, while others appear to degenerate. These data suggest that neurons in adult animals are susceptible to PIP2 induced actin polymerization and membrane growth. Since many of the signaling pathways activated by PIP2 are not known, we are screening for second site genetic suppressors of the uncoordinated phenotype associated with animals overexpressing PPK-1. One of the suppressors was identified as a mutation in the unc-80 gene. We have cloned unc-80 and confirmed what others had previously shown ("unc-80 is a stupid gene" Hudson, et al, WBG114; 20 1990). It encodes a novel neuronal protein that has a single ortholog in all animals. Interestingly, unc-80 was also identified as a suppressor of synaptojanin mutants. Synaptojanin is a lipid phosphatase that is required to degrade PIP2 during synaptic vesicle recycling. Taken together, our current data suggests UNC-80 functions in PIP2 signaling in neurons.


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