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Resources » Paper

Hiroki, S. et al. (2019) International Worm Meeting "Exploring regulatory mechanism of chemotaxis towards preferred salt concentration through DAG/PKC signaling."

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  • Comments on Hiroki, S. et al. (2019) International Worm Meeting "Exploring regulatory mechanism of chemotaxis towards preferred salt concentration through DAG/PKC signaling." (0)

  • Overview

    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00058515

    Hiroki, S., Kunitomo, H., Ikeda, M., Mori, I., & Iino, Y (2019). Exploring regulatory mechanism of chemotaxis towards preferred salt concentration through DAG/PKC signaling presented in International Worm Meeting. Unpublished information; cite only with author permission.

    The nematode C. elegans has an ability to navigate towards various attractants- i.e. odorants, temperature, and soluble chemicals. Previously, we reported that worms can memorize and migrate towards the concentration of NaCl at which they were cultivated. In addition, our recent study showed that the DAG/PKC signaling pathway in gustatory sensory neuron ASER plays a critical role in this behavior, salt concentration chemotaxis. These studies suggested that synaptic abundance of DAG encode the difference between current concentration and cultivation concentration of NaCl, and subsequent increase or decrease of PKC-1 activity determines whether they climb up or down the NaCl gradient. In this study, we explore how PKC-1 activation leads to chemotaxis towards high NaCl concentration. We evaluated impacts of ablation of first-layer interneurons on salt chemotaxis of the transgenic strain ASERp::pkc-1(gf) carrying an activated form of PKC-1 in ASER. Triple ablation of first-layer interneurons, AIA, AIB and AIY, spared chemotaxis to high NaCl, while ablation of AIZ interneuron, which was not considered directly connected to ASER, diminished chemotaxis to higher salt concentration. Indeed, ASER-specific expression of unc-64 syntaxin, which is required for synaptic transmission, rescued the response of AIZ to NaCl downstep stimulation in the unc-64(e246) mutant background, suggesting that AIZ directly receives input from ASER. On the other hand, chemotaxis to lower salt concentration under the pkc-1(WT) background required AIB, AIY, and AIZ.Thus, we assumed that PKC-1 activation alters recruitment of circuit usage of sensory information processing. We are now performing further analyses on how PKC-1 activation regulates presynaptic activity of ASER using a genetic approach and imaging techniques.

    Affiliations:
    - Department of Molecular Biology, Graduate School of Science, Nagoya University
    - Department of Biology, Graduate School of Science, University of Tokyo


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