Our Research
Movement precision, a key feature of animal movement, is ultimately determined by the resolution of the motor circuit at the level of single neurons and synapses. However, other factors such as muscle quality/quantity and joint flexibility also affect locomotion. Hence, it is not clear to what extent the fineness of the motor circuit determines physical ability. We tackle this question using Caenorhabditis elegans as a model system. C. elegans has a simple nervous system that consists of only 302 neurons, much less compared with the number of neurons in human (more than 1 billion), mouse (70,000,000) or fly (100,000). Individual neurons can be visualized with cell-specific markers in vivo. The complete neural connection map and cell lineage are available (Sulston and Horvitz, 1977; Sulston et al., 1983; White et al., 1986). Most importantly, the nervous system is largely dispensable under laboratory conditions, allowing us to study any neurological abnormalities in vivo. These features make C. elegans a powerful genetic model system for studying development of the nervous system. In worms locomotion is regulated by 6 types of motor neurons. Each neuron in the same class innervates a non-overlapping segment of the muscle field by restricting its synapses to a distinct sub-axonal region. This type of innervation generates a phenomenon we term “synaptic tiling”. Previously we developed a genetic marker to visualize synaptic tiling between two motor neurons, and showed that Semaphorin/Plexin signaling and Wnt signaling cooperatively regulate synaptic tiling (Mizumoto and Shen. Neuron 2013; Mizumoto and Shen Cell Rep 2013).
Currently, we are conducting following research projects amongst others:
- Molecular mechanisms of Sema/Plexin signaling in synaptic tiling.
- The roles of cell fate determinants in synapse pattern formation
- Functions of gap junction proteins in neurodevelopment
- Gradient-dependent and independent Wnt signaling in neurodevelopment
- Genetic mechanisms of synapse assembly