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Published on: November 29, 2016
Neuronal development in Caenorhabditis elegans is regulated by inhibition of an MLK MAP kinase pathway
Scott T Baker1, Shane M Turgeon2, Erik D Tulgren3
1Department of Neuroscience, The Scripps Research Institute, Scripps Florida, Jupiter, Florida 33458 Department of Pharmacology, University of Minnesota, Minneapolis, Minnesota 55455.
Abstract:
We show that loss-of-function mutations in kinases of the MLK-1 pathway (mlk-1, mek-1, and kgb-1/jnk) function cell-autonomously in neurons to suppress defects in synapse formation and axon termination caused by rpm-1 loss of function. Our genetic analysis also suggests that the phosphatase PPM-1, like RPM-1, is a potential inhibitor of kinases in the MLK-1 pathway.
Insights
Loss-of-function mutations in the MLK-1 pathway kinases suppress neuronal defects caused by rpm-1 mutations. This suggests PPM-1 phosphatase may also inhibit MLK-1 pathway kinases, similar to RPM-1.
Area of Science:
- Neurobiology
- Molecular Biology
- Genetics
Background:
- The MLK-1 pathway is involved in neuronal development.
- RPM-1 plays a role in synapse formation and axon termination.
Purpose of the Study:
- To investigate the role of MLK-1 pathway kinases in neuronal development.
- To explore the relationship between RPM-1 and the MLK-1 pathway.
Main Methods:
- Genetic analysis in model organisms.
- Loss-of-function mutation studies.
Main Results:
- Mutations in mlk-1, mek-1, and kgb-1/jnk suppress rpm-1 loss-of-function defects in neurons.
- These kinase mutations act cell-autonomously in neurons.
- Genetic data suggest PPM-1 phosphatase inhibits MLK-1 pathway kinases.
Conclusions:
- The MLK-1 pathway kinases are critical for proper synapse formation and axon termination.
- RPM-1 and PPM-1 may function in a common pathway to regulate neuronal development.
