Neuronal development in Caenorhabditis elegans is regulated by inhibition of an MLK MAP kinase pathway

Genetics. 2015 Jan;199(1):151-6. doi: 10.1534/genetics.114.170589. Epub 2014 Oct 22.

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.

Keywords: JNK; MAP kinase; RPM-1; axon; synapse.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Axons / metabolism
  • Caenorhabditis elegans / genetics*
  • Caenorhabditis elegans / growth & development
  • Caenorhabditis elegans Proteins / genetics*
  • Caenorhabditis elegans Proteins / metabolism
  • Guanine Nucleotide Exchange Factors / genetics
  • Guanine Nucleotide Exchange Factors / metabolism
  • JNK Mitogen-Activated Protein Kinases / genetics*
  • JNK Mitogen-Activated Protein Kinases / metabolism
  • MAP Kinase Kinase 1 / genetics*
  • MAP Kinase Kinase 1 / metabolism
  • MAP Kinase Signaling System*
  • Neurogenesis*
  • Synapses / metabolism

Substances

  • Caenorhabditis elegans Proteins
  • Guanine Nucleotide Exchange Factors
  • RPM-1 protein, C elegans
  • JNK Mitogen-Activated Protein Kinases
  • KGB-1 protein, C elegans
  • MAP Kinase Kinase 1