title: C. elegans anaplastic lymphoma kinase ortholog SCD-2 controls dauer formation by modulating TGF-beta signaling.
abstract: BACKGROUND
  Different environmental stimuli, including exposure to dauer pheromone, food deprivation, and high temperature, can induce C. elegans larvae to enter the dauer stage, a developmentally arrested diapause state. Although molecular and cellular pathways responsible for detecting dauer pheromone and temperature have been defined in part, other sensory inputs are poorly understood, as are the mechanisms by which these diverse sensory inputs are integrated to achieve a consistent developmental outcome.
  
  
  RESULTS
  In this paper, we analyze a wild C. elegans strain isolated from a desert oasis. Unlike wild-type laboratory strains, the desert strain fails to respond to dauer pheromone at 25 degrees C, but it does respond at higher temperatures, suggesting a unique adaptation to the hot desert environment. We map this defect in dauer response to a mutation in the scd-2 gene, which, we show, encodes the nematode anaplastic lymphoma kinase (ALK) homolog, a proto-oncogene receptor tyrosine kinase. scd-2 acts in a genetic pathway shown here to include the HEN-1 ligand, the RTK adaptor SOC-1, and the MAP kinase SMA-5. The SCD-2 pathway modulates TGF-beta signaling, which mediates the response to dauer pheromone, but SCD-2 might mediate a nonpheromone sensory input, such as food.
  
  
  CONCLUSIONS
  Our studies identify a new sensory pathway controlling dauer formation and shed light on ALK signaling, integration of signaling pathways, and adaptation to extreme environmental conditions.
authors.affiliation: Howard Hughes Medical Institute and Department of Cell Biology, University of California, Berkeley, CA 94720, USA. dreiner@med.unc.edu
authors.forename: David J
authors.initials: DJ
authors.lastname: Reiner
authors.forename: Michael
authors.initials: M
authors.lastname: Ailion
authors.forename: James H
authors.initials: JH
authors.lastname: Thomas
authors.forename: Barbara J
authors.initials: BJ
authors.lastname: Meyer
mesh_terms: D000220:Adaptation, Biological; D000818:Animals; D017173:Caenorhabditis elegans / Q000201:enzymology* / Q000235:genetics / Q000502:physiology; D029742:Caenorhabditis elegans Proteins / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D003889:Desert Climate; D005247:Feeding Behavior; D008024:Ligands; D009154:Mutation; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism; D010641:Phenotype; D010675:Pheromones / Q000378:metabolism; D011505:Protein-Tyrosine Kinases / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D015398:Signal Transduction; D051785:Smad Proteins / Q000235:genetics / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000378:metabolism*
chemical_list: D029742:Caenorhabditis elegans Proteins; C108738:DAF-3 protein, C elegans; C459682:HEN-1 protein, C elegans; D008024:Ligands; D009419:Nerve Tissue Proteins; D010675:Pheromones; C503591:SMA-5 protein, C elegans; D051785:Smad Proteins; D016212:Transforming Growth Factor beta; C439708:soc-1 protein, C elegans; D011505:Protein-Tyrosine Kinases; C532034:Scd-2 protein, C elegans