title: The JNK-like MAPK KGB-1 of Caenorhabditis elegans promotes reproduction, lifespan, and gene expressions for protein biosynthesis and germline homeostasis but interferes with hyperosmotic stress tolerance.
abstract: OBJECTIVE
  This study focused on the role of the JNK-like MAPK (mitogen-activated protein kinase) KGB-1 (kinase, GLH-binding 1) for osmoprotection and other vital functions.
  
  
  METHODS
  We mapped KGB-1 expression patterns and determined lifespan, reproduction and survival rates as well as changes in body volume, motility, and GPDH (glycerol-3-phosphate dehydrogenase) activity for glycerol production in wildtype (WT), different signaling mutants (including a kgb-1 deletion mutant, kgb-1∆) and RNAi-treated worms under control and hyperosmotic conditions. KGB-1-mediated gene expressions were studied, for instance, by RNA Sequencing, with the resulting transcriptome data analyzed using orthology-based approaches.
  
  
  RESULTS
  Surprisingly, mutation/RNAi of kgb-1 and fos-1 (gene for an AP-1, activator protein 1, element) significantly promoted hyperosmotic resistance, even though hyperosmotic GPDH activity was higher in WT than in kgb-1∆. KGB-1 and moderate hyperosmolarity promoted and severe hyperosmolarity repressed kgb-1, fos-1, and jun-1 (gene for another AP-1 element) expression. Transcriptome profiling revealed, for instance, down-regulated genes for protein biosynthesis and up-regulated genes for membrane transporters in kgb-1∆ and up-regulated genes for GPDH-1 or detoxification in WT, with the latter indicating cellular damage and less effective osmoprotection in WT.
  
  
  CONCLUSIONS
  KGB-1 promotes reproduction and lifespan and fosters gene expressions for AP-1 elements, protein biosynthesis, and balanced gametogenesis, but inhibits expressions for membrane transporters perhaps in order to control energy consumption. Reduced protein biosyntheses and enhanced membrane transports in kgb-1∆ most likely contribute to the high hyperosmotic tolerance of the mutant by easing the burden of the existing chaperone machinery and promoting regulatory volume increases upon hyperosmotic stress.
authors.affiliation: Institute of Zoophysiology, University of Münster (WWU), Münster, Germany.
authors.forename: Peter
authors.initials: P
authors.lastname: Gerke
authors.forename: Alex
authors.initials: A
authors.lastname: Keshet
authors.forename: Ansgar
authors.initials: A
authors.lastname: Mertenskötter
authors.forename: Rüdiger J
authors.initials: RJ
authors.lastname: Paul
mesh_terms: D000818:Animals; D017173:Caenorhabditis elegans / Q000235:genetics* / Q000254:growth & development; D029742:Caenorhabditis elegans Proteins / Q000235:genetics*; D018507:Gene Expression Regulation, Developmental; D005854:Germ Cells / Q000378:metabolism; D048031:JNK Mitogen-Activated Protein Kinases / Q000235:genetics*; D009997:Osmotic Pressure; D014176:Protein Biosynthesis / Q000235:genetics; D012098:Reproduction / Q000235:genetics*
chemical_list: D029742:Caenorhabditis elegans Proteins; D048031:JNK Mitogen-Activated Protein Kinases; C524496:KGB-1 protein, C elegans