MAP kinase and Wnt pathways converge to downregulate an HMG-domain repressor in Caenorhabditis elegans

Marc D. Meneghini, Tohru Ishitani, J. Clayton Carter, Naoki Hisamoto, Jun Ninomiya-Tsuji, Christopher J. Thorpe, Danielle R. Hamill, Kunihiro Matsumoto and Bruce Bowerman ()
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Marc D. Meneghini: Institute of Molecular Biology, University of Oregon
Tohru Ishitani: Graduate School of Science, Nagoya University
J. Clayton Carter: Institute of Molecular Biology, University of Oregon
Naoki Hisamoto: Graduate School of Science, Nagoya University
Jun Ninomiya-Tsuji: Graduate School of Science, Nagoya University
Christopher J. Thorpe: Institute of Molecular Biology, University of Oregon
Danielle R. Hamill: Institute of Molecular Biology, University of Oregon
Kunihiro Matsumoto: Graduate School of Science, Nagoya University
Bruce Bowerman: Institute of Molecular Biology, University of Oregon

Nature, 1999, vol. 399, issue 6738, 793-797

Abstract: Abstract The signalling protein Wnt regulates transcription factors containing high-mobility-group (HMG) domains to direct decisions on cell fate during animal development1. In Caenorhabditis elegans, the HMG-domain-containing repressor POP-1 distinguishes the fates of anterior daughter cells from their posterior sisters throughout development2,3, and Wnt signalling downregulates POP-1 activity in one posterior daughter cell called E (refs 2, 4, 5). Here we show that the genes mom-4 and lit-1 are also required to downregulate POP-1, not only in E but also in other posterior daughter cells. Consistent with action in a common pathway, mom-4 and lit-1 exhibit similar mutant phenotypes and encode components of the mitogen-activated protein kinase (MAPK) pathway that are homologous to vertebrate transforming-growth-factor-β-activated kinase (TAK1) and NEMO-like kinase (NLK), respectively. Furthermore, MOM-4 and TAK1 bind related proteins that promote their kinase activities. We conclude that a MAPK-related pathway cooperates with Wnt signal transduction to downregulate POP-1 activity. These functions are likely to be conserved in vertebrates, as TAK1 and NLK can downregulate HMG-domain-containing proteins related to POP-1 (ref. 6).

Date: 1999
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DOI: 10.1038/21666

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