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First published online March 24, 2005
doi: 10.1242/10.1242/dev.01776
1 Division of Neuroanatomy, Osaka University Graduate School of Medicine, Kobe
University, Kobe 650-0017, Japan
2 Department of Genome Sciences, Graduate School of Medicine, Kobe University,
Kobe 650-0017, Japan
3 CREST, Japan Science and Technology Corporation, Japan
4 Department of Physiology, Keio University School of Medicine, Tokyo 160-8582,
Japan
5 PRESTO, Japan Science and Technology Corporation, Japan
6 Division of Bioinformation, Department of Biosystems Science, Graduate School
of Science and Technology, Kobe University, Kobe 650-0017, Japan
7 Laboratory for Cell Fate Decision, Riken, Center for Developmental Biology,
Kobe 650-0047, Japan
* Author for correspondence (e-mail: sawa{at}cdb.riken.jp)
Accepted 10 February 2005
Asymmetric cell division is a fundamental process that produces cellular diversity during development. In C. elegans, the Wnt signaling pathway regulates the asymmetric divisions of a number of cells including the T blast cell. We found that the let-19 and dpy-22 mutants have defects in their T-cell lineage, and lineage analyses showed that the defects were caused by disruption in the asymmetry of the T-cell division. We found that let-19 and dpy-22 encode homologs of the human proteins MED13/TRAP240 and MED12/TRAP230, respectively, which are components of the Mediator complex. Mediator is a multi-component complex that can regulate transcription by transducing the signals between activators and RNA polymerase in vitro. We also showed that LET-19 and DPY-22 form a complex in vivo with other components of Mediator, SUR-2/MED23 and LET-425/MED6. In the let-19 and dpy-22 mutants, tlp-1, which is normally expressed asymmetrically between the T-cell daughters through the function of the Wnt pathway, was expressed symmetrically in both daughter cells. Furthermore, we found that the let-19 and dpy-22 mutants were defective in the fusion of the Pn.p cell, a process that is regulated by bar-1/ß-catenin. Ectopic cell fusion in bar-1 mutants was suppressed by the let-19 or dpy-22 mutations, while defective cell fusion in let-19 mutants was suppressed by lin-39/Hox mutations, suggesting that let-19 and dpy-22 repress the transcription of lin-39. These results suggest that LET-19 and DPY-22 in the Mediator complex repress the transcription of Wnt target genes.
Key words: Mediator, Wnt, Asymmetric cell division, C. elegans
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