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The Mediator subunit MDT-15 confers metabolic adaptation to ingested material.

In eukaryotes, RNA polymerase II (Pol(II)) dependent gene expression requires accessory factors termed transcriptional coregulators. One coregulator that universally contributes to Pol(II)-dependent transcription is the Mediator, a multisubunit complex that is targeted by many transcriptional regulatory factors. For example, the Caenorhabditis elegans Mediator subunit MDT-15 confers the regulatory actions of the sterol response element binding protein SBP-1 and the nuclear hormone receptor NHR-49 on fatty acid metabolism. Here, we demonstrate that MDT-15 displays a broader spectrum of activities, and that it integrates metabolic responses to materials ingested by C. elegans. Depletion of MDT-15 protein or mutation of the mdt-15 gene abrogated induction of specific detoxification genes in response to certain xenobiotics or heavy metals, rendering these animals hypersensitive to toxin exposure. Intriguingly, MDT-15 appeared to selectively affect stress responses related to ingestion, as MDT-15 functional defects did not abrogate other stress responses, e.g., thermotolerance. Together with our previous finding that MDT-15:NHR-49 regulatory complexes coordinate a sector of the fasting response, we propose a model whereby MDT-15 integrates several transcriptional regulatory pathways to monitor both the availability and quality of ingested materials, including nutrients and xenobiotic compounds.

Pubmed ID: 18454197


  • Taubert S
  • Hansen M
  • Van Gilst MR
  • Cooper SB
  • Yamamoto KR


PLoS genetics

Publication Data

February 5, 2008

Associated Grants

  • Agency: NCI NIH HHS, Id: 5R01CA020535-29

Mesh Terms

  • Adaptation, Physiological
  • Animals
  • Caenorhabditis elegans
  • Caenorhabditis elegans Proteins
  • Food
  • Gene Expression Profiling
  • Genes, Helminth
  • Heat-Shock Response
  • Inactivation, Metabolic
  • Lipid Metabolism
  • Metals, Heavy
  • Models, Biological
  • Mutation
  • Protein Subunits
  • RNA Interference
  • Trans-Activators
  • Xenobiotics