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The TOR pathway interacts with the insulin signaling pathway to regulate C. elegans larval development, metabolism

Kailiang Jia1, Di Chen, Donald L Riddle

  • 1Molecular Biology Program and Division of Biological Sciences, University of Missouri, Columbia, MO 65211, USA.

Development (Cambridge, England)
|July 16, 2004
PubMed

Insights

Target-of-rapamycin (TOR) pathway regulates C. elegans development and lifespan. Insulin/IGF signaling converges with nutrient signaling on raptor to control larval arrest, fat metabolism, and longevity.

Area of Science:

  • Cell Biology
  • Genetics
  • Developmental Biology

Background:

  • The highly conserved target-of-rapamycin (TOR) protein kinases are crucial regulators of cell growth, responding to nutrient availability and growth factors.
  • In mammals, TOR interacts with raptor to mediate nutrient signals to the translational machinery.

Purpose of the Study:

  • To investigate the role of the TOR pathway in Caenorhabditis elegans development and lifespan.
  • To elucidate the regulatory mechanisms controlling the TOR pathway in response to developmental and environmental cues.

Main Methods:

  • Genetic analysis of C. elegans mutants in CeTOR (let-363) and raptor (daf-15).
  • Phenotypic characterization of dauer-like larval arrest, fat metabolism, and adult lifespan.
  • Investigation of transcriptional regulation of daf-15 by DAF-16 (FOXO transcription factor) and its link to daf-2 insulin/IGF signaling.

Main Results:

  • Mutations in CeTOR and raptor lead to dauer-like larval arrest in C. elegans.
  • daf-15 (raptor) and let-363 (CeTOR) mutants exhibit altered metabolism with increased fat accumulation.
  • Mutations in raptor extend the adult lifespan of C. elegans.
  • daf-15 transcription is regulated by DAF-16, which is itself controlled by daf-2 insulin/IGF signaling.

Conclusions:

  • The TOR pathway, comprising CeTOR and raptor, plays a critical role in regulating C. elegans dauer diapause and larval development.
  • A novel regulatory mechanism is identified where daf-2 insulin/IGF signaling converges with nutrient signaling on DAF-15 (raptor) to control C. elegans development, metabolism, and lifespan.

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