TOR Signaling and Nutrient Sensing

Annu Rev Plant Biol. 2016 Apr 29;67:261-85. doi: 10.1146/annurev-arplant-043014-114648. Epub 2016 Feb 22.

Abstract

All living organisms rely on nutrients to sustain cell metabolism and energy production, which in turn need to be adjusted based on available resources. The evolutionarily conserved target of rapamycin (TOR) protein kinase is a central regulatory hub that connects environmental information about the quantity and quality of nutrients to developmental and metabolic processes in order to maintain cellular homeostasis. TOR is activated by both nitrogen and carbon metabolites and promotes energy-consuming processes such as cell division, mRNA translation, and anabolism in times of abundance while repressing nutrient remobilization through autophagy. In animals and yeasts, TOR acts antagonistically to the starvation-induced AMP-activated kinase (AMPK)/sucrose nonfermenting 1 (Snf1) kinase, called Snf1-related kinase 1 (SnRK1) in plants. This review summarizes the immense knowledge on the relationship between TOR signaling and nutrients in nonphotosynthetic organisms and presents recent findings in plants that illuminate the crucial role of this pathway in conveying nutrient-derived signals and regulating many aspects of metabolism and growth.

Keywords: SnRK1 kinase; TOR kinase; nitrogen; nutrient signaling; sugars.

Publication types

  • Review

MeSH terms

  • Autophagy
  • Carbon / metabolism*
  • Nitrogen / metabolism*
  • Plant Development
  • Plants / metabolism*
  • Protein-Serine-Threonine Kinases / metabolism*
  • Signal Transduction
  • TOR Serine-Threonine Kinases / metabolism*

Substances

  • Carbon
  • SNF1-related protein kinases
  • TOR Serine-Threonine Kinases
  • Protein-Serine-Threonine Kinases
  • Nitrogen