ABSTRACT
Administration of the small macrolide antibiotic rapamycin to eukaryotic cells results in physiological responses that mimic nutrient starvation, and in many ways resembles nitrogen starvation. The target for rapamycin action in these cells is a family of con served kinases known as TOR (target of rapamycin). Tor kinases are essential for the normal function of eukaryotic cells and participate in the integration and control of nutrient-sensing signals. Inhibition of Tor by rapamycin triggers a variety of molecular responses. These include global changes in gene expression, which are mediated by effects on both transcription and translation, as well as direct effects on other cellular processes. Within this context, inhibition of TOR has a number of effects on membrane trafficking, including the induction of auto phagy. This chapter represents a compendium of our current state of knowledge on the role of TOR family proteins, their architecture and molecular interactions, as well as the mechanisms by which inhibition of TO R leads to various cellular responses. This general perspective is aimed at understanding the relative role of the induction of autophagy within the broader response of cells to rapamycin and starvation.
