PodcastCell Biology

Science Signaling Podcast: 16 December 2014

+ See all authors and affiliations

Sci. Signal.  16 Dec 2014:
Vol. 7, Issue 356, pp. pc32
DOI: 10.1126/scisignal.aaa4034

You are currently viewing the abstract.

View Full Text

Abstract

This Podcast features an interview with Benjamin Tu, author of a Research Article that appears in the 16 December 2014 issue of Science Signaling, about metabolic rewiring that enables cells to survive nutrient limitation. Under nutrient-replete conditions, signaling through the target of rapamycin complex 1 (TORC1) promotes protein synthesis and cell growth. Inhibition of TORC1 signaling under nutrient-limiting conditions promotes autophagy, a set of processes through which cells can break down nonessential or damaged cellular components to recycle their chemical constituents. In yeast, a complex containing Npr2 mediates TORC1 inhibition when nutrients are limiting to promote autophagy. Knocking out npr2 prevents yeast from initiating autophagy under nutrient-limiting conditions, yet yeast lacking Npr2 actually proliferate faster than normal cells under nutrient-limiting conditions. Laxman et al. found that, when grown on a nonfermentable carbon source instead of glucose, npr2-deficient cells synthesized glutamine and used it as a nitrogen donor to make nitrogen-containing metabolites. These cells also had increased abundance of S-adenosyl methionine (SAM), which drives cell growth.

View Full Text