Science Signaling Podcast: 16 December 2014

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 nutrientreplete conditions, signaling through the target of rapamycin complex 1 (TORC1) promotes protein synthesis and cell growth. Inhibition of TORC1 signaling under nutrientlimiting 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 nutrientlimiting conditions, yet yeast lacking Npr2 actually proliferate faster than normal cells under nutrientlimiting 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 nitrogencontaining metabolites. These cells also had increased abundance of Sadenosyl methionine (SAM), which drives cell growth.