Stress-Induced Growth Rate Reduction Restricts Metabolic Resource Utilization to Modulate Osmo-Adaptation Time
Provided here is the .xls annotated source data used to generate all figures included in the manuscript. When we studied this interplay between cell cycle and stress response in the S. cerevisiae hyperosmotic shock response (HOG), we found that decoupling the stress response program from the cell cycle machinery in a mutant background led to an adaptive stress response that was substantially accelerated compared to the wild type strain. We pursued this observation mechanistically to uncover that stress-induced growth slowdown tapered the flux of internal carbon sources, specifically glycogen into glycerol. By contrast, concomitant growth progression diverted a surplus of glycogen catabolism products into the stress adaptation program. We then went further, asking why a wild type cell would ration its metabolic resources, mediated through cell cycle control, even under acute stress. Our experiments uncovered a fitness tradeoff that makes this rationing of resources vitally important under repeated stress.