Data from single-cell microscopy experiments for "Distributing tasks via multiple input pathways increases cellular survival in stress" by Granados, Crane, Montano-Gutierrez, Tanaka, Voliotis, & Swain. Improving in one aspect of a task can undermine performance in another, but how such opposing demands play out in single cells and impact on fitness is mostly unknown. Here we study budding yeast in dynamic environments of hyperosmotic stress and show how the corresponding signalling network increases cellular survival both by assigning the requirements of high response speed and high response accuracy to two separate input pathways and by having these pathways interact to converge on Hog1, a p38 MAP kinase. Cells with only the less accurate, reflex-like pathway are fitter in sudden stress, whereas cells with only the slow, more accurate pathway are fitter in fluctuating but increasing stress. Our results demonstrate that cellular signalling is vulnerable to trade-offs in performance, but that these trade-offs can be mitigated by assigning the opposing tasks to different signalling subnetworks. Such division of labour could function broadly within cellular signal transduction.Text files of single-cell data in six ramps and six steps of osmotic stress for wild-type and STE11 and SSK1 deletion mutants of budding yeast. See README.txt.