PT - JOURNAL ARTICLE AU - David F Moreno AU - Eva Parisi AU - Galal Yahya AU - Federico Vaggi AU - Attila Csikász-Nagy AU - Martí Aldea TI - Competition in the chaperone-client network subordinates cell-cycle entry to growth and stress AID - 10.26508/lsa.201800277 DP - 2019 Apr 01 TA - Life Science Alliance PG - e201800277 VI - 2 IP - 2 4099 - https://www.life-science-alliance.org/content/2/2/e201800277.short 4100 - https://www.life-science-alliance.org/content/2/2/e201800277.full SO - Life Sci. Alliance2019 Apr 01; 2 AB - The precise coordination of growth and proliferation has a universal prevalence in cell homeostasis. As a prominent property, cell size is modulated by the coordination between these processes in bacterial, yeast, and mammalian cells, but the underlying molecular mechanisms are largely unknown. Here, we show that multifunctional chaperone systems play a concerted and limiting role in cell-cycle entry, specifically driving nuclear accumulation of the G1 Cdk–cyclin complex. Based on these findings, we establish and test a molecular competition model that recapitulates cell-cycle-entry dependence on growth rate. As key predictions at a single-cell level, we show that availability of the Ydj1 chaperone and nuclear accumulation of the G1 cyclin Cln3 are inversely dependent on growth rate and readily respond to changes in protein synthesis and stress conditions that alter protein folding requirements. Thus, chaperone workload would subordinate Start to the biosynthetic machinery and dynamically adjust proliferation to the growth potential of the cell.