Cellular quiescence is a nonproliferative state required for cell survival under stress and during development. In most quiescent cells, proliferation is stopped in a reversible state of low Cdk1 kinase activity; in many organisms, however, quiescent states with high-Cdk1 activity can also be established through still uncharacterized stress or developmental mechanisms. Here, we used a microfluidics approach coupled to phenotypic classification by machine learning to identify stress pathways associated with starvation-triggered high-Cdk1 quiescent states in Saccharomyces cerevisiae. We found that low- and high-Cdk1 quiescent states shared a core of stress-associated processes, such as autophagy, protein aggregation, and mitochondrial up-regulation, but differed in the nuclear accumulation of the stress transcription factors Xbp1, Gln3, and Sfp1. The decision between low- or high-Cdk1 quiescence was controlled by cell cycle–independent accumulation of Xbp1, which acted as a time-delayed integrator of the duration of stress stimuli. Our results show how cell cycle–independent stress-activated factors promote cellular quiescence outside G1/G0.
Cell cycle–independent integration of stress signals by Xbp1 promotes Non-G1/G0 quiescence entry
O. Argüello-Miranda’s present address is Department of Plant and Microbial Biology, North Carolina State University, Raleigh, NC.
A preprint of this paper was posted in bioRxiv on March 24, 2021.
- Award Id(s): RP150596,RR150058
- Award Id(s): I-1919-20170325
- Award Id(s): K99GM135487
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Orlando Argüello-Miranda, Ashley J. Marchand, Taylor Kennedy, Marielle A.X. Russo, Jungsik Noh; Cell cycle–independent integration of stress signals by Xbp1 promotes Non-G1/G0 quiescence entry. J Cell Biol 3 January 2022; 221 (1): e202103171. doi: https://doi.org/10.1083/jcb.202103171
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