2021 journal article
Cell cycle–independent integration of stress signals by Xbp1 promotes Non-G1/G0 quiescence entry
Journal of Cell Biology.
MeSH headings : Cell Cycle; Cell Nucleus / metabolism; Cell Proliferation; Microfluidics; Repressor Proteins / metabolism; Saccharomyces cerevisiae / cytology; Saccharomyces cerevisiae / metabolism; Saccharomyces cerevisiae Proteins / metabolism; Signal Transduction; Stress, Physiological; Transcription Factors / metabolism
TL;DR:
This work uses machine learning and spectral imaging to show how the stress-activated transcriptional repressor Xbp1 can drive cellular quiescence—a reversible arrest of proliferation crucial for stress survival and development—even outside the G1 cell cycle stage.
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open access via rupress.org (publisher PDF)
Source: ORCID
Added: July 11, 2022
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.