The environmental stress response regulates ribosome content in cell cycle-arrested S. cerevisiae .

Autor:	Terhorst A; David H. Koch Institute for Integrative Cancer Research, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA, United States., Sandikci A; David H. Koch Institute for Integrative Cancer Research, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA, United States., Whittaker CA; David H. Koch Institute for Integrative Cancer Research, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA, United States., Szórádi T; Institute for Systems Genetics, New York University Langone Health, New York City, NY, United States., Holt LJ; Institute for Systems Genetics, New York University Langone Health, New York City, NY, United States., Neurohr GE; David H. Koch Institute for Integrative Cancer Research, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA, United States.; Institute of Biochemistry, ETH Zurich, Zurich, Switzerland., Amon A; David H. Koch Institute for Integrative Cancer Research, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA, United States.
Jazyk:	angličtina
Zdroj:	Frontiers in cell and developmental biology [Front Cell Dev Biol] 2023 Apr 12; Vol. 11, pp. 1118766. Date of Electronic Publication: 2023 Apr 12 (Print Publication: 2023).
DOI:	10.3389/fcell.2023.1118766
Abstrakt:	Prolonged cell cycle arrests occur naturally in differentiated cells and in response to various stresses such as nutrient deprivation or treatment with chemotherapeutic agents. Whether and how cells survive prolonged cell cycle arrests is not clear. Here, we used S. cerevisiae to compare physiological cell cycle arrests and genetically induced arrests in G1-, meta- and anaphase. Prolonged cell cycle arrest led to growth attenuation in all studied conditions, coincided with activation of the Environmental Stress Response (ESR) and with a reduced ribosome content as determined by whole ribosome purification and TMT mass spectrometry. Suppression of the ESR through hyperactivation of the Ras/PKA pathway reduced cell viability during prolonged arrests, demonstrating a cytoprotective role of the ESR. Attenuation of cell growth and activation of stress induced signaling pathways also occur in arrested human cell lines, raising the possibility that the response to prolonged cell cycle arrest is conserved. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2023 Terhorst, Sandikci, Whittaker, Szórádi, Holt, Neurohr and Amon.)
Databáze:	MEDLINE
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