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Competition in the chaperone-client network subordinates cell-cycle entry to growth and stress

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Competition in the chaperone-client network subordinates cell-cycle entry to growth and stress. / Moreno, David F.; Parisi, Eva; Yahya, Galal; Vaggi, Federico; Csikász-Nagy, Attila; Aldea, Martí.

In: Life Science Alliance, Vol. 2, No. 2, e201800277, 15.04.2019.

Research output: Contribution to journalArticle

Harvard

Moreno, DF, Parisi, E, Yahya, G, Vaggi, F, Csikász-Nagy, A & Aldea, M 2019, 'Competition in the chaperone-client network subordinates cell-cycle entry to growth and stress', Life Science Alliance, vol. 2, no. 2, e201800277. https://doi.org/10.26508/lsa.201800277

APA

Moreno, D. F., Parisi, E., Yahya, G., Vaggi, F., Csikász-Nagy, A., & Aldea, M. (2019). Competition in the chaperone-client network subordinates cell-cycle entry to growth and stress. Life Science Alliance, 2(2), [e201800277]. https://doi.org/10.26508/lsa.201800277

Vancouver

Moreno DF, Parisi E, Yahya G, Vaggi F, Csikász-Nagy A, Aldea M. Competition in the chaperone-client network subordinates cell-cycle entry to growth and stress. Life Science Alliance. 2019 Apr 15;2(2). e201800277. https://doi.org/10.26508/lsa.201800277

Author

Moreno, David F. ; Parisi, Eva ; Yahya, Galal ; Vaggi, Federico ; Csikász-Nagy, Attila ; Aldea, Martí. / Competition in the chaperone-client network subordinates cell-cycle entry to growth and stress. In: Life Science Alliance. 2019 ; Vol. 2, No. 2.

Bibtex Download

@article{d7152b85192e469a87375abd4859183d,
title = "Competition in the chaperone-client network subordinates cell-cycle entry to growth and stress",
abstract = "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.",
author = "Moreno, {David F.} and Eva Parisi and Galal Yahya and Federico Vaggi and Attila Csik{\'a}sz-Nagy and Mart{\'i} Aldea",
year = "2019",
month = "4",
day = "15",
doi = "10.26508/lsa.201800277",
language = "English",
volume = "2",
journal = "Life Science Alliance",
issn = "2575-1077",
publisher = "Rockefeller University Press",
number = "2",

}

RIS (suitable for import to EndNote) Download

TY - JOUR

T1 - Competition in the chaperone-client network subordinates cell-cycle entry to growth and stress

AU - Moreno, David F.

AU - Parisi, Eva

AU - Yahya, Galal

AU - Vaggi, Federico

AU - Csikász-Nagy, Attila

AU - Aldea, Martí

PY - 2019/4/15

Y1 - 2019/4/15

N2 - 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.

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.

UR - http://www.scopus.com/inward/record.url?scp=85065728840&partnerID=8YFLogxK

U2 - 10.26508/lsa.201800277

DO - 10.26508/lsa.201800277

M3 - Article

AN - SCOPUS:85065728840

VL - 2

JO - Life Science Alliance

JF - Life Science Alliance

SN - 2575-1077

IS - 2

M1 - e201800277

ER -

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