dc.contributor.author | Moreno, David F. | |
dc.contributor.author | Parisi, Eva | |
dc.contributor.author | Yahya, Galal | |
dc.contributor.author | Vaggi, Federico | |
dc.contributor.author | Csikász-Nagy, Attila | |
dc.contributor.author | Aldea Malo, Martí | |
dc.date.accessioned | 2019-10-24T15:09:45Z | |
dc.date.available | 2019-10-24T15:09:45Z | |
dc.date.issued | 2019-04-15 | |
dc.identifier.citation | Moreno, David F.; Parisi, Eva; Yahya, Galal; Vaggi, Federico; Csikasz-Nagy, Attila; Aldea Malo, Martí. «Competition in the chaperone-client network subordinates cell-cycle entry to growth and stress». Life Science Alliance, 2019, vol. 2, núm. 2, art. e201800277. Disponible en: <https://www.life-science-alliance.org/content/2/2/e201800277/tab-rc>. Fecha de acceso: 24 oct. 2019. DOI: 10.26508/lsa.201800277 | ca |
dc.identifier.issn | 2575-1077 | ca |
dc.identifier.uri | http://hdl.handle.net/20.500.12328/1271 | |
dc.description.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. | ca |
dc.format.extent | 16 | ca |
dc.language.iso | eng | ca |
dc.publisher | Life Science Alliance | ca |
dc.relation.ispartof | Life Science Alliance | ca |
dc.relation.ispartofseries | 2;2 | |
dc.rights | http://creativecommons.org/licenses/by-nc-nd/4.0/ | ca |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 International | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.subject.other | Cicle cel·lular | ca |
dc.subject.other | Cell cycle | ca |
dc.subject.other | Cells | ca |
dc.subject.other | Cells--Growth-Molecular aspects | ca |
dc.subject.other | Células | ca |
dc.subject.other | Cèl·lules | ca |
dc.subject.other | Cèl·lules--Creixement--Aspectes moleculars | ca |
dc.title | Competition in the chaperone-client network subordinates cell-cycle entry to growth and stress | ca |
dc.type | info:eu-repo/semantics/article | ca |
dc.description.version | info:eu-repo/semantics/acceptedVersion | ca |
dc.embargo.terms | cap | ca |
dc.subject.udc | 61 | ca |
dc.identifier.doi | https://doi.org/10.26508/lsa.201800277 | ca |