Dataset Information
Moreno2019 - Stochastic model of G1 arrest due to proteostasis decline delimits replicative lifespan in yeast
Ontology highlight
ABSTRACT: This model is described within the paper: A G1 arrest due to proteostasis decline delimits replicative lifespan in yeastDavid F. Moreno, Kirsten Jenkins, Sandrine Morlot, Gilles Charvin, Attila Csikász-Nagy, Martí AldeaTo be implemented in Copasi.Missing Event due to difficulties in SBML conversion to run model upon loading model in COPASI, create an event called Budding. Set the trigger expression to: {Whi5.ParticleNumber} lt 250*({Whi5i.ParticleNumber}+{Whi5.ParticleNumber})/({Whi5.InitialParticleNumber}+{Whi5i.InitialParticleNumber}) AND {Values[Budding]} lt 1. Uncheck boxes for fire at initial time if true and trigger must remain true.Leave priority box blank. Set delay to None.There are 3 targets: the value of budding which should be set to one;the time at budding which should be set to the time; and the unsynced generation which should be set to generation.
SUBMITTER: Krishna Kumar Tiwari
PROVIDER: MODEL1901210001 | biostudies-other |
SECONDARY ACCESSION(S): 31518229
REPOSITORIES: biostudies-other
Publications
Proteostasis collapse, a hallmark of aging, hinders the chaperone-Start network and arrests cells in G1.
eLife 20190913
Loss of proteostasis and cellular senescence are key hallmarks of aging, but direct cause-effect relationships are not well understood. We show that most yeast cells arrest in G1 before death with low nuclear levels of Cln3, a key G1 cyclin extremely sensitive to chaperone status. Chaperone availability is seriously compromised in aged cells, and the G1 arrest coincides with massive aggregation of a metastable chaperone-activity reporter. Moreover, G1-cyclin overexpression increases lifespan in ...[more]
