title: Autophagy is required for G₁/G₀ quiescence in response to nitrogen starvation in Saccharomyces cerevisiae.
abstract: In response to starvation, cells undergo increased levels of autophagy and cell cycle arrest but the role of autophagy in starvation-induced cell cycle arrest is not fully understood. Here we show that autophagy genes regulate cell cycle arrest in the budding yeast Saccharomyces cerevisiae during nitrogen starvation. While exponentially growing wild-type yeasts preferentially arrest in G₁/G₀ in response to starvation, yeasts carrying null mutations in autophagy genes show a significantly higher percentage of cells in G₂/M. In these autophagy-deficient yeast strains, starvation elicits physiological properties associated with quiescence, such as Snf1 activation, glycogen and trehalose accumulation as well as heat-shock resistance. However, while nutrient-starved wild-type yeasts finish the G₂/M transition and arrest in G₁/G 0₀ autophagy-deficient yeasts arrest in telophase. Our results suggest that autophagy is crucial for mitotic exit during starvation and appropriate entry into a G₁/G₀ quiescent state.
authors.affiliation: Center for Autophagy Research; University of Texas Southwestern Medical Center; Dallas, TX USA; Department of Internal Medicine; University of Texas Southwestern Medical Center; Dallas, TX USA.
authors.forename: Zhenyi
authors.initials: Z
authors.lastname: An
authors.affiliation: Department of Internal Medicine; University of Texas Southwestern Medical Center; Dallas, TX USA.
authors.forename: Amina
authors.initials: A
authors.lastname: Tassa
authors.affiliation: Department of Internal Medicine; University of Texas Southwestern Medical Center; Dallas, TX USA.
authors.forename: Collin
authors.initials: C
authors.lastname: Thomas
authors.affiliation: Department of Clinical Sciences; University of Texas Southwestern Medical Center; Dallas, TX USA.
authors.forename: Rui
authors.initials: R
authors.lastname: Zhong
authors.affiliation: Department of Clinical Sciences; University of Texas Southwestern Medical Center; Dallas, TX USA.
authors.forename: Guanghua
authors.initials: G
authors.lastname: Xiao
authors.affiliation: Sanford Burnham Medical Research Institute; La Jolla, CA USA.
authors.forename: Rati
authors.initials: R
authors.lastname: Fotedar
authors.affiliation: Department of Biochemistry; University of Texas Southwestern Medical Center; Dallas, TX USA.
authors.forename: Benjamin P
authors.initials: BP
authors.lastname: Tu
authors.affiliation: Life Sciences Institute; University of Michigan; Ann Arbor, MI USA.
authors.forename: Daniel J
authors.initials: DJ
authors.lastname: Klionsky
authors.affiliation: Center for Autophagy Research; University of Texas Southwestern Medical Center; Dallas, TX USA; Department of Internal Medicine; University of Texas Southwestern Medical Center; Dallas, TX USA; Department of Microbiology; University of Texas Southwestern Medical Center; Dallas, TX USA; Howard Hughes Medical Institute; University of Texas Southwestern Medical Center; Dallas, TX USA.
authors.forename: Beth
authors.initials: B
authors.lastname: Levine
mesh_terms: D001343:Autophagy / Q000187:drug effects*; D016193:G1 Phase / Q000187:drug effects*; D009584:Nitrogen / Q000172:deficiency* / Q000494:pharmacology*; D010641:Phenotype; D016192:Resting Phase, Cell Cycle / Q000187:drug effects*; D012441:Saccharomyces cerevisiae / Q000166:cytology* / Q000187:drug effects / Q000254:growth & development
chemical_list: D009584:Nitrogen
keywords: autophagy; cell cycle; quiescence; starvation; yeast