title: Zinc starvation induces autophagy in yeast.
abstract: Zinc is an essential nutrient for all forms of life. Within cells, most zinc is bound to protein. Because zinc serves as a catalytic or structural cofactor for many proteins, cells must maintain zinc homeostasis under severely zinc-deficient conditions. In yeast, the transcription factor Zap1 controls the expression of genes required for uptake and mobilization of zinc, but to date the fate of existing zinc-binding proteins under zinc starvation remains poorly understood. Autophagy is an evolutionarily conserved cellular degradation/recycling process in which cytoplasmic proteins and organelles are sequestered for degradation in the vacuole/lysosome. In this study, we investigated how autophagy functions under zinc starvation. Zinc depletion induced non-selective autophagy, which is important for zinc-limited growth. Induction of autophagy by zinc starvation was not directly related to transcriptional activation of Zap1. Instead, TORC1 inactivation directed zinc starvation-induced autophagy. Abundant zinc proteins, such as Adh1, Fba1, and ribosomal protein Rpl37, were degraded in an autophagy-dependent manner. But the targets of autophagy were not restricted to zinc-binding proteins. When cellular zinc is severely depleted, this non-selective autophagy plays a role in releasing zinc from the degraded proteins and recycling zinc for other essential purposes.
authors.affiliation: Research Unit for Cell Biology, Institute of Innovative Research, Tokyo Institute of Technology, Yokohama 226-8503.
authors.forename: Tomoko
authors.initials: T
authors.lastname: Kawamata
authors.affiliation: Research Unit for Cell Biology, Institute of Innovative Research, Tokyo Institute of Technology, Yokohama 226-8503; Research Center for Odontology, School of Life Dentistry at Tokyo, The Nippon Dental University, Chiyoda-ku, Tokyo 102-8159, Japan.
authors.forename: Tetsuro
authors.initials: T
authors.lastname: Horie
authors.affiliation: Research Unit for Cell Biology, Institute of Innovative Research, Tokyo Institute of Technology, Yokohama 226-8503.
authors.forename: Miou
authors.initials: M
authors.lastname: Matsunami
authors.affiliation: Research Unit for Cell Biology, Institute of Innovative Research, Tokyo Institute of Technology, Yokohama 226-8503.
authors.forename: Michiko
authors.initials: M
authors.lastname: Sasaki
authors.affiliation: Research Unit for Cell Biology, Institute of Innovative Research, Tokyo Institute of Technology, Yokohama 226-8503. Electronic address: yohsumi@iri.titech.ac.jp.
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Ohsumi
mesh_terms: D000426:Alcohol Dehydrogenase / Q000235:genetics / Q000378:metabolism; D001343:Autophagy; D000076222:Mechanistic Target of Rapamycin Complex 1; D046912:Multiprotein Complexes / Q000235:genetics / Q000378:metabolism; D059748:Proteolysis; D012441:Saccharomyces cerevisiae / Q000235:genetics / Q000378:metabolism*; D029701:Saccharomyces cerevisiae Proteins / Q000235:genetics / Q000378:metabolism; D058570:TOR Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism; D015032:Zinc / Q000378:metabolism*
chemical_list: D046912:Multiprotein Complexes; D029701:Saccharomyces cerevisiae Proteins; D014157:Transcription Factors; C103264:ZAP1 protein, S cerevisiae; C516801:ADH1 protein, S cerevisiae; D000426:Alcohol Dehydrogenase; D000076222:Mechanistic Target of Rapamycin Complex 1; D058570:TOR Serine-Threonine Kinases; D015032:Zinc
keywords: TOR complex (TORC); autophagy; metal; starvation; yeast; zinc