title: Programmed cell death-involved aluminum toxicity in yeast alleviated by antiapoptotic members with decreased calcium signals.
abstract: The molecular mechanisms of aluminum (Al) toxicity and tolerance in plants have been the focus of ongoing research in the area of stress phytophysiology. Recent studies have described Al-induced apoptosis-like cell death in plant and animal cells. In this study, we show that yeast (Saccharomyces cerevisiae) exposed to low effective concentrations of Al for short times undergoes enhanced cell division in a manner that is dose and cell density dependent. At higher concentrations of Al or longer exposure times, Al induces cell death and growth inhibition. Several apoptotic features appear during Al treatment, including cell shrinkage, vacuolation, chromatin marginalization, nuclear fragmentation, DNA degradation, and DNA strand breaks, as well as concomitant cell aggregation. Yeast strains expressing Ced-9, Bcl-2, and PpBI-1 (a plant Bax inhibitor-1 isolated from Phyllostachys praecox), respectively, display more resistance to Al toxicity compared with control cells. Data from flow cytometric studies show these three antiapoptotic members do not affect reactive oxygen species levels, but decrease calcium ion (Ca(2+)) signals in response to Al stress, although both intracellular reactive oxygen species and Ca(2+) levels were increased. The data presented suggest that manipulation of the negative regulation process of programmed cell death may provide a novel mechanism for conferring Al tolerance.
authors.affiliation: State Key Lab of Plant Physiology and Biochemistry, College of Life Sciences, Zhejiang University, Hangzhou 310058, China.
authors.forename: Ke
authors.initials: K
authors.lastname: Zheng
authors.forename: Jian-Wei
authors.initials: JW
authors.lastname: Pan
authors.forename: Lan
authors.initials: L
authors.lastname: Ye
authors.forename: Yu
authors.initials: Y
authors.lastname: Fu
authors.forename: Hua-Zheng
authors.initials: HZ
authors.lastname: Peng
authors.forename: Bai-Yu
authors.initials: BY
authors.lastname: Wan
authors.forename: Qing
authors.initials: Q
authors.lastname: Gu
authors.forename: Hong-Wu
authors.initials: HW
authors.lastname: Bian
authors.forename: Ning
authors.initials: N
authors.lastname: Han
authors.forename: Jun-Hui
authors.initials: JH
authors.lastname: Wang
authors.forename: Bo
authors.initials: B
authors.lastname: Kang
authors.forename: Jun-Hang
authors.initials: JH
authors.lastname: Pan
authors.forename: Hong-Hong
authors.initials: HH
authors.lastname: Shao
authors.forename: Wen-Zhe
authors.initials: WZ
authors.lastname: Wang
authors.forename: Mu-Yuan
authors.initials: MY
authors.lastname: Zhu
mesh_terms: D000535:Aluminum / Q000633:toxicity*; D000595:Amino Acid Sequence; D017209:Apoptosis / Q000187:drug effects*; D002118:Calcium / Q000378:metabolism*; D049109:Cell Proliferation / Q000187:drug effects; D004249:DNA Damage; D008969:Molecular Sequence Data; D017382:Reactive Oxygen Species / Q000378:metabolism; D012441:Saccharomyces cerevisiae / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D029701:Saccharomyces cerevisiae Proteins / Q000235:genetics / Q000378:metabolism; D016415:Sequence Alignment; D015398:Signal Transduction
chemical_list: D017382:Reactive Oxygen Species; D029701:Saccharomyces cerevisiae Proteins; D000535:Aluminum; D002118:Calcium