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Published on July 21, 2006; 10.1104/pp.106.082495

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Received April 23, 2006
Accepted July 10, 2006

Programmed Cell Death-Involved Aluminum Toxicity in Saccharomyces cerevisiae Alleviated by Antiapoptotic Members with Declined Calcium Signals

Ke Zheng , Jian-Wei Pan , Lan Ye , Yu Fu , Hua-Zheng Peng , Bai-Yu Wan , Qing Gu , Hong-Wu Bian , Ning Han , Jun-Hui Wang , Bo Kang , Jun-Hang Pan , Hong-Hong Shao , Wen-Zhe Wang , and Mu-Yuan Zhu *

State Key Lab of Plant Physiology and Biochemistry, College of Life Sciences, Zhejiang University, Hangzhou 310058, China
State Key Lab of Plant Physiology and Biochemistry, College of Life Sciences, Zhejiang University, Hangzhou 310058, China; Zhejiang Forestry Academy, Hangzhou 310023, China
State Key Lab of Plant Physiology and Biochemistry, College of Life Sciences, Zhejiang University, Hangzhou 310058, China; Department of Biotechnology, Hangzhou University of Commerce, Hangzhou 310012, China

* Corresponding author; email: myzhu{at}zju.edu.cn.

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 undergo 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 respectively expressing Ced-9, Bcl-2 and PpBI-1 (a plant Bax inhibitor-1 isolated from Phyllostachys praecox) display more resistance to Al toxicity, compared to the control cells. Data from flow cytometric studies show these three antiapoptotic members do not affect reactive oxygen species (ROS) levels but decrease calcium ions (Ca2+) signals in response to Al stress, though both intracellular ROS and Ca2+ levels were increased. The data presented suggest that manipulation of the negative regulation process of PCD may provide a novel mechanism for conferring Al tolerance.




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[Abstract] [Full Text] [PDF]


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