regulating cytoplasmic calcium homeostasis can reduce aluminum toxicity in yeast调节胞质钙稳态可以减少铝的毒性在酵母.pdfVIP

Regulating Cytoplasmic Calcium Homeostasis Can Reduce Aluminum Toxicity in Yeast 1 1 1 1 1 1 1 1 Xuan Li , Jia Qian , Chaoqun Wang , Ke Zheng , Lan Ye , Yu Fu , Ning Han , Hongwu Bian *, Jianwei 2 1 1 Pan , Junhui Wang , Muyuan Zhu * 1 State Key Laboratory of Plant Physiology and Biochemistry, Key Laboratory for Cell and Gene Engineering of Zhejiang Province, College of Life Sciences, Zhejiang University, Hangzhou, China, 2 College of Chemistry and Life Sciences, Zhejiang Normal University, Jinhua, China Abstract Our previous study suggested that increased cytoplasmic calcium (Ca) signals may mediate aluminum (Al) toxicity in yeast (Saccharomyces cerevisiae). In this report, we found that a yeast mutant, pmc1, lacking the vacuolar calcium ion (Ca2+) pump Ca2+-ATPase (Pmc1p), was more sensitive to Al treatment than the wild-type strain. Overexpression of either PMC1 or an anti-apoptotic factor, such as Bcl-2, Ced-9 or PpBI-1, decreased cytoplasmic Ca2+ levels and rescued yeast from Al sensitivity in both the wild-type and pmc1 mutant. Moreover, pretreatment with the Ca2+ chelator BAPTA-AM sustained cytoplasmic Ca2+ at low levels in the presence of Al, effectively making the cells more tolerant to Al exposure. Quantitative RT-PCR revealed that the expression of calmodulin (CaM) and phospholipase C (PLC), which are in the Ca2+ signaling pathway, was down-regulated under Al stress. This effect was largely counteracted when cells overexpressed anti-apoptotic Ced-9 or were pretreated with BAPTA-AM. Taken together, our results suggest that the negative regulation of Al-induced cytoplasmic Ca signaling is a novel mechanism underlying internal resistance to Al toxicity