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Ced-9 inhibits Al-induced programmed cell death and promotes Al tolerance in tobacco

Our previous data showed that apoptotic suppressors inhibit aluminum (Al)-induced programmed cell death (PCD) and promote Al tolerance in yeast cells, however, very little is known about the underlying mechanisms, especially in plants. Here, we show that the Caenorhabditis elegans apoptotic suppress...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2009-05, Vol.383 (1), p.141-145
Main Authors: Wang, Wenzhe, Pan, Jianwei, Zheng, Ke, Chen, Hong, Shao, Honghong, Guo, Yajuan, Bian, Hongwu, Han, Ning, Wang, Junhui, Zhu, Muyuan
Format: Article
Language:English
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Summary:Our previous data showed that apoptotic suppressors inhibit aluminum (Al)-induced programmed cell death (PCD) and promote Al tolerance in yeast cells, however, very little is known about the underlying mechanisms, especially in plants. Here, we show that the Caenorhabditis elegans apoptotic suppressor Ced-9, a Bcl-2 homologue, inhibited both the Al-induced PCD and Al-induced activity of caspase-like vacuolar processing enzyme (VPE), a crucial executioner of PCD, in tobacco. Furthermore, we show that Ced-9 significantly alleviated Al inhibition of root elongation, decreased Al accumulation in the root tip and greatly inhibited Al-induced gene expression in early response to Al, leading to enhancing the tolerance of tobacco plants to Al toxicity. Our data suggest that Ced-9 promotes Al tolerance in plants via inhibition of Al-induced PCD, indicating that conserved negative regulators of PCD are involved in integrated regulation of cell survival and Al-induced PCD by an unidentified mechanism.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2009.03.125