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ABSTRACT
Nitric oxide (NO), a vital cell‐signaling molecule, has been reported to regulate toxic metal responses in plants. This work investigated the effects of NO and the relationship between NO and mitogen‐activated protein kinase (MAPK) in Arabidopsis (Arabidopsis thaliana) programmed cell death (PCD) induced by cadmium (Cd2+) exposure. With fluorescence resonance energy transfer (FRET) analysis, caspase‐3‐like protease activation was detected after Cd2+ treatment. This was further confirmed with a caspase‐3 substrate assay. Cd2+‐induced caspase‐3‐like activity was inhibited in the presence of the NO‐specific scavenger 2‐(4‐carboxyphenyl)‐4,4,5,5‐tetramethylimidazoline‐1‐oxyl‐3‐oxide (cPTIO), suggesting that NO mediated caspase‐3‐like protease activation under Cd2+stress conditions. Pretreatment with cPTIO effectively inhibited Cd2+‐induced MAPK activation, indicating that NO also affected the MAPK pathway. Interestingly, Cd2+‐induced caspase‐3‐like activity was significantly suppressed in the mpk6 mutant, suggesting that MPK6 was required for caspase‐3‐like protease activation. To our knowledge, this is the first demonstration that NO promotes Cd2+‐induced Arabidopsis PCD by promoting MPK6‐mediated caspase‐3‐like activation.
© 2012 Blackwell Publishing Ltd
| Authors: | Yun Ye, Zhe Li, Da Xing | |
| Journal: | Plant, Cell & Environment | |
| Year: | 2012 | |
| Pages: | no | |
| DOI: | 10.1111/j.1365-3040.2012.02543.x | |
| Publication date: | 24-05-2012 |
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