Publication Type: | Journal Article |
Year of Publication: | 2013 |
Authors: | YE, YUN, LI, ZHE, XING, DA |
Journal: | Plant, Cell & Environment |
Volume: | 36 |
Issue: | 1 |
Date Published: | 2013 |
ISBN Number: | 1365-3040 |
Keywords: | Arabidopsis PCD, caspase-3-like protease, Cd2+ stress, MAPK pathway, nitric oxide signal |
Abstract: | Nitric oxide (NO), a vital cell-signalling 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. |
URL: | http://dx.doi.org/10.1111/j.1365-3040.2012.02543.x |
Short Title: | Plant, Cell & Environment |