Polyamines inhibit NADPH oxidase-mediated superoxide generation and putrescine prevents programmed cell death induced by polyamine oxidase-generated hydrogen peroxide

Planta ◽  
2004 ◽  
Vol 220 (6) ◽  
pp. 826-837 ◽  
Author(s):  
Anastasia K. Papadakis ◽  
Kalliopi A. Roubelakis-Angelakis
2005 ◽  
Vol 168 (1) ◽  
pp. 17-20 ◽  
Author(s):  
Tsanko S. Gechev ◽  
Jacques Hille

Hydrogen peroxide (H2O2) has established itself as a key player in stress and programmed cell death responses, but little is known about the signaling pathways leading from H2O2 to programmed cell death in plants. Recently, identification of key regulatory mutants and near-full genome coverage microarray analysis of H2O2-induced cell death have begun to unravel the complexity of the H2O2 network. This review also describes a novel link between H2O2 and sphingolipids, two signals that can interplay and regulate plant cell death.


2008 ◽  
Vol 9 (4) ◽  
pp. 435-445 ◽  
Author(s):  
OLIVIA J. DESMOND ◽  
JOHN M. MANNERS ◽  
AMBER E. STEPHENS ◽  
DONALD J. MACLEAN ◽  
PEER M. SCHENK ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Huilan Yi ◽  
Xin Liu ◽  
Min Yi ◽  
Gang Chen

Sulfur dioxide (SO2) is a major air pollutant and has significant impacts on plant physiology. Plant can adapt to SO2 stress by controlling stomatal movement, gene expression, and metabolic changes. Here we show clear evidences that SO2-triggered hydrogen peroxide (H2O2) production mediated stomatal closure and cell death in Arabidopsis leaves. High levels of SO2 caused irreversible stomatal closure and decline in guard cell viability, but low levels of SO2 caused reversible stomatal closure. Exogenous antioxidants ascorbic acid (AsA) and catalase (CAT) or Ca2+ antagonists EGTA and LaCl3 blocked SO2-induced stomatal closure and decline in viability. AsA and CAT also blocked SO2-induced H2O2 and [Ca2+]cyt elevation. However, EGTA and LaCl3 inhibited SO2-induced [Ca2+]cyt increase but did not suppress SO2-induced H2O2 elevation. These results indicate that H2O2 elevation triggered stomatal closure and cell death via [Ca2+]cyt signaling in SO2-stimulated Arabidopsis guard cells. NADPH oxidase inhibitor DPI blocked SO2-induced cell death but not the stomatal closure triggered by low levels of SO2, indicating that NADPH oxidase-dependent H2O2 production plays critical role in SO2 toxicity but is not necessary for SO2-induced stomatal closure. Our results suggest that H2O2 production and accumulation in SO2-stimulated plants trigger plant adaptation and toxicity via reactive oxygen species mediating Ca2+ signaling.


2015 ◽  
Vol 42 (4) ◽  
pp. 337 ◽  
Author(s):  
Juan Liu ◽  
Yanhong Xu ◽  
Zheng Zhang ◽  
Jianhe Wei

Aquilaria sinensis (Lour.) Gilg produces a highly valuable agarwood characterised by a diverse array of sesquiterpenes and chromone derivatives that can protect wounded trees against potential herbivores and pathogens. A defensive reaction on the part of the plant has been proposed as the key reason for agarwood formation, but the issue of whether programmed cell death (PCD), an important process of plant immune responding, is involved in agarwood formation, still needs to be clarified. In this study, treatment of cultured cell suspensions with hydrogen peroxide (H2O2) induced the production of sesquiterpenes due to endogenous accumulation of salicylic acid (SA) and elevations in the expression of sesquiterpene biosynthetic genes. Moreover, PCD was stimulated by H2O2 in cultured cell suspensions of A. sinensis due to the induction of caspase activity, upregulated expression of metacaspases and cytochrome c, and SA accumulation. Our findings demonstrate for the first time that H2O2 stimulates PCD, SA accumulation and sesquiterpene production in cultured cell suspensions of A. sinensis. Furthermore, results from this study provide a valuable insight into investigations of the potential interactions between sesquiterpene synthesis and PCD during agarwood formation.


2007 ◽  
Vol 6 (10) ◽  
pp. 1745-1757 ◽  
Author(s):  
Nancy Lee ◽  
Sreenivas Gannavaram ◽  
Angamuthu Selvapandiyan ◽  
Alain Debrabant

ABSTRACT In this report, we have characterized two metacaspases of Leishmania donovani, L. donovani metacaspase-1 (LdMC1) and LdMC2. These two proteins show 98% homology with each other, and both contain a characteristic C-terminal proline-rich domain. Both genes are transcribed in promastigotes and axenic amastigotes of L. donovani; however, LdMC1 shows increased mRNA levels in axenic amastigotes. An anti-LdMC antibody was obtained and showed reactivity with a single ∼42-kDa protein band in both promastigote and axenic amastigote parasite whole-cell lysates by Western blotting. Pulse-chase experiments suggest that LdMCs are not synthesized as proenzymes, and immunofluorescence studies show that LdMCs are associated with the acidocalcisome compartments of L. donovani. Enzymatic assays of immunoprecipitated LdMCs show that native LdMCs efficiently cleave trypsin substrates and are unable to cleave caspase-specific substrates. Consistently, LdMC activity is insensitive to caspase inhibitors and is efficiently inhibited by trypsin inhibitors, such as leupeptin, antipain, and N α-tosyl-l-lysine-chloromethyl ketone (TLCK). In addition, our results show that LdMC activity was induced in parasites treated with hydrogen peroxide, a known trigger of programmed cell death (PCD) in Leishmania and that parasites overexpressing metacaspases are more sensitive to hydrogen peroxide-induced PCD. These findings suggest that Leishmania metacaspases are not responsible for the caspase-like activities reported in this organism and suggest a possible role for LdMCs as effector molecules in Leishmania PCD.


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