scholarly journals Hydrogen peroxide as a signal controlling plant programmed cell death

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.

1994 ◽  
Vol 142 (1) ◽  
pp. 53-91 ◽  
Author(s):  
Elena Baixeras ◽  
Lisbardo Bosca ◽  
Claudia Stauber ◽  
Ana Gonzalez ◽  
Ana C. Carrera ◽  
...  

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

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.


Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 4492-4492
Author(s):  
Changhong Yin ◽  
Sanghoon Lee ◽  
Timmy O'Connell ◽  
Janet Ayello ◽  
Carmella van de Ven ◽  
...  

Abstract BACKGROUND: Primary Mediastinal large B-cell lymphoma (PMBL) is a rare form of Non Hodgkin Lymphoma (NHL) representing 2% of mature B-cell non-Hodgkin lymphoma in patients less than 18 years of age (Lones/Cairo et al, JCO 2000; Burkhardt et al, BJH 2005). PMBL has histological features somewhere between Diffuse Large B-Cell Lymphoma (DLBCL) and classical HL (cHL) (Abramson et al, Blood 2005). Gene expression studies suggested that the molecular signature of PMBL had a striking resemblance to the expression profile of cHL (Rosenwald et al, JEM 2003). We have recently reported that a significant decrease in EFS among children and adolescent PMBL patients compared with other stage III non-PMBL pediatric DLBCL patients following FAB/LMB 96 therapy, suggesting that children and adolescent with PMBL required alternative treatment strategies (Gerrard/Cairo et al, Blood 2013). PMBL has been demonstrated to have an over-activated NF-kB pathway by gene expression profiling (Rosenwald et al, JEM 2003). Since over 95% of PMBL express CD20, targeting the CD20 receptor with a CD20 antibody is of high clinical interest. Obinutuzumab (GA101) is novel glycoengineered anti-CD20 targeted monoclonal antibody recognizing a unique CD20 type II epitope and it has been demonstrated to have greater efficacy in reducing tumor size, inducing remission and improving survival in other B-NHL xenograft models (Mössner et al, Blood 2010). Obinutuzumab has been recently approved by FDA for first line treatment of chronic lymphocytic leukemia (CLL) in combination with chlorambucil. OBJECTIVES: We hypothesize that obinutuzumab may be a future potential targeted agent for the treatment of PMBL, and therefore, we investigated whether obinutuzumab treatment results in significant changes in signaling pathways, genes expression, programmed cell death and cell proliferation in PMBL. METHODS: Karpas-1106P cells (DSMZ) were treated with obinutuzumab (generously provided by Dr. Klein, Roche) at every 24 hours (1-100ug/ml). qRT-PCR, western blot, MTS, Caspase 3/7 assay (Promega) and FACS analysis were performed. The BeadChip array (Illumina, HumanHT-12) was used for gene expression profiling. RESULTS: There was a significant decrease of cell proliferation in obinutuzumab-treated Karpas cells with 10ug/ml (0.69 ± 0.025, p<0.005) vs control (1.00 ± 0.000) at 48 hours. Concomitantly, there was a significant increase in programmed cell death in 10ug/ml obinutuzumab treated Karpas (37.80 ± 10.096, p<0.05) vs control (1.19 ± 0.762) at 48 hours. We also observed a significant decrease of CD20 expression (0.74± 0.010, p<0.05) with 10ug/ml obinutuzumab treatment at 48 hours. A total of 133 differentially expressed genes were identified by gene expression profiling (>1.5-fold, 0.57%) and 77.5% of genes including apoptosis related genes (CASP2 and PAK2) and MAPK signaling pathways (RASA1 and JUN) and EGR1 were upregulated and 22.5% of genes including ID3, GRAP and RAB6B were downregulated in obinutuzumab treated Karpas vs control (Fig 1). There were significant decreases of p-STAT6 (0.72± 0.011, p=0.01), p-Akt (0.69± 0.011, p<0.05), p-ikBα (0.70± 0.017, p<0.05) and p-Erk (0.56± 0.019, p<0.05) with 10ug/ml obinutuzumab treatment at 48 hours (Fig 2). Additionally, There were significant down-regulation of mRNA expression of Bcl-xL (0.91±0.011, p<0.04) and Bax (0.66±0.022, p<0.02) vs control. CONCLUSIONS: We observed that obinutuzumab significantly inhibited cell proliferation and induced programmed cell death and downregulated downstream of PI3k/Akt and NF-kB signaling pathways. Gene expression analysis indicated obinutuzumab induced changes in the expression of genes in Karpas that were involved in apoptosis and signaling pathways including CASP2, EGR1 and ID3. Future studies 1) will investigate the efficacy of combination therapies to enhance programmed cell death, and 2) will assess the proteomic signature induced by obinutuzumab in obinutuzumab sensitive and resistant PMBL, and furthermore, 3) will focus on the in vivo effects of obinutuzumab in a NOD/SCID PMBL xenograft mouse model. Obinutuzumab may be a future potential targeted agent for the adjuvant treatment of PMBL lymphoma. Disclosures No relevant conflicts of interest to declare.


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