scholarly journals Enhanced Resistance to Salt, Cold and Wound Stresses by Overproduction of Animal Cell Death Suppressors Bcl-xL and Ced-9 in Tobacco Cells — Their Possible Contribution Through Improved Function of Organella

2002 ◽  
Vol 43 (9) ◽  
pp. 992-1005 ◽  
Author(s):  
Jingbo Qiao ◽  
Ichiro Mitsuhara ◽  
Yosiaki Yazaki ◽  
Katsuhiro Sakano ◽  
Yoko Gotoh ◽  
...  
Keyword(s):  
Cell Death ◽  
Animal Cell ◽  
Tobacco Cells ◽  
Enhanced Resistance ◽  
Improved Function

scholarly journals BAX INHIBITOR-1 Is Required for Full Susceptibility of Barley to Powdery Mildew

2010 ◽  
Vol 23 (9) ◽  
pp. 1217-1227 ◽  
Author(s):  
Ruth Eichmann ◽  
Melanie Bischof ◽  
Corina Weis ◽  
Jane Shaw ◽  
Christophe Lacomme ◽  
...  
Keyword(s):  
Cell Death ◽  
Powdery Mildew ◽  
Gene Silencing ◽  
Defense Responses ◽  
Negative Control ◽  
Cellular Level ◽  
Virus Induced Gene Silencing ◽  
Powdery Mildew Fungus ◽  
Basal Resistance ◽  
Enhanced Resistance

BAX INHIBITOR-1 (BI-1) is one of the few proteins known to have cross-kingdom conserved functions in negative control of programmed cell death. Additionally, barley BI-1 (HvBI-1) suppresses defense responses and basal resistance to the powdery mildew fungus Blumeria graminis f. sp. hordei and enhances resistance to cell death–provoking fungi when overexpressed in barley. Downregulation of HvBI-1 by transient-induced gene silencing or virus-induced gene silencing limited susceptibility to B. graminis f. sp. hordei, suggesting that HvBI-1 is a susceptibility factor toward powdery mildew. Transient silencing of BI-1 did not limit supersusceptibility induced by overexpression of MLO. Transgenic barley plants harboring an HvBI-1 RNA interference (RNAi) construct displayed lower levels of HvBI-1 transcripts and were less susceptible to powdery mildew than wild-type plants. At the cellular level, HvBI-1 RNAi plants had enhanced resistance to penetration by B. graminis f. sp. hordei. These data support a function of BI-1 in modulating cell-wall-associated defense and in establishing full compatibility of B. graminis f. sp. hordei with barley.

scholarly journals Induction of Hypersensitive Cell Death by a Fungal Protein in Cultures of Tobacco Cells

1998 ◽  
Vol 11 (2) ◽  
pp. 115-123 ◽  
Author(s):  
Akira Yano ◽  
Kaoru Suzuki ◽  
Hirofumi Uchimiya ◽  
Hideaki Shinshi
Keyword(s):  
Cell Death ◽  
Specific Interaction ◽  
Trichoderma Viride ◽  
Defense Responses ◽  
Hypersensitive Reaction ◽  
Hypersensitive Cell Death ◽  
Tobacco Cells ◽  
Bright Yellow ◽  
Cell Death Program ◽  
Cellular Signal

Treatment of suspension-cultured tobacco (Nicotiana tabacum cv. Xanthi) cells (line XD6S) with fungal proteinaceous elicitors, namely, xylanase (EC 3.2.1.8) from Trichoderma viride (TvX) and xylanase from T. reesei (TrX), induced shrinkage of the cytoplasm, condensation of the nucleus, and, finally, cell death, which were accompanied by typical defense responses that included an oxidative burst and expression of defense genes. A Ca2+ channel blocker, Gd3+, inhibited the typical response of XD6S cells to TvX, which resembled the hypersensitive reaction (HR). These results suggested that the influx of Ca2+ ions plays an important role as a secondary signal. The HR was not observed in TvX-treated tobacco cells (line BY-2) derived from cv. Bright Yellow 2. This result suggests that key features of cultivar-specific interaction can be observed in cultures of tobacco cells. Xylanase from Bacillus circulans (BcX) and B. subtilis (BsX), which has enzymatic properties similar to those of TvX but an amino acid sequence different from that of TvX, did not induce the HR-like response in XD6S cells. These results suggest that the elicitor action of TvX is not due to its ability to hydrolyze cell walls but requires the TvX-specific recognition factors in plant cells. Thus, TvX-induced cell death was not due to some general toxic effect, but seems to be mediated by the activation of a specific cellular signal-transduction cascade that converges with a pathway that activates the intracellular cell death program.

scholarly journals Animal cell-death suppressors Bcl-xL and Ced-9 inhibit cell death in tobacco plants

1999 ◽  
Vol 9 (14) ◽  
pp. 775-S1 ◽  
Author(s):  
Ichiro Mitsuhara ◽  
Kamal A. Malik ◽  
Masayuki Miura ◽  
Yuko Ohashi
Keyword(s):  
Cell Death ◽  
Animal Cell ◽  
Tobacco Plants

scholarly journals Expression of an Oxalate Decarboxylase Impairs the Necrotic Effect Induced by Nep1-like Protein (NLP) of Moniliophthora perniciosa in Transgenic Tobacco

2011 ◽  
Vol 24 (7) ◽  
pp. 839-848 ◽  
Author(s):  
Leonardo F. da Silva ◽  
Cristiano V. Dias ◽  
Luciana C. Cidade ◽  
Juliano S. Mendes ◽  
Carlos P. Pirovani ◽  
...  
Keyword(s):  
Cell Death ◽  
Transgenic Plants ◽  
Plant Pathogens ◽  
Oxygen Species ◽  
Oxalate Decarboxylase ◽  
Moniliophthora Perniciosa ◽  
Enhanced Resistance ◽  
Broom Disease ◽  
Ros Formation ◽  
Theobroma Cacao L

Oxalic acid (OA) and Nep1-like proteins (NLP) are recognized as elicitors of programmed cell death (PCD) in plants, which is crucial for the pathogenic success of necrotrophic plant pathogens and involves reactive oxygen species (ROS). To determine the importance of oxalate as a source of ROS for OA- and NLP-induced cell death, a full-length cDNA coding for an oxalate decarboxylase (FvOXDC) from the basidiomycete Flammulina velutipes, which converts OA into CO2 and formate, was overexpressed in tobacco plants. The transgenic plants contained less OA and more formic acid compared with the control plants and showed enhanced resistance to cell death induced by exogenous OA and MpNEP2, an NLP of the hemibiotrophic fungus Moniliophthora perniciosa. This resistance was correlated with the inhibition of ROS formation in the transgenic plants inoculated with OA, MpNEP2, or a combination of both PCD elicitors. Taken together, these results have established a pivotal function for oxalate as a source of ROS required for the PCD-inducing activity of OA and NLP. The results also indicate that FvOXDC represents a potentially novel source of resistance against OA- and NLP-producing pathogens such as M. perniciosa, the causal agent of witches' broom disease of cacao (Theobroma cacao L.).

Heat-induced oxidative activity protects suspension-cultured plant cells from low temperature damage

2006 ◽  
Vol 33 (1) ◽  
pp. 67 ◽  
Author(s):  
Andrew C. Allan ◽  
Ratnasiri Maddumage ◽  
Joanne L. Simons ◽  
Samuel O. Neill ◽  
Ian B. Ferguson
Keyword(s):  
Heat Treatment ◽  
Cell Death ◽  
Low Temperature ◽  
Real Time ◽  
Peroxidase Activity ◽  
Low Temperatures ◽  
Temperature Tolerance ◽  
H2o2 Production ◽  
Tobacco Cells ◽  
Pre Treatment

A short heat pre-treatment (1 h at 38°C) was found to protect both suspension-cultured apple fruit cells and tobacco cells from cold-induced cell death. Tobacco cells were more sensitive to low temperatures than apple cells, with significant cell death after 48 h at 0 or –2°C. Real-time measurements of H2O2 levels during the heat pre-treatment revealed a substantial burst of this reactive oxygen species in both cell types. Real-time and longer-term measurements also showed a large burst of H2O2 production from tobacco cells, but not apple cells, when exposed to low temperatures. Lower temperatures reduced levels of peroxidase activity (both total and intracellular), with the heat pre-treatment preventing some of the cold-induced reduction of this activity in both apple and tobacco cells. The greater sensitivity to low temperature of the tobacco cells may be related to higher H2O2 production, with the heat treatment maintaining higher peroxidase activity. The lesser sensitivity of the apple cells may be due to the lack of a H2O2 burst and maintenance of peroxidase activity by the heat treatment. These results support a role for oxidative metabolism in the beneficial effects of heat in inducing low temperature tolerance.

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