GLYCINE-RICH RNA-BINDING PROTEIN1 interacts with RECEPTOR-LIKE CYTOPLASMIC PROTEIN KINASE1 and suppresses cell death and defense responses in pepper (Capsicum annuum)

Systemic necrosis is one of the most severe symptoms caused by plant RNA viruses. Recently, systemic necrosis has been suggested to have similar features to a defense response referred to as the hypersensitive response (HR), a form of programmed cell death. In virus-infected plant cells, host intracellular membrane structures are changed dramatically for more efficient viral replication. However, little is known about whether this replication-associated membrane modification is the cause of the symptoms. In this study, we identified an amino-terminal amphipathic helix of the helicase encoded by Radish mosaic virus (RaMV) (genus Comovirus) as an elicitor of cell death in RaMV-infected plants. Cell death caused by the amphipathic helix had features similar to HR, such as SGT1-dependence. Mutational analyses and inhibitor assays using cerulenin demonstrated that the amphipathic helix–induced cell death was tightly correlated with dramatic alterations in endoplasmic reticulum (ER) membrane structures. Furthermore, the cell death–inducing activity of the amphipathic helix was conserved in Cowpea mosaic virus (genus Comovirus) and Tobacco ringspot virus (genus Nepovirus), both of which are classified in the family Secoviridae. Together, these results indicate that ER membrane modification associated with viral intracellular replication may be recognized to prime defense responses against plant viruses.

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ArabidopsisHSP90 protein modulates RPP4-mediated temperature-dependent cell death and defense responses

New Phytologist ◽

10.1111/nph.12760 ◽

2014 ◽

Vol 202 (4) ◽

pp. 1320-1334 ◽

Cited By ~ 28

Author(s):

Fei Bao ◽

Xiaozhen Huang ◽

Chipan Zhu ◽

Xiaoyan Zhang ◽

Xin Li ◽

...

Keyword(s):

Cell Death ◽

Defense Responses ◽

Temperature Dependent ◽

Dependent Cell

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

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi-23-9-1217 ◽

2010 ◽

Vol 23 (9) ◽

pp. 1217-1227 ◽

Cited By ~ 58

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.

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Nitrate Efflux Is an Essential Component of the Cryptogein Signaling Pathway Leading to Defense Responses and Hypersensitive Cell Death in Tobacco

The Plant Cell ◽

10.1105/tpc.002295 ◽

2002 ◽

Vol 14 (8) ◽

pp. 1937-1951 ◽

Cited By ~ 95

Author(s):

David Wendehenne ◽

Olivier Lamotte ◽

Jean-Marie Frachisse ◽

Hélène Barbier-Brygoo ◽

Alain Pugin

Keyword(s):

Cell Death ◽

Signaling Pathway ◽

Defense Responses ◽

Hypersensitive Cell Death ◽

Essential Component

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

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi.1998.11.2.115 ◽

1998 ◽

Vol 11 (2) ◽

pp. 115-123 ◽

Cited By ~ 59

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.

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The Arabidopsis Gain-of-Function Mutant ssi4 Requires RAR1 and SGT1b Differentially for Defense Activation and Morphological Alterations

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi-21-1-0040 ◽

2008 ◽

Vol 21 (1) ◽

pp. 40-49 ◽

Cited By ~ 27

Author(s):

Fasong Zhou ◽

Stephen Mosher ◽

Miaoying Tian ◽

Giovanna Sassi ◽

Jane Parker ◽

...

Keyword(s):

Cell Death ◽

Defense Responses ◽

R Gene ◽

Lesion Formation ◽

Triple Mutant ◽

Gain Of Function ◽

Pathogen Infection ◽

Basal Resistance ◽

Morphological Alterations ◽

Induced Disease Resistance

A gain-of-function mutation in resistance (R) gene SSI4 causes constitutive activation of defense responses, spontaneous necrotic lesion formation, enhanced resistance against virulent pathogens, and a severe dwarf phenotype. Genetic analysis revealed that ssi4-induced H2O2 accumulation and spontaneous cell death require RAR1, whereas ssi4-mediated stunting is dependent on SGT1b. By contrast, both RAR1 and SGT1b are required in a genetically additive manner for ssi4-induced disease resistance, SA accumulation, and lesion formation after pathogen infection. These data point to cooperative yet distinct functions of RAR1 and SGT1b in responses conditioned by a deregulated nucleotide-binding leucine-rich repeat protein. We also found that RAR1 and SGT1b together contribute to basal resistance because an ssi4 rar1 sgt1b triple mutant exhibited enhanced susceptibility to virulent pathogen infection compared with wild-type SSI4 plants. All ssi4-induced phenotypes were suppressed when plants were grown at 22°C under high relative humidity. However, low temperature (16°C) triggered ssi4-mediated cell death via an RAR1-dependent pathway even in the presence of high humidity. Thus, multiple environmental factors impact on ssi4 signaling, as has been observed for other constitutive defense mutants and R gene-triggered pathways.

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