Identification of the Novel Effector RsIA_NP8 in Rhizoctonia solani AG1 IA That Induces Cell Death and Triggers Defense Responses in Non-Host Plants

Erwinia amylovora is the bacterium responsible for fire blight, a necrotic disease affecting plants of the rosaceous family. E. amylovora pathogenicity requires a functional type three secretion system (T3SS). We show here that E. amylovora triggers a T3SS-dependent cell death on Arabidopsis thaliana. The plants respond by inducing T3SS-dependent defense responses, including salicylic acid (SA)-independent callose deposition, activation of the SA defense pathway, reactive oxygen species (ROS) accumulation, and part of the jasmonic acid/ethylene defense pathway. Several of these reactions are similar to what is observed in host plants. We show that the cell death triggered by E. amylovora on A. thaliana could not be simply explained by the recognition of AvrRpt2ea by the resistance gene product RPS2. We then analyzed the role of type three-secreted proteins (T3SPs) DspA/E, HrpN, and HrpW in the induction of cell death and defense reactions in A. thaliana following infection with the corresponding E. amylovora mutant strains. HrpN and DspA/E were found to play an important role in the induction of cell death, activation of defense pathways, and ROS accumulation. None of the T3SPs tested played a major role in the induction of SA-independent callose deposition. The relative importance of T3SPs in A. thaliana is correlated with their relative importance in the disease process on host plants, indicating that A. thaliana can be used as a model to study their role.

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The novel anti-cell death compound MS41 and its cytoprotective mechanism

Neuroscience Research ◽

10.1016/s0168-0102(00)81156-6 ◽

2000 ◽

Vol 38 ◽

pp. S51

Author(s):

R Asakai

Keyword(s):

Cell Death ◽

The Novel

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Faculty Opinions recommendation of Nitrate efflux is an essential component of the cryptogein signaling pathway leading to defense responses and hypersensitive cell death in tobacco.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1011782.182572 ◽

2003 ◽

Author(s):

Eric Lam

Keyword(s):

Cell Death ◽

Signaling Pathway ◽

Defense Responses ◽

Hypersensitive Cell Death ◽

Essential Component

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Faculty Opinions recommendation of Cell death and immunity in cancer: From danger signals to mimicry of pathogen defense responses.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.732002205.793538244 ◽

2017 ◽

Author(s):

D John Doyle

Keyword(s):

Cell Death ◽

Defense Responses ◽

Pathogen Defense ◽

Danger Signals

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Targeting AKT/mTOR and Bcl-2 for Autophagic and Apoptosis Cell Death in Lung Cancer: Novel Activity of a Polyphenol Compound

Antioxidants ◽

10.3390/antiox10040534 ◽

2021 ◽

Vol 10 (4) ◽

pp. 534

Author(s):

Sucharat Tungsukruthai ◽

Onrapak Reamtong ◽

Sittiruk Roytrakul ◽

Suchada Sukrong ◽

Chanida Vinayanwattikun ◽

...

Keyword(s):

Lung Cancer ◽

Cell Death ◽

Cancer Cells ◽

Proteomic Analysis ◽

Interaction Analysis ◽

Time Dependent ◽

The Novel ◽

Protein Protein Interaction ◽

Autophagy Induction ◽

Acidic Vesicle

Autophagic cell death (ACD) is an alternative death mechanism in resistant malignant cancer cells. In this study, we demonstrated how polyphenol stilbene compound PE5 exhibits potent ACD-promoting activity in lung cancer cells that may offer an opportunity for novel cancer treatment. Cell death caused by PE5 was found to be concomitant with dramatic autophagy induction, as indicated by acidic vesicle staining, autophagosome, and the LC3 conversion. We further confirmed that the main death induction caused by PE5 was via ACD, since the co-treatment with an autophagy inhibitor could reverse PE5-mediated cell death. Furthermore, the defined mechanism of action and upstream regulatory signals were identified using proteomic analysis. Time-dependent proteomic analysis showed that PE5 affected 2142 and 1996 proteins after 12 and 24 h of treatment, respectively. The crosstalk network comprising 128 proteins that control apoptosis and 25 proteins involved in autophagy was identified. Protein–protein interaction analysis further indicated that the induction of ACD was via AKT/mTOR and Bcl-2 suppression. Western blot analysis confirmed that the active forms of AKT, mTOR, and Bcl-2 were decreased in PE5-treated cells. Taken together, we demonstrated the novel mechanism of PE5 in shifting autophagy toward cell death induction by targeting AKT/mTOR and Bcl-2 suppression.

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The novel synthesized 2-(3-(methylamino)phenyl)-6-(pyrrolidin-1-yl)quinolin-4-one (Smh-3) compound induces G2/M phase arrest and mitochondrial-dependent apoptotic cell death through inhibition of CDK1 and AKT activity in HL-60 human leukemia cells

International Journal of Oncology ◽

10.3892/ijo.2011.952 ◽

2011 ◽

Vol 38 (5) ◽

Cited By ~ 5

Author(s):

Huang

Keyword(s):

Cell Death ◽

Apoptotic Cell ◽

Apoptotic Cell Death ◽

Leukemia Cells ◽

Human Leukemia ◽

The Novel ◽

Human Leukemia Cells ◽

Phase Arrest ◽

M Phase

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Cell Death Triggered by a Putative Amphipathic Helix of Radish mosaic virus Helicase Protein Is Tightly Correlated With Host Membrane Modification

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi-01-15-0004-r ◽

2015 ◽

Vol 28 (6) ◽

pp. 675-688 ◽

Cited By ~ 15

Author(s):

Masayoshi Hashimoto ◽

Ken Komatsu ◽

Ryo Iwai ◽

Takuya Keima ◽

Kensaku Maejima ◽

...

Keyword(s):

Cell Death ◽

Mosaic Virus ◽

Defense Responses ◽

Plant Viruses ◽

Amphipathic Helix ◽

Membrane Structures ◽

Membrane Modification ◽

Systemic Necrosis ◽

Amino Terminal ◽

Er Membrane

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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