scholarly journals Loss-of-function ofArabidopsisreceptor-like kinase BIR1 activates cell death and defense responses mediated by BAK1 and SOBIR1

2016 ◽  
Vol 212 (3) ◽  
pp. 637-645 ◽  
Author(s):  
Yanan Liu ◽  
Xingchuan Huang ◽  
Meng Li ◽  
Ping He ◽  
Yuelin Zhang
Keyword(s):  
Cell Death ◽  
Defense Responses ◽  
Loss Of Function

scholarly journals Arabidopsis EDR1 Protein Kinase Regulates the Association of EDS1 and PAD4 to Inhibit Cell Death

2020 ◽  
Vol 33 (4) ◽  
pp. 693-703 ◽  
Author(s):  
Matthew Neubauer ◽  
Irene Serrano ◽  
Natalie Rodibaugh ◽  
Deepak D. Bhandari ◽  
Jaqueline Bautor ◽  
...  
Keyword(s):  
Cell Death ◽  
Protein Kinase ◽  
Defense Responses ◽  
Loss Of Function ◽  
Wild Type ◽  
Independent Function ◽  
Signaling Function ◽  
Golovinomyces Cichoracearum ◽  
Powdery Mildew Pathogen ◽  
Heteromeric Association

ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) and PHYTOALEXIN DEFICIENT4 (PAD4) are sequence-related lipase-like proteins that function as a complex to regulate defense responses in Arabidopsis by both salicylic acid–dependent and independent pathways. Here, we describe a gain-of-function mutation in PAD4 (S135F) that enhances resistance and cell death in response to infection by the powdery mildew pathogen Golovinomyces cichoracearum. The mutant PAD4 protein accumulates to wild-type levels in Arabidopsis cells, thus these phenotypes are unlikely to be due to PAD4 over accumulation. The phenotypes are similar to loss-of-function mutations in the protein kinase EDR1 (Enhanced Disease Resistance1), and previous work has shown that loss of PAD4 or EDS1 suppresses edr1-mediated phenotypes, placing these proteins downstream of EDR1. Here, we show that EDR1 directly associates with EDS1 and PAD4 and inhibits their interaction in yeast and plant cells. We propose a model whereby EDR1 negatively regulates defense responses by interfering with the heteromeric association of EDS1 and PAD4. Our data indicate that the S135F mutation likely alters an EDS1-independent function of PAD4, potentially shedding light on a yet-unknown PAD4 signaling function.

scholarly journals OsPG1 encodes a polygalacturonase that determines cell wall architecture and affects resistance to bacterial blight pathogen in rice

2020 ◽  
Author(s):  
Qunen Liu ◽  
Yongrun Cao ◽  
Yue Zhang ◽  
Yuyu Chen ◽  
Ning Yu ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Wall ◽  
Defense Response ◽  
Cell Walls ◽  
Bacterial Blight ◽  
Defense Responses ◽  
Base Substitution ◽  
Loss Of Function ◽  
Wild Type ◽  
Bacterial Blight Pathogen

Abstract Background Plant cell walls are the main physical barrier encountered by pathogens colonizing plant tissues. Alteration of cell wall integrity (CWI) can activate specific defenses by impairing proteins involved in cell wall biosynthesis, degradation and remodeling, or cell wall damage due to biotic or abiotic stress. Polygalacturonase (PG) depolymerize pectin by hydrolysis, thereby altering pectin composition and structures and activating cell wall defense. Although many studies of CWI have been reported, the mechanism of how PGs regulate cell wall immune response is not well understood.Results Necrosis appeared in leaf tips at the tillering stage, finally resulting in 3–5 cm of dark brown necrotic tissue. ltn-212 showed obvious cell death and accumulation of H2O2 in leaf tips. The defense responses were activated in ltn-212 to resist bacterial blight pathogen of rice. Map based cloning revealed that a single base substitution (G-A) in the first intron caused incorrect splicing of OsPG1, resulting in a necrotic phenotype. OsPG1 is constitutively expressed in all organs, and the wild-type phenotype was restored in complementation individuals and knockout of wild-type lines resulted in necrosis as in ltn-212. Transmission electron microscopy showed that thicknesses of cell walls were significantly reduced and cell size and shape were significantly diminished in ltn-212.Conclusion These results demonstrate that OsPG1 encodes a PG in response to the leaf tip necrosis phenotype of ltn-212. Loss-of-function mutation of ltn-212 destroyed CWI, resulting in spontaneous cell death and an auto-activated defense response including reactive oxygen species (ROS) burst and pathogenesis-related (PR) gene expression, as well as enhanced resistance to Xanthomonas oryzae pv. oryzae (Xoo). These findings promote our understanding of the CWI mediated defense response.

scholarly journals OsPG1 encodes a polygalacturonase that determines cell wall architecture and affects resistance to bacterial blight pathogen in rice

2021 ◽  
Author(s):  
Yongrun Cao ◽  
Yue Zhang ◽  
Yuyu Chen ◽  
Ning Yu ◽  
Shah Liaqat ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Wall ◽  
Defense Response ◽  
Cell Walls ◽  
Bacterial Blight ◽  
Defense Responses ◽  
Base Substitution ◽  
Loss Of Function ◽  
Wild Type ◽  
Bacterial Blight Pathogen

Abstract Background: Plant cell walls are the main physical barrier encountered by pathogens colonizing plant tissues. Alteration of cell wall integrity (CWI) can activate specific defenses by impairing proteins involved in cell wall biosynthesis, degradation and remodeling, or cell wall damage due to biotic or abiotic stress. Polygalacturonase (PG) depolymerize pectin by hydrolysis, thereby altering pectin composition and structures and activating cell wall defense. Although many studies of CWI have been reported, the mechanism of how PGs regulate cell wall immune response is not well understood. Results: Necrosis appeared in leaf tips at the tillering stage, finally resulting in 3-5 cm of dark brown necrotic tissue. ltn-212 showed obvious cell death and accumulation of H2O2 in leaf tips. The defense responses were activated in ltn-212 to resist bacterial blight pathogen of rice. Map based cloning revealed that a single base substitution (G-A) in the first intron caused incorrect splicing of OsPG1, resulting in a necrotic phenotype. OsPG1 is constitutively expressed in all organs, and the wild-type phenotype was restored in complementation individuals and knockout of wild-type lines resulted in necrosis as in ltn-212. Transmission electron microscopy showed that thicknesses of cell walls were significantly reduced and cell size and shape were significantly diminished in ltn-212.Conclusion: These results demonstrate that OsPG1 encodes a PG in response to the leaf tip necrosis phenotype of ltn-212. Loss-of-function mutation of ltn-212 destroyed CWI, resulting in spontaneous cell death and an auto-activated defense response including reactive oxygen species (ROS) burst and pathogenesis-related (PR) gene expression, as well as enhanced resistance to Xanthomonas oryzae pv. oryzae (Xoo). These findings promote our understanding of the CWI mediated defense response.

scholarly journals Arabidopsis ENHANCED DISEASE RESISTANCE1 Protein Kinase Regulates the Association of ENHANCED DISEASE SUSCEPTIBILITY1 and PHYTOALEXIN DEFICIENT4 to Inhibit Cell Death

2019 ◽  
Author(s):  
Matthew Neubauer ◽  
Irene Serrano ◽  
Natalie Rodibaugh ◽  
Deepak D. Bhandari ◽  
Jaqueline Bautor ◽  
...  
Keyword(s):  
Cell Death ◽  
Protein Kinase ◽  
Defense Responses ◽  
Loss Of Function ◽  
Wild Type ◽  
Independent Function ◽  
Signaling Function ◽  
Golovinomyces Cichoracearum ◽  
Powdery Mildew Pathogen ◽  
Heteromeric Association

ABSTRACTENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) and PHYTOALEXIN DEFICIENT4 (PAD4) are sequence-related lipase-like proteins that function as a complex to regulate defense responses in Arabidopsis by both salicylic acid-dependent and independent pathways. Here we describe a gain-of-function mutation in PAD4 (S135F) that enhances resistance and cell death in response to infection by the powdery mildew pathogen Golovinomyces cichoracearum. The mutant PAD4 protein accumulates to wild-type levels in Arabidopsis cells, thus these phenotypes are unlikely to be due to PAD4 over accumulation. The phenotypes are similar to loss of function mutations in the protein kinase Enhanced Disease Resistance1 (EDR1), and previous work has shown that loss of PAD4 or EDS1 suppresses edr1-mediated phenotypes, placing these proteins downstream of EDR1. Here we show that EDR1 directly associates with EDS1 and PAD4 and inhibits their interaction in yeast and plant cells. We propose a model whereby EDR1 negatively regulates defense responses by interfering with the heteromeric association of EDS1 and PAD4. Our data indicate that the S135F mutation likely alters an EDS1-independent function of PAD4, potentially shedding light on a yet unknown PAD4 signaling function.

scholarly journals OsPG1 Encodes a Polygalacturonase that Determines Cell Wall Architecture and Affects Resistance to Bacterial Blight Pathogen in Rice

Rice ◽  
2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Yongrun Cao ◽  
Yue Zhang ◽  
Yuyu Chen ◽  
Ning Yu ◽  
Shah Liaqat ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Wall ◽  
Defense Response ◽  
Cell Walls ◽  
Bacterial Blight ◽  
Defense Responses ◽  
Base Substitution ◽  
Loss Of Function ◽  
Wild Type ◽  
Bacterial Blight Pathogen

Abstract Background Plant cell walls are the main physical barrier encountered by pathogens colonizing plant tissues. Alteration of cell wall integrity (CWI) can activate specific defenses by impairing proteins involved in cell wall biosynthesis, degradation and remodeling, or cell wall damage due to biotic or abiotic stress. Polygalacturonase (PG) depolymerize pectin by hydrolysis, thereby altering pectin composition and structures and activating cell wall defense. Although many studies of CWI have been reported, the mechanism of how PGs regulate cell wall immune response is not well understood. Results Necrosis appeared in leaf tips at the tillering stage, finally resulting in 3–5 cm of dark brown necrotic tissue. ltn-212 showed obvious cell death and accumulation of H2O2 in leaf tips. The defense responses were activated in ltn-212 to resist bacterial blight pathogen of rice. Map based cloning revealed that a single base substitution (G-A) in the first intron caused incorrect splicing of OsPG1, resulting in a necrotic phenotype. OsPG1 is constitutively expressed in all organs, and the wild-type phenotype was restored in complementation individuals and knockout of wild-type lines resulted in necrosis as in ltn-212. Transmission electron microscopy showed that thicknesses of cell walls were significantly reduced and cell size and shape were significantly diminished in ltn-212. Conclusion These results demonstrate that OsPG1 encodes a PG in response to the leaf tip necrosis phenotype of ltn-212. Loss-of-function mutation of ltn-212 destroyed CWI, resulting in spontaneous cell death and an auto-activated defense response including reactive oxygen species (ROS) burst and pathogenesis-related (PR) gene expression, as well as enhanced resistance to Xanthomonas oryzae pv. oryzae (Xoo). These findings promote our understanding of the CWI mediated defense response.

scholarly journals Echovirus infection causes rapid loss-of-function and cell death in human dendritic cells

2007 ◽  
Vol 9 (6) ◽  
pp. 1507-1518 ◽  
Author(s):  
Matthijs Kramer ◽  
Barbara M. Schulte ◽  
Liza W. J. Toonen ◽  
Mike A. M. de Bruijni ◽  
Jochem M. D. Galama ◽  
...  
Keyword(s):  
Cell Death ◽  
Dendritic Cells ◽  
Loss Of Function ◽  
Rapid Loss ◽  
Human Dendritic Cells

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

2015 ◽  
Vol 28 (6) ◽  
pp. 675-688 ◽  
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.

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

2014 ◽  
Vol 202 (4) ◽  
pp. 1320-1334 ◽  
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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