scholarly journals EXTRA LARGE G-PROTEIN 2 (XLG2) mediates cell death and hyperimmunity via a novel, apoplastic ROS-independent pathway in Arabidopsis thaliana

2021 ◽  
Author(s):  
Elena Kristin Petutschnig ◽  
Julia Anders ◽  
Marnie Stolze ◽  
Christopher Meusel ◽  
Ronja Hacke ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Surface Receptor ◽  
Ros Generation ◽  
Cell Periphery ◽  
Heterotrimeric G Proteins ◽  
Cell Death Pathway ◽  
Powdery Mildews ◽  
Suppressor Effect ◽  
Receptor Component ◽  
Surface Receptor

Heterotrimeric G-Proteins are signal transduction complexes comprised of three subunits, Gα, Gβand Gγ, and are involved in many aspects of plant life. The non-canonical Gα subunit XLG2 mediates PAMP-induced ROS generation and immunity downstream of PRRs. A mutant of the chitin receptor component CERK1, cerk1-4, maintains normal chitin signalling capacity, but shows excessive cell death upon infection with powdery mildews. We identified XLG2 mutants as suppressors of the cerk1-4 phenotype. We generated stably transformed Arabidopsis lines expressing Venus-XLG2 and numerous mutated variants. These were analysed by confocal microscopy, Western blotting and pathogen infection. We also crossed cerk1-4 with several mutants involved in immunity and analysed their phenotype. Phosphorylation of XLG2 was investigated by quantitative proteomics. Mutations in XLG2 complex partners AGB1 and AGG1 have a partial cerk1-4 suppressor effect. The cerk1-4 phenotype is independent of NADPH oxidase-generated ROS, BAK1 and SOBIR1, but requires PUB2. XLG2 mediates cerk1-4 cell death at the cell periphery. Integrity of the XLG2 N-terminal domain, but not its phosphorylation, is essential for correct XLG2 localisation and cerk1-4 signalling. Our results suggest that XLG2 transduces signals from an unknown cell surface receptor that activates an apoplastic ROS-independent cell death pathway in Arabidopsis.

scholarly journals Estradiol-inducible AvrRps4 expression reveals distinct properties of TIR-NLR-mediated effector-triggered immunity

2020 ◽  
Vol 71 (6) ◽  
pp. 2186-2197 ◽  
Author(s):  
Bruno Pok Man Ngou ◽  
Hee-Kyung Ahn ◽  
Pingtao Ding ◽  
Amey Redkar ◽  
Hannah Brown ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Surface Receptor ◽  
Leucine Rich Repeat ◽  
Nucleotide Binding Domain ◽  
Hypersensitive Cell Death ◽  
Cell Death Response ◽  
Defence Genes ◽  
Surface Receptor ◽  
Effector Triggered Immunity ◽  
Bacterial Effectors

Abstract Plant nucleotide-binding domain, leucine-rich repeat receptor (NLR) proteins play important roles in recognition of pathogen-derived effectors. However, the mechanism by which plant NLRs activate immunity is still largely unknown. The paired Arabidopsis NLRs RRS1-R and RPS4, that confer recognition of bacterial effectors AvrRps4 and PopP2, are well studied, but how the RRS1/RPS4 complex activates early immediate downstream responses upon effector detection is still poorly understood. To study RRS1/RPS4 responses without the influence of cell surface receptor immune pathways, we generated an Arabidopsis line with inducible expression of the effector AvrRps4. Induction does not lead to hypersensitive cell death response (HR) but can induce electrolyte leakage, which often correlates with plant cell death. Activation of RRS1 and RPS4 without pathogens cannot activate mitogen-associated protein kinase cascades, but still activates up-regulation of defence genes, and therefore resistance against bacteria.

scholarly journals The helper NLR immune protein NRC3 mediates the hypersensitive cell death caused by the cell-surface receptor Cf-4

2021 ◽  
Author(s):  
Jiorgos Kourelis ◽  
Mauricio P. Contreras ◽  
Adeline Harant ◽  
Hiroaki Adachi ◽  
Lida Derevnina ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Surface ◽  
Immune Responses ◽  
Coiled Coil ◽  
Chimeric Protein ◽  
Cell Surface Receptor ◽  
Surface Pattern ◽  
Hypersensitive Cell Death ◽  
Cell Death Response ◽  
Surface Receptor

Cell surface pattern recognition receptors (PRRs) activate immune responses that can include the hypersensitive cell death. However, the pathways that link PRRs to the cell death response are poorly understood. Here, we show that the cell surface receptor-like protein Cf-4 requires the intracellular nucleotide-binding domain leucine-rich repeat containing receptor (NLR) NRC3 to trigger a confluent cell death response upon detection of the fungal effector Avr4 in leaves of Nicotiana benthamiana. This NRC3 activity requires an intact N-terminal MADA motif, a conserved signature of coiled-coil (CC)-type plant NLRs that is required for resistosome-mediated immune responses. A chimeric protein with the N-terminal α1 helix of Arabidopsis ZAR1 swapped into NRC3 retains the capacity to mediate Cf-4 hypersensitive cell death. Pathogen effectors acting as suppressors of NRC3 can suppress Cf-4-triggered hypersensitive cell-death. Our findings link the NLR resistosome model to the hypersensitive cell death caused by a cell surface PRR.

scholarly journals Programmed Cell Death-1 Receptor (PD-1)-Mediated Regulation of Innate Lymphoid Cells

2019 ◽  
Vol 20 (11) ◽  
pp. 2836 ◽  
Author(s):  
Grace Mallett ◽  
Arian Laurence ◽  
Shoba Amarnath
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Cell Surface Receptor ◽  
Programmed Cell Death 1 ◽  
Surface Receptor ◽  
A Cell ◽  
And Function

Programmed cell death-1 (PD-1) is a cell surface receptor that dampens adaptive immune responses. PD-1 is activated by the engagement of its ligands PDL-1 or PDL-2. This results in the inhibition of T cell proliferation, differentiation, cytokine secretion, and cytolytic function. Although a great deal is known about PD-1 mediated regulation of CD4+ and CD8+ T cells, its expression and function in innate lymphoid cells (ILCs) are yet to be fully deciphered. This review summarizes the role of PD-1 in (1) modulating ILC development, (2) ILC function, and (3) PD-1 signaling in ILC. Finally, we explore how PD-1 based immunotherapies may be beneficial in boosting ILC responses in cancer, infections, and other immune-related disorders.

scholarly journals Molecular cloning of Porimin, a novel cell surface receptor mediating oncotic cell death

2001 ◽  
Vol 98 (17) ◽  
pp. 9778-9783 ◽  
Author(s):  
F. Ma ◽  
C. Zhang ◽  
K. V. S. Prasad ◽  
G. J. Freeman ◽  
S. F. Schlossman
Keyword(s):  
Cell Death ◽  
Cell Surface ◽  
Molecular Cloning ◽  
Cell Surface Receptor ◽  
Surface Receptor

scholarly journals Multiple Sclerosis: Fas Signaling in Oligodendrocyte Cell Death

1996 ◽  
Vol 184 (6) ◽  
pp. 2361-2370 ◽  
Author(s):  
Sameer D. D'Souza ◽  
Bruno Bonetti ◽  
Vijayabalan Balasingam ◽  
Neil R. Cashman ◽  
Philip A. Barker ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Monoclonal Antibody ◽  
Cell Death ◽  
Fas Ligand ◽  
Demyelinating Disease ◽  
Cellular Systems ◽  
Cell Surface Receptor ◽  
Fas Signaling ◽  
Surface Receptor ◽  
A Cell

Fas is a cell surface receptor that transduces cell death signals when cross-linked by agonist antibodies or by fas ligand. In this study, we examined the potential of fas to contribute to oligodendrocyte (OL) injury and demyelination as they occur in the human demyelinating disease multiple sclerosis (MS). Immunohistochemical study of central nervous system (CNS) tissue from MS subjects demonstrated elevated fas expression on OLs in chronic active and chronic silent MS lesions compared with OLs in control tissue from subjects with or without other neurologic diseases. In such lesions, microglia and infiltrating lymphocytes displayed intense immunoreactivity to fas ligand. In dissociated glial cell cultures prepared from human adult CNS tissue, fas expression was restricted to OLs. Fas ligation with the anti-fas monoclonal antibody M3 or with the fas–ligand induced rapid OL cell membrane lysis, assessed by LDH release and trypan blue uptake and subsequent cell death. In contrast to the activity of fas in other cellular systems, dying OLs did not exhibit evidence of apoptosis, assessed morphologically and by terminal transferase–mediated d-uridine triphosphate-biotin nick-end-labeling staining for DNA fragmentation. Other stimuli such as C2-ceramide were capable of inducing rapid apoptosis in OLs. Antibodies directed at other surface molecules expressed on OLs or the M33 nonactivating anti-fas monoclonal antibody did not induce cytolysis of OLs. Our results suggest that fas-mediated signaling might contribute in a novel cytolytic manner to immune-mediated OL injury in MS.

scholarly journals DHEA protects mitochondria against dual modes of apoptosis and necroptosis in human granulosa HO23 cells

Reproduction ◽  
2017 ◽  
Vol 154 (2) ◽  
pp. 101-110 ◽  
Author(s):  
Kuan-Hao Tsui ◽  
Peng-Hui Wang ◽  
Li-Te Lin ◽  
Chia-Jung Li
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Culture Conditions ◽  
Human Oocyte ◽  
Ros Generation ◽  
Mitochondrial Morphology ◽  
Ros Scavenging ◽  
Chinese Translation ◽  
Cell Death Pathway

Because ovarian granulosa cells are essential for oocyte maturation and development, we validated human granulosa HO23 cells to evaluate the ability of the DHEA to prevent cell death after starvation. The present study was aimed to investigate whether DHEA could protect against starvation-induced apoptosis and necroptosis in human oocyte granulosa HO23 cells. The starvation was induced by treatment of serum-free (SF) medium for 4 h in vitro. Starvation-induced mitochondrial depolarization, cytochrome c release and caspase-3 activation were largely prevented by DHEA in HO23 cells. We found that treatment with DHEA can restore starvation-induced reactive oxygen species (ROS) generation and mitochondrial membrane potential imbalance. In addition, treatment of DHEA prevents cell death via upregulation of cytochrome c and downregulation of BAX in mitochondria. Most importantly, DHEA is ameliorated to mitochondrial function mediated through the decrease in mitochondrial ROS, maintained mitochondrial morphology, and enhancing the ability of cell proliferation and ROS scavenging. Our present data strongly indicate that DHEA reduces programmed cell death (apoptosis and necroptosis) in granulosa HO23 cells through multiple interactions with the mitochondrion-dependent programmed cell death pathway. Taken together, our data suggest that the presence of DHEA could be beneficial to protect human oocyte granulosa HO23 cells under in vitro culture conditions during various assisted reproductive technology (ART) programs. Free Chinese abstract: A Chinese translation of this abstract is freely available at http://www.reproduction-online.org/content/154/2/101/suppl/DC1

scholarly journals Altered neutrophil phenotype and function in non-ICU COVID-19 patients correlated with disease severity

2021 ◽  
Author(s):  
Kylie BR Belchamber ◽  
Onn S Thein ◽  
Jon Hazeldine ◽  
Frances S Grudzinska ◽  
Michael J Hughes ◽  
...  
Keyword(s):  
Disease Severity ◽  
Ex Vivo ◽  
Surface Expression ◽  
Neutrophil Function ◽  
Receptor Expression ◽  
Cell Surface Receptor ◽  
Ros Generation ◽  
Cell Functions ◽  
Surface Receptor ◽  
Neutrophil Dysfunction

Rational: Infection with the SARS-CoV2 virus is associated with elevated neutrophil counts. Evidence of neutrophil dysfunction in COVID-19 is based predominantly on transcriptomics or single functional assays. Cell functions are interwoven pathways, and so understanding the effect of COVID-19 across the spectrum of neutrophil function may identify tractable therapeutic targets. Objectives: Examine neutrophil phenotype and functional capacity in COVID-19 patients versus age-matched controls (AMC) Methods: Isolated neutrophils from 41 hospitalised, non-ICU COVID-19 patients and 23 AMC underwent ex vivo analyses for migration, bacterial phagocytosis, ROS generation, NET formation (NETosis) and cell surface receptor expression. DNAse 1 activity was measured, alongside circulating levels of cfDNA, MPO, VEGF, IL-6 and sTNFRI. All measurements were correlated to clinical outcome. Serial sampling on day 3-5 post hospitalisation were also measured. Results: Compared to AMC, COVID-19 neutrophils demonstrated elevated transmigration (p=0.0397) and NETosis (p=0.0366), but impaired phagocytosis (p=0.0236) associated with impaired ROS generation (p<0.0001). Surface expression of CD54 (p<0.0001) and CD11c (p=0.0008) was significantly increased and CD11b significantly decreased (p=0.0229) on COVID-19 patient neutrophils. COVID-19 patients showed increased systemic markers of NETosis including increased cfDNA (p=0.0153) and impaired DNAse activity (p<0.0.001). MPO (p<0.0001), VEGF (p<0.0001), TNFRI (p<0.0001) and IL-6 (p=0.009) were elevated in COVID-19, which positively correlated with disease severity by 4C score. Conclusion: COVID-19 is associated with neutrophil dysfunction across all main effector functions, with altered phenotype, elevated migration, impaired antimicrobial responses and elevated NETosis. These changes represent a clear mechanism for tissue damage and highlight that targeting neutrophil function may help modulate COVID-19 severity.

scholarly journals Harpin and hydrogen peroxide both initiate programmed cell death but have differential effects on defence gene expression in Arabidopsis suspension cultures

1998 ◽  
Vol 330 (1) ◽  
pp. 115-120 ◽  
Author(s):  
Radhika DESIKAN ◽  
Adele REYNOLDS ◽  
T. John HANCOCK ◽  
J. Steven NEILL
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Plant Defence ◽  
Suspension Cultures ◽  
Ros Generation ◽  
Resistance Response ◽  
Signalling Molecules ◽  
Cell Death Pathway ◽  
A Cell

Programmed cell death is increasingly viewed as a key component of the hypersensitive disease resistance response of plants. The generation of reactive oxygen species (ROS) such as H2O2 triggers a cell death programme in Arabidopsis suspension cultures following challenge with the bacterial elicitor harpin. Both harpin and exogenous H2O2 initiate a cell death pathway that requires gene expression, and also act as signalling molecules to induce the expression of plant defence genes encoding enzymes such as phenylalanine ammonia-lyase (PAL), glutathione S-transferase (GST) and anthranilate synthase (ASA1), an enzyme of phytoalexin biosynthesis in Arabidopsis. H2O2 induces the expression of PAL1 and GST but not that of ASA1. Harpin initiates two signalling pathways, one leading to increased ROS generation and expression of PAL1 and GST mRNA, and another leading to increased GST and ASA1 expression, independent of H2O2.

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