scholarly journals PLANT NATRIURETIC PEPTIDE A antagonizes salicylic acid-primed cell death

2019 ◽  
Author(s):  
Keun Pyo Lee ◽  
Kaiwei Liu ◽  
Eun Yu Kim ◽  
Laura Medina-Puche ◽  
Jianli Duan ◽  
...  
Keyword(s):  
Cell Death ◽  
Salicylic Acid ◽  
Natriuretic Peptide ◽  
Intracellular Signaling ◽  
Cell Communication ◽  
Biological Processes ◽  
Receptor Proteins ◽  
Functional Analog ◽  
Primed Cell ◽  
Secreted Peptides

ABSTRACTPeptide hormones perceived in the cell surface via receptor proteins enable cell-to-cell communication and act in multiple biological processes through the activation of intracellular signaling. Even though Arabidopsis is predicted to have more than 1,000 secreted peptides, the biological relevance of the majority of these is yet to be established. Here, we demonstrate that PLANT NATRIURETIC PEPTIDE A (PNP-A), a functional analog to vertebrate atrial natriuretic peptides, antagonizes the salicylic acid (SA)-mediated cell death in the Arabidopsis lesion-stimulating disease 1 (lsd1) mutant. While loss of PNP-A potentiates SA signaling, exogenous application of the PNP-A synthetic peptide or overexpression of PNP-A significantly compromises the SA-mediated cell death. Moreover, we identified a plasma membrane-localized receptor-like protein, which we name PNPAR (for PNP-A receptor), that binds PNP-A and is required to counteract SA responses. Our work identifies a novel peptide-receptor pair which modulates SA responses in Arabidopsis.

scholarly journals N-Terminal Acetylation Stabilizes SIGMA FACTOR BINDING PROTEIN1 Involved in Salicylic Acid-Primed Cell Death

2020 ◽  
Vol 183 (1) ◽  
pp. 358-370 ◽  
Author(s):  
Zihao Li ◽  
Vivek Dogra ◽  
Keun Pyo Lee ◽  
Rongxia Li ◽  
Mingyue Li ◽  
...  
Keyword(s):  
Cell Death ◽  
Salicylic Acid ◽  
Sigma Factor ◽  
Factor Binding ◽  
Primed Cell

scholarly journals PLANT NATRIURETIC PEPTIDE A and Its Putative Receptor PNP-R2 Antagonize Salicylic Acid–Mediated Signaling and Cell Death

2020 ◽  
Vol 32 (7) ◽  
pp. 2237-2250 ◽  
Author(s):  
Keun Pyo Lee ◽  
Kaiwei Liu ◽  
Eun Yu Kim ◽  
Laura Medina-Puche ◽  
Haihong Dong ◽  
...  
Keyword(s):  
Cell Death ◽  
Salicylic Acid ◽  
Natriuretic Peptide ◽  
Putative Receptor

scholarly journals Age-Related Resistance of Nicotiana benthamiana Against Hemibiotrophic Pathogen Phytophthora infestans Requires Both Ethylene- and Salicylic Acid–Mediated Signaling Pathways

2010 ◽  
Vol 23 (9) ◽  
pp. 1130-1142 ◽  
Author(s):  
Yusuke Shibata ◽  
Kazuhito Kawakita ◽  
Daigo Takemoto
Keyword(s):  
Cell Death ◽  
Salicylic Acid ◽  
Gene Silencing ◽  
Phytophthora Infestans ◽  
Nicotiana Benthamiana ◽  
Virus Induced Gene Silencing ◽  
Expression Of Genes ◽  
Age Related ◽  
Functional Analog ◽  
Blight Disease

Phytophthora infestans, the agent of late blight disease of potato, is a hemibiotrophic pathogen with biotrophic action during early infection and necrotrophic in the later stage of colonization. Mature Nicotiana benthamiana was resistant to P. infestans, whereas relatively young plants were susceptible to this pathogen. Young plants became resistant following a pretreatment with acibenzolar-S-methyl, a functional analog of salicylic acid (SA), indicating that susceptibility of young plants is due to a lack of induction of SA signaling. Further analysis with virus-induced gene silencing indicated that NbICS1 and NbEIN2, the genes for SA biosynthesis and ethylene (ET) signaling, respectively, are required for the resistance of mature N. benthamiana against P. infestans. Furthermore, these genes are required for the production of reactive oxygen species (ROS) induced by treatment of the INF1 elicitor. In NbICS1-silenced plants, cell death induced by either INF1 or necrosis-inducing protein NPP1.1 was significantly accelerated. Expression of genes for phytoalexin (capsidiol) biosynthesis, NbEAS and NbEAH, were regulated by ET, and gene silencing of either of them compromised resistance of N. benthamiana to P. infestans. Together, these results suggest that resistance of N. benthamiana against hemibiotrophic P. infestans requires both SA-regulated appropriate induction of cell death and ET-induced production of phytoalexin.

scholarly journals Salicylic Acid Accumulation Controlled by LSD1 Is Essential in Triggering Cell Death in Response to Abiotic Stress

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 962
Author(s):  
Maciej Jerzy Bernacki ◽  
Anna Rusaczonek ◽  
Weronika Czarnocka ◽  
Stanisław Karpiński
Keyword(s):  
Cell Death ◽  
Salicylic Acid ◽  
Abiotic Stress ◽  
Wild Type ◽  
Pr Genes ◽  
Genes Expression ◽  
Salicylic Acid Accumulation ◽  
Cell Death Phenotype ◽  
Insight Into

Salicylic acid (SA) is well known hormonal molecule involved in cell death regulation. In response to a broad range of environmental factors (e.g., high light, UV, pathogens attack), plants accumulate SA, which participates in cell death induction and spread in some foliar cells. LESION SIMULATING DISEASE 1 (LSD1) is one of the best-known cell death regulators in Arabidopsis thaliana. The lsd1 mutant, lacking functional LSD1 protein, accumulates SA and is conditionally susceptible to many biotic and abiotic stresses. In order to get more insight into the role of LSD1-dependent regulation of SA accumulation during cell death, we crossed the lsd1 with the sid2 mutant, caring mutation in ISOCHORISMATE SYNTHASE 1(ICS1) gene and having deregulated SA synthesis, and with plants expressing the bacterial nahG gene and thus decomposing SA to catechol. In response to UV A+B irradiation, the lsd1 mutant exhibited clear cell death phenotype, which was reversed in lsd1/sid2 and lsd1/NahG plants. The expression of PR-genes and the H2O2 content in UV-treated lsd1 were significantly higher when compared with the wild type. In contrast, lsd1/sid2 and lsd1/NahG plants demonstrated comparability with the wild-type level of PR-genes expression and H2O2. Our results demonstrate that SA accumulation is crucial for triggering cell death in lsd1, while the reduction of excessive SA accumulation may lead to a greater tolerance toward abiotic stress.

scholarly journals Uncoupling Salicylic Acid-Dependent Cell Death and Defense-Related Responses From Disease Resistance in the Arabidopsis Mutant acd5

Genetics ◽  
2000 ◽  
Vol 156 (1) ◽  
pp. 341-350
Author(s):  
Jean T Greenberg ◽  
F Paul Silverman ◽  
Hua Liang
Keyword(s):  
Cell Death ◽  
Salicylic Acid ◽  
Disease Resistance ◽  
Pseudomonas Syringae ◽  
Higher Plants ◽  
Ethylene Signaling ◽  
Symptom Development ◽  
Wild Type ◽  
Dependent Cell ◽  
Arabidopsis Mutant

Abstract Salicylic acid (SA) is required for resistance to many diseases in higher plants. SA-dependent cell death and defense-related responses have been correlated with disease resistance. The accelerated cell death 5 mutant of Arabidopsis provides additional genetic evidence that SA regulates cell death and defense-related responses. However, in acd5, these events are uncoupled from disease resistance. acd5 plants are more susceptible to Pseudomonas syringae early in development and show spontaneous SA accumulation, cell death, and defense-related markers later in development. In acd5 plants, cell death and defense-related responses are SA dependent but they do not confer disease resistance. Double mutants with acd5 and nonexpressor of PR1, in which SA signaling is partially blocked, show greatly attenuated cell death, indicating a role for NPR1 in controlling cell death. The hormone ethylene potentiates the effects of SA and is important for disease symptom development in Arabidopsis. Double mutants of acd5 and ethylene insensitive 2, in which ethylene signaling is blocked, show decreased cell death, supporting a role for ethylene in cell death control. We propose that acd5 plants mimic P. syringae-infected wild-type plants and that both SA and ethylene are normally involved in regulating cell death during some susceptible pathogen infections.

scholarly journals Insights into how environment shapes post-mortem RNA transcription in mouse brain

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Raphael Severino Bonadio ◽  
Larissa Barbosa Nunes ◽  
Patricia Natália S. Moretti ◽  
Juliana Forte Mazzeu ◽  
Stefano Cagnin ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Mouse Brain ◽  
Molecular Mechanisms ◽  
Cell Communication ◽  
Rna Degradation ◽  
The Body ◽  
Biological Processes ◽  
Post Mortem ◽  
Gene Expression Alterations ◽  
Upregulated Genes

AbstractMost biological features that occur on the body after death were already deciphered by traditional medicine. However, the molecular mechanisms triggered in the cellular microenvironment are not fully comprehended yet. Previous studies reported gene expression alterations in the post-mortem condition, but little is known about how the environment could influence RNA degradation and transcriptional regulation. In this work, we analysed the transcriptome of mouse brain after death under three concealment simulations (air exposed, buried, and submerged). Our analyses identified 2,103 genes differentially expressed in all tested groups 48 h after death. Moreover, we identified 111 commonly upregulated and 497 commonly downregulated genes in mice from the concealment simulations. The gene functions shared by the individuals from the tested environments were associated with RNA homeostasis, inflammation, developmental processes, cell communication, cell proliferation, and lipid metabolism. Regarding the altered biological processes, we identified that the macroautophagy process was enriched in the upregulated genes and lipid metabolism was enriched in the downregulated genes. On the other hand, we also described a list of biomarkers associated with the submerged and buried groups, indicating that these environments can influence the post-mortem RNA abundance in its particular way.

scholarly journals Neurotoxic Effect of Flavonol Myricetin in the Presence of Excess Copper

Molecules ◽  
2021 ◽  
Vol 26 (4) ◽  
pp. 845
Author(s):  
Anja Sadžak ◽  
Ignacija Vlašić ◽  
Zoran Kiralj ◽  
Marijana Batarelo ◽  
Nada Oršolić ◽  
...  
Keyword(s):  
Cell Death ◽  
Intracellular Signaling ◽  
Chromatin Condensation ◽  
Membrane Integrity ◽  
Toxic Effects ◽  
Trypan Blue Exclusion ◽  
Atp Production ◽  
Mtt Method ◽  
Biophysical Approach ◽  
Induced Changes

Oxidative stress (OS) induced by the disturbed homeostasis of metal ions is one of the pivotal factors contributing to neurodegeneration. The aim of the present study was to investigate the effects of flavonoid myricetin on copper-induced toxicity in neuroblastoma SH-SY5Y cells. As determined by the MTT method, trypan blue exclusion assay and measurement of ATP production, myricetin heightened the toxic effects of copper and exacerbated cell death. It also increased copper-induced generation of reactive oxygen species, indicating the prooxidative nature of its action. Furthermore, myricetin provoked chromatin condensation and loss of membrane integrity without caspase-3 activation, suggesting the activation of both caspase-independent programmed cell death and necrosis. At the protein level, myricetin-induced upregulation of PARP-1 and decreased expression of Bcl-2, whereas copper-induced changes in the expression of p53, p73, Bax and NME1 were not further affected by myricetin. Inhibitors of ERK1/2 and JNK kinases, protein kinase A and L-type calcium channels exacerbated the toxic effects of myricetin, indicating the involvement of intracellular signaling pathways in cell death. We also employed atomic force microscopy (AFM) to evaluate the morphological and mechanical properties of SH-SY5Y cells at the nanoscale. Consistent with the cellular and molecular methods, this biophysical approach also revealed a myricetin-induced increase in cell surface roughness and reduced elasticity. Taken together, we demonstrated the adverse effects of myricetin, pointing out that caution is required when considering powerful antioxidants for adjuvant therapy in copper-related neurodegeneration.

scholarly journals PRDX1 is essential for the viability and maintenance of reactive oxygen species in chicken DT40

2021 ◽  
Vol 43 (1) ◽  
Author(s):  
Takahito Moriwaki ◽  
Akari Yoshimura ◽  
Yuki Tamari ◽  
Hiroyuki Sasanuma ◽  
Shunichi Takeda ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Intracellular Signaling ◽  
Reactive Oxygen ◽  
Fine Tuning ◽  
Oxygen Species ◽  
Ros Homeostasis ◽  
Intracellular Ros ◽  
Chromosomal Breaks ◽  
Dt40 Cells

Abstract Background Peroxiredoxin 1 (PRDX1) is a member of a ubiquitous family of thiol peroxidases that catalyze the reduction of peroxides, including hydrogen peroxide. It functions as an antioxidant enzyme, similar to catalase and glutathione peroxidase. PRDX1 was recently shown act as a sensor of reactive oxygen species (ROS) and play a role in ROS-dependent intracellular signaling pathways. To investigate its physiological functions, PRDX1 was conditionally disrupted in chicken DT40 cells in the present study. Results The depletion of PRDX1 resulted in cell death with increased levels of intracellular ROS. PRDX1-depleted cells did not show the accumulation of chromosomal breaks or sister chromatid exchange (SCE). These results suggest that cell death in PRDX1-depleted cells was not due to DNA damage. 2-Mercaptoethanol protected against cell death in PRDX1-depleted cells and also suppressed elevations in ROS. Conclusions PRDX1 is essential in chicken DT40 cells and plays an important role in maintaining intracellular ROS homeostasis (or in the fine-tuning of cellular ROS levels). Cells deficient in PRDX1 may be used as an endogenously deregulated ROS model to elucidate the physiological roles of ROS in maintaining proper cell growth.

The intracellular carboxyl tail of the PAR-2 receptor controls intracellular signaling and cell death

2014 ◽  
Vol 359 (3) ◽  
pp. 817-827 ◽  
Author(s):  
Zhihui Zhu ◽  
Rolf Stricker ◽  
Rong yu Li ◽  
Gregor Zündorf ◽  
Georg Reiser
Keyword(s):  
Cell Death ◽  
Intracellular Signaling ◽  
Carboxyl Tail

scholarly journals Death Receptor-Induced Activation of Initiator Caspase 8 Is Antagonized by Serine/Threonine Kinase PAK4

2003 ◽  
Vol 23 (21) ◽  
pp. 7838-7848 ◽  
Author(s):  
Nerina Gnesutta ◽  
Audrey Minden
Keyword(s):  
Cell Death ◽  
Cell Survival ◽  
Intracellular Signaling ◽  
Death Receptor ◽  
Caspase 8 ◽  
Death Domain ◽  
Serine Threonine Kinase ◽  
Threonine Kinase ◽  
Different Types ◽  
Promote Cell Survival

ABSTRACT Normal cell growth requires a precisely controlled balance between cell death and survival. This involves activation of different types of intracellular signaling cascades within the cell. While some types of signaling proteins regulate apoptosis, or programmed cell death, other proteins within the cell can promote survival. The serine/threonine kinase PAK4 can protect cells from apoptosis in response to several different types of stimuli. As is the case for other members of the p21-activated kinase (PAK) family, one way that PAK4 may promote cell survival is by phosphorylating and thereby inhibiting the proapoptotic protein Bad. This leads in turn to the inhibition of effector caspases such as caspase 3. Here we show that in response to cytokines which activate death domain-containing receptors, such as the tumor necrosis factor and Fas receptors, PAK4 can inhibit the death signal by a different mechanism. Under these conditions, PAK4 inhibits apoptosis early in the caspase cascade, antagonizing the activation of initiator caspase 8. This inhibition, which does not require PAK4's kinase activity, may involve inhibition of caspase 8 recruitment to the death domain receptors. This role in regulating initiator caspases is an entirely novel role for the PAK proteins and suggests a new mechanism by which these proteins promote cell survival.

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