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 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 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 Restoration of Defective Cross Talk in ssi2 Mutants: Role of Salicylic Acid, Jasmonic Acid, and Fatty Acids in SSI2-Mediated Signaling

2003 ◽  
Vol 16 (11) ◽  
pp. 1022-1029 ◽  
Author(s):  
Pradeep Kachroo ◽  
Aardra Kachroo ◽  
Ludmila Lapchyk ◽  
David Hildebrand ◽  
Daniel F. Klessig
Keyword(s):  
Cell Death ◽  
Salicylic Acid ◽  
Jasmonic Acid ◽  
Cross Talk ◽  
Pr Genes ◽  
Exogenous Application ◽  
Basal Level Expression ◽  
Sa Signaling ◽  
Spontaneous Cell Death

The Arabidopsis mutants ssi2 and fab2 are defective in stearoyl ACP desaturase, which causes altered salicylic acid (SA)- and jasmonic acid (JA)-mediated defense signaling. Both ssi2 and fab2 plants show spontaneous cell death, express PR genes constitutively, accumulate high levels of SA, and exhibit enhanced resistance to bacterial and oomycete pathogens. In contrast to constitutive activation of the SA pathway, ssi2 and fab2 plants are repressed in JA-mediated induction of the PDF1.2 gene, which suggests that the SSI2-mediated signaling pathway modulates cross talk between the SA and JA pathways. In this study, we have characterized two recessive nonallelic mutants in the ssi2 background, designated as rdc (restorer of defective cross talk) 2 and rdc8. Both ssi2 rdc mutants are suppressed in constitutive SA signaling, show basal level expression of PR-1 gene, and induce high levels of PDF1.2 in response to exogenous application of JA. Interestingly, while the rdc8 mutation completely abolishes spontaneous cell death in ssi2 rdc8 plants, the ssi2 rdc2 plants continue to show some albeit reduced cell death. Fatty acid (FA) analysis showed a reduction in 16:3 levels in ssi2 rdc8 plants, which suggests that this mutation may limit the flux of FAs into the pro-karyotic pathway of glycerolipid biosynthesis. Both rdc2 and rdc8 continue to accumulate high levels of 18:0, which suggests that 18:0 levels were responsible for neither constitutive SA signaling nor repression of JA-induced expression of the PDF1.2 gene in ssi2 plants. We also analyzed SA and JA responses of the fab2-derived shs1 mutant, which accumulates levels of 18:0 over 50% lower than those in the fab2 plants. Even though fab2 shs1 plants were morphologically bigger than fab2 plants, they expressed PR genes constitutively, showed HR-like cell death, and accumulated elevated levels of SA. However, unlike the ssi2 rdc plants, fab2 shs1 plants were unable to induce high levels of PDF1.2 expression in response to exogenous application of JA. Together, these results show that defective cross talk in ssi2 can be restored by second site mutations and is independent of morphological size of the plants, cell death, and elevated levels of 18:0.

Construction of Synthetic Promoters by Assembling the Sigma Factor Binding −35 and −10 Boxes

2018 ◽  
pp. 1800298 ◽  
Author(s):  
Yang Wang ◽  
Qingtao Liu ◽  
Huanjiao Weng ◽  
Yanan Shi ◽  
Jian Chen ◽  
...  
Keyword(s):  
Sigma Factor ◽  
Factor Binding ◽  
Synthetic Promoters

scholarly journals Immune regulators SIB1 and LSD1 antagonistically regulate PhANGs via the GLK transcription factors

2020 ◽  
Author(s):  
Mengping Li ◽  
Keun Pyo Lee ◽  
Tong Liu ◽  
Vivek Dogra ◽  
Jianli Duan ◽  
...  
Keyword(s):  
Cell Death ◽  
Transcription Factors ◽  
Critical Level ◽  
Negative Regulator ◽  
Chloroplast Biogenesis ◽  
Sensor Protein ◽  
Primed Cell ◽  
Light Harvesting Antenna ◽  
Signaling Components ◽  
Fine Tune

AbstractGOLDEN2-LIKE (GLK) transcription factors drive the expression of photosynthesis-associated nuclear genes (PhANGs), indispensable for chloroplast biogenesis. We previously demonstrated that the salicylic acid (SA)-induced SIGMA FACTOR-BINDING PROTEIN1 (SIB1), a transcription coregulator and positive regulator of SA-primed cell death, interacts with GLKs. The SIB1-GLK interaction raises the level of light-harvesting antenna proteins in the photosystem II, aggravating photoinhibition and singlet oxygen (1O2) burst. 1O2 then contributes to SA-primed cell death via EXECUTER1 (EX1, 1O2 sensor protein)-mediated retrograde signaling upon reaching a critical level. We now reveal that LESION-SIMULATING DISEASE 1 (LSD1), a transcription coregulator and negative regulator of SA-primed cell death, interacts with GLKs to repress their activities. Consistently, the overexpression of LSD1 represses the expression of PhANGs, but the loss of LSD1 increases their expression. The SA-induced SIB1 then counteractively interacts with GLKs, leading to EX1-mediated cell death. Collectively, we provide a working model that mutually exclusive SA-signaling components SIB1 and LSD1 antagonistically regulate GLKs to fine-tune the expression of PhANGs, priming SA-induced cell death, and sustaining 1O2 homeostasis, respectively.

scholarly journals Arabidopsis SIGMA FACTOR BINDING PROTEIN1 (SIB1) and SIB2 inhibit WRKY75 function in abscisic acid-mediated leaf senescence and seed germination

2021 ◽  
Author(s):  
Haiyan Zhang ◽  
Liping Zhang ◽  
Yunrui Ji ◽  
Yifen Jing ◽  
Lanxin Li ◽  
...  
Keyword(s):  
Abscisic Acid ◽  
Seed Germination ◽  
Leaf Senescence ◽  
Chromatin Immunoprecipitation ◽  
Sigma Factor ◽  
Dependent Manner ◽  
Negative Regulators ◽  
Factor Binding ◽  
Physiological Processes ◽  
Increased Sensitivity

Abstract The plant-specific VQ gene family participates in diverse physiological processes but little information is available on their role in leaf senescence. Here, we show that the VQ motif-containing proteins, Arabidopsis SIGMA FACTOR BINDING PROTEIN1 (SIB1) and SIB2 are negative regulators of abscisic acid (ABA)-mediated leaf senescence. Loss of SIB1 and SIB2 function resulted in increased sensitivity of ABA-induced leaf senescence. In contrast, overexpression of SIB1 significantly delayed this process. Moreover, biochemical studies revealed that SIBs interact with WRKY75 transcription factor. Loss of WRKY75 function decreased sensitivity to ABA-induced leaf senescence, while overexpression of WRKY75 significantly accelerated this process. Chromatin immunoprecipitation assays revealed that WRKY75 directly binds to the promoters of GOLDEN 2-LIKE1(GLK1) and GLK2, to repress their expression. SIBs repress the transcriptional function of WRKY75 and negatively regulate ABA-induced leaf senescence in a WRKY75-dependent manner. In contrast, WRKY75 positively modulates ABA-mediated leaf senescence in a GLK-dependent manner. In addition, SIBs inhibit WRKY75 function in ABA-mediated seed germination. These results demonstrate that SIBs can form a complex with WRKY75 to regulate ABA-mediated leaf senescence and seed germination.

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