scholarly journals Age-Related Resistance in Arabidopsis thaliana Involves the MADS-Domain Transcription Factor SHORT VEGETATIVE PHASE and Direct Action of Salicylic Acid on Pseudomonas syringae

2017 ◽  
Vol 30 (11) ◽  
pp. 919-929 ◽  
Author(s):  
Daniel C. Wilson ◽  
Christine J. Kempthorne ◽  
Philip Carella ◽  
David K. Liscombe ◽  
Robin K. Cameron
Keyword(s):  
Arabidopsis Thaliana ◽  
Transcription Factor ◽  
Salicylic Acid ◽  
Disease Resistance ◽  
Antimicrobial Agent ◽  
Pseudomonas Syringae ◽  
Antibiofilm Activity ◽  
Vegetative Phase ◽  
Short Vegetative Phase ◽  
Age Related

Arabidopsis thaliana exhibits a developmentally regulated disease-resistance response known as age-related resistance (ARR), a process that requires intercellular accumulation of salicylic acid (SA), which is thought to act as an antimicrobial agent. ARR is characterized by enhanced resistance to some pathogens at the late adult-vegetative and reproductive stages. While the transition to flowering does not cause the onset of ARR, both processes involve the MADS-domain transcription factor SHORT VEGETATIVE PHASE (SVP). In this study, ARR-defective svp mutants were found to accumulate reduced levels of intercellular SA compared with wild type in response to Pseudomonas syringae pv. tomato. Double mutant and overexpression analyses suggest that SVP and SOC1 (SUPPRESSOR OF OVEREXPRESSION OF CO 1) act antagonistically, such that SVP is required for ARR to alleviate the negative effects of SOC1 on SA accumulation. In vitro, SA exhibited antibacterial and antibiofilm activity at concentrations similar to those measured in the intercellular space during ARR. In vivo, P. syringae pv. tomato formed biofilm-like aggregates in young susceptible plants, while this was drastically reduced in mature ARR-competent plants, which accumulate intercellular SA. Collectively, these results reveal a novel role for the floral regulators SVP and SOC1 in disease resistance and provide evidence that SA acts directly on pathogens as an antimicrobial agent. [Formula: see text] Copyright © 2017 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license .

scholarly journals PtrWRKY73, a salicylic acid-inducible poplar WRKY transcription factor, is involved in disease resistance in Arabidopsis thaliana

2015 ◽  
Vol 34 (5) ◽  
pp. 831-841 ◽  
Author(s):  
Yanjiao Duan ◽  
Yuanzhong Jiang ◽  
Shenglong Ye ◽  
Abdul Karim ◽  
Zhengyi Ling ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Transcription Factor ◽  
Salicylic Acid ◽  
Disease Resistance ◽  
Wrky Transcription Factor

Overexpression of a moso bamboo (Phyllostachys edulis) transcription factor gene PheWRKY1 enhances disease resistance in transgenic Arabidopsis thaliana

Botany ◽  
2013 ◽  
Vol 91 (7) ◽  
pp. 486-494 ◽  
Author(s):  
Xiao-Wei Cui ◽  
Ying Zhang ◽  
Fei-Yan Qi ◽  
Jian Gao ◽  
Yuan-Wen Chen ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Transcription Factor ◽  
Disease Resistance ◽  
Pseudomonas Syringae ◽  
Transgenic Arabidopsis ◽  
Defense Responses ◽  
Moso Bamboo ◽  
Photosynthetic Parameters ◽  
Phyllostachys Edulis ◽  
Pr Genes

Members of plant WRKY transcription factor families are implicated in defense responses and various other physiological processes. To study the function of WRKY transcription factors in moso bamboo (Phyllostachys edulis (Carrière) J. Houz.), a PheWRKY1 gene (GenBank accession number: GU944762) was cloned by reverse transcription polymerase chain reaction. An overexpression vector for this gene was constructed and transformed into Arabidopsis thaliana (L.) Heynh. by an agrobacterium-mediated method. To determine the effect of PheWRKY1 gene overexpression on disease resistance in A. thaliana, the photosynthetic parameters and the expression of pathogenesis-related (PR) genes were examined after Pseudomonas syringae PV Tomato DC3000 (Pst DC3000) infection. Compared to wild-type plants, most PheWRKY1-overexpressing plants did not exhibit spreading maceration to systemic leaves and had a better photosynthetic capacity after Pst DC3000 infection. Furthermore, PheWRKY1-overexpressing plants accumulated significantly more PR1, PR2, PR5, and nonexpressor of PR genes (NPR1) transcripts. These results demonstrated that transgenic Arabidopsis overexpressing PheWRKY1 gene exhibited improved resistance to bacterial infection.

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 PHOSPHORYLETHANOLAMINE CYTIDYLYLTRANSFERASE 1 modulates flowering in a florigen-independent manner by regulating SVP

Development ◽  
2020 ◽  
Vol 148 (1) ◽  
pp. dev193870
Author(s):  
Hendry Susila ◽  
Zeeshan Nasim ◽  
Katarzyna Gawarecka ◽  
Ji-Yul Jung ◽  
Suhyun Jin ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Flowering Time ◽  
Shoot Apical Meristem ◽  
Apical Meristem ◽  
Artificial Microrna ◽  
Flowering Locus T ◽  
Independent Manner ◽  
Vegetative Phase ◽  
Twin Sister ◽  
Short Vegetative Phase

ABSTRACTPHOSPHORYLETHANOLAMINE CYTIDYLYLTRANSFERASE 1 (PECT1) regulates phosphatidylethanolamine biosynthesis and controls the phosphatidylethanolamine:phosphatidylcholine ratio in Arabidopsis thaliana. Previous studies have suggested that PECT1 regulates flowering time by modulating the interaction between phosphatidylcholine and FLOWERING LOCUS T (FT), a florigen, in the shoot apical meristem (SAM). Here, we show that knockdown of PECT1 by artificial microRNA in the SAM (pFD::amiR-PECT1) accelerated flowering under inductive and even non-inductive conditions, in which FT transcription is almost absent, and in ft-10 twin sister of ft-1 double mutants under both conditions. Transcriptome analyses suggested that PECT1 affects flowering by regulating SHORT VEGETATIVE PHASE (SVP) and GIBBERELLIN 20 OXIDASE 2 (GA20ox2). SVP misexpression in the SAM suppressed the early flowering of pFD::amiR-PECT1 plants. pFD::amiR-PECT1 plants showed increased gibberellin (GA) levels in the SAM, concomitant with the reduction of REPRESSOR OF GA1-3 levels. Consistent with this, GA treatment had little effect on flowering time of pFD::amiR-PECT1 plants and the GA antagonist paclobutrazol strongly affected flowering in these plants. Together, these results suggest that PECT1 also regulates flowering time through a florigen-independent pathway, modulating SVP expression and thus regulating GA production.

scholarly journals LSD1 Regulates Salicylic Acid Induction of Copper Zinc Superoxide Dismutase in Arabidopsis thaliana

1999 ◽  
Vol 12 (11) ◽  
pp. 1022-1026 ◽  
Author(s):  
Daniel J. Kliebenstein ◽  
Robert A. Dietrich ◽  
Adam C. Martin ◽  
Robert L. Last ◽  
Jeffery L. Dangl
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Death ◽  
Salicylic Acid ◽  
Pseudomonas Syringae ◽  
Lesion Formation ◽  
Copper Zinc Superoxide Dismutase ◽  
Zinc Superoxide Dismutase ◽  
A Cell ◽  
Copper Zinc ◽  
Cell Death Cascade

We characterized the accumulation patterns of Arabidopsis thaliana proteins, two CuZnSODs, FeSOD, MnSOD, PR1, PR5, and GST1, in response to various pathogen-associated treatments. These treatments included inoculation with virulent and avirulent Pseudomonas syringae strains, spontaneous lesion formation in the lsd1 mutant, and treatment with the salicylic acid (SA) analogs INA (2,6-dichloroisonicotinic acid) and BTH (benzothiadia-zole). The PR1, PR5, and GST1 proteins were inducible by all treatments tested, as expected from previous mRNA blot analysis. The two CuZnSOD proteins were induced by SA analogs and in conjunction with lsd1-mediated spreading cell death. Additionally, LSD1 is a part of a signaling pathway for the induction of the CuZnSOD proteins in response to SA but not in lsd1-mediated cell death. We suggest that the spreading lesion phenotype of lsd1 results from a lack of up-regulation of a CuZnSOD responsible for detoxification of accumulating superoxide before the reactive oxygen species can trigger a cell death cascade.

scholarly journals Facilitation of Fusarium graminearum Infection by 9-Lipoxygenases in Arabidopsis and Wheat

2015 ◽  
Vol 28 (10) ◽  
pp. 1142-1152 ◽  
Author(s):  
Vamsi J. Nalam ◽  
Syeda Alam ◽  
Jantana Keereetaweep ◽  
Barney Venables ◽  
Dehlia Burdan ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Salicylic Acid ◽  
Disease Resistance ◽  
Jasmonic Acid ◽  
Fusarium Graminearum ◽  
Head Blight ◽  
Enhanced Resistance ◽  
Susceptibility Factors ◽  
Ja Signaling ◽  
Important Disease

Fusarium graminearum causes Fusarium head blight, an important disease of wheat. F. graminearum can also cause disease in Arabidopsis thaliana. Here, we show that the Arabidopsis LOX1 and LOX5 genes, which encode 9-lipoxygenases (9-LOXs), are targeted during this interaction to facilitate infection. LOX1 and LOX5 expression were upregulated in F. graminearum–inoculated plants and loss of LOX1 or LOX5 function resulted in enhanced disease resistance in the corresponding mutant plants. The enhanced resistance to F. graminearum infection in the lox1 and lox5 mutants was accompanied by more robust induction of salicylic acid (SA) accumulation and signaling and attenuation of jasmonic acid (JA) signaling in response to infection. The lox1- and lox5-conferred resistance was diminished in plants expressing the SA-degrading salicylate hydroxylase or by the application of methyl-JA. Results presented here suggest that plant 9-LOXs are engaged during infection to control the balance between SA and JA signaling to facilitate infection. Furthermore, since silencing of TaLpx-1 encoding a 9-LOX with homology to LOX1 and LOX5, resulted in enhanced resistance against F. graminearum in wheat, we suggest that 9-LOXs have a conserved role as susceptibility factors in disease caused by this important fungus in Arabidopsis and wheat.

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