Preexisting Systemic Acquired Resistance Suppresses Hypersensitive Response-Associated Cell Death in Arabidopsishrl1 Mutant

Because of their sessile nature, plants evolved integrated defense and acclimation mechanisms to simultaneously cope with adverse biotic and abiotic conditions. Among these are systemic acquired resistance (SAR) and systemic acquired acclimation (SAA). Growing evidence suggests that SAR and SAA activate similar cellular mechanisms and employ common signaling pathways for the induction of acclimatory and defense responses. It is therefore possible to consider these processes together, rather than separately, as a common systemic acquired acclimation and resistance (SAAR) mechanism. Arabidopsis thaliana flavin-dependent monooxygenase 1 (FMO1) was previously described as a regulator of plant resistance in response to pathogens as an important component of SAR. In the current study, we investigated its role in SAA, induced by a partial exposure of Arabidopsis rosette to local excess light stress. We demonstrate here that FMO1 expression is induced in leaves directly exposed to excess light stress as well as in systemic leaves remaining in low light. We also show that FMO1 is required for the systemic induction of ASCORBATE PEROXIDASE 2 (APX2) and ZINC-FINGER OF ARABIDOPSIS 10 (ZAT10) expression and spread of the reactive oxygen species (ROS) systemic signal in response to a local application of excess light treatment. Additionally, our results demonstrate that FMO1 is involved in the regulation of excess light-triggered systemic cell death, which is under control of LESION SIMULATING DISEASE 1 (LSD1). Our study indicates therefore that FMO1 plays an important role in triggering SAA response, supporting the hypothesis that SAA and SAR are tightly connected and use the same signaling pathways.

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Hrip1, a novel protein elicitor from necrotrophic fungus,Alternaria tenuissima, elicits cell death, expression of defence-related genes and systemic acquired resistance in tobacco

Plant Cell & Environment ◽

10.1111/j.1365-3040.2012.02539.x ◽

2012 ◽

Vol 35 (12) ◽

pp. 2104-2120 ◽

Cited By ~ 36

Author(s):

MAHESH KULYE ◽

HUA LIU ◽

YULIANG ZHANG ◽

HONGMEI ZENG ◽

XIUFEN YANG ◽

...

Keyword(s):

Cell Death ◽

Systemic Acquired Resistance ◽

Acquired Resistance ◽

Alternaria Tenuissima ◽

Protein Elicitor ◽

Novel Protein

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The Elicitor Protein AsES Induces a Systemic Acquired Resistance Response Accompanied by Systemic Microbursts and Micro–Hypersensitive Responses in Fragaria ananassa

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi-05-17-0121-fi ◽

2018 ◽

Vol 31 (1) ◽

pp. 46-60 ◽

Cited By ~ 15

Author(s):

Verónica Hael-Conrad ◽

Silvia Marisa Perato ◽

Marta Eugenia Arias ◽

Martín Gustavo Martínez-Zamora ◽

Pía de los Ángeles Di Peto ◽

...

Keyword(s):

Cell Death ◽

Systemic Acquired Resistance ◽

Calcium Influx ◽

Wide Spectrum ◽

Acquired Resistance ◽

Defense Responses ◽

Death Process ◽

Fragaria Ananassa ◽

Hypersensitive Cell Death ◽

Acremonium Strictum

The elicitor AsES (Acremonium strictum elicitor subtilisin) is a 34-kDa subtilisin-like protein secreted by the opportunistic fungus Acremonium strictum. AsES activates innate immunity and confers resistance against anthracnose and gray mold diseases in strawberry plants (Fragaria × ananassa Duch.) and the last disease also in Arabidopsis. In the present work, we show that, upon AsES recognition, a cascade of defense responses is activated, including: calcium influx, biphasic oxidative burst (O2⋅− and H2O2), hypersensitive cell-death response (HR), accumulation of autofluorescent compounds, cell-wall reinforcement with callose and lignin deposition, salicylic acid accumulation, and expression of defense-related genes, such as FaPR1, FaPG1, FaMYB30, FaRBOH-D, FaRBOH-F, FaCHI23, and FaFLS. All these responses occurred following a spatial and temporal program, first induced in infiltrated leaflets (local acquired resistance), spreading out to untreated lateral leaflets, and later, to distal leaves (systemic acquired resistance). After AsES treatment, macro-HR and macro–oxidative bursts were localized in infiltrated leaflets, while micro-HRs and microbursts occurred later in untreated leaves, being confined to a single cell or a cluster of a few epidermal cells that differentiated from the surrounding ones. The differentiated cells initiated a time-dependent series of physiological and anatomical changes, evolving to idioblasts accumulating H2O2 and autofluorescent compounds that blast, delivering its content into surrounding cells. This kind of systemic cell-death process in plants is described for the first time in response to a single elicitor. All data presented in this study suggest that AsES has the potential to activate a wide spectrum of biochemical and molecular defense responses in F. ananassa that may explain the induced protection toward pathogens of opposite lifestyle, like hemibiotrophic and necrotrophic fungi.

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Elicitin Genes Expressed In Vitro by Certain Tobacco Isolates of Phytophthora parasitica Are Down Regulated During Compatible Interactions

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi.2001.14.3.326 ◽

2001 ◽

Vol 14 (3) ◽

pp. 326-335 ◽

Cited By ~ 27

Author(s):

Virginie Colas ◽

Sandrine Conrod ◽

Paul Venard ◽

Harald Keller ◽

Pierre Ricci ◽

...

Keyword(s):

Hypersensitive Response ◽

Systemic Acquired Resistance ◽

Acquired Resistance ◽

Compatible Interaction ◽

Phytophthora Parasitica ◽

In Planta ◽

Black Shank ◽

Phytophthora Spp ◽

Compatible Interactions

Phytophthora spp. secrete proteins called elicitins in vitro that can specifically induce hypersensitive response and systemic acquired resistance in tobacco. In Phytophthora parasitica, the causal agent of black shank, most isolates virulent on tobacco are unable to produce elicitins in vitro. Recently, however, a few elicitin-producing P. parasitica strains virulent on tobacco have been isolated. We investigated the potential diversity of elicitin genes in P. parasitica isolates belonging to different genotypes and with various virulence levels toward tobacco as well as elicitin expression pattern in vitro and in planta. Although elicitins are encoded by a multigene family, parA1 is the main elicitin gene expressed. This gene is highly conserved among isolates, regardless of the elicitin production and virulence levels toward tobacco. Moreover, we show that elicitin-producing P. parasitica isolates virulent on tobacco down regulate parA1 expression during compatible interactions, whichever host plant is tested. Conversely, one elicitin-producing P. parasitica isolate that is pathogenic on tomato and avirulent on tobacco still expresses parA1 in the compatible interaction. Therefore, some P. parasitica isolates may evade tobacco recognition by down regulating parA1 in planta. The in planta down regulation of parA1 may constitute a suitable mechanism for P. parasitica to infect tobacco without deleterious consequences for the pathogen.

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