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Biology subjects

Burketova, L.

Publications and source records attributed to Burketova, L..

5 recordsLinked to original sources

Unfolded Protein Response signaling restricts PTI and limits salicylic acid-dependent cell death under ER stress

The Unfolded Protein Response (UPR) maintains endoplasmic reticulum (ER) homeostasis during proteotoxic stress while also contributing to plant immunity. However, the functional relationship between UPR signaling, pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and salicylic acid (SA) remains poorly understood. Here, we investigated this interplay using Arabidopsis mutants impaired in the two major UPR branches. Mutants defective in the INOSITOL-REQUIRING ENZYME 1 (IRE1)-bZIP60 branch displayed enhanced resistance to Pseudomonas syringae pv. tomato DC3000 and to the type III secretion-deficient strain hrcC-, indicating potentiation of PTI. Consistently, the ire1a ire1b double mutant exhibited increased flg22-induced callose deposition, whereas reactive oxygen species production was unaffected. Despite enhanced basal resistance, all UPR mutants retained full responsiveness to benzothiadiazole, demonstrating that downstream SA signaling remains functional independently of UPR integrity. Conversely, acute ER stress induced by tunicamycin promoted SA accumulation and extensive leaf necrosis. Reverse genetics revealed that SA-deficient mutants were largely protected from ER stress-induced cell death, whereas mutants over-accumulating SA exhibited enhanced susceptibility, demonstrating that endogenous SA is required for the full execution of this response. Analysis of an independent transcriptomic dataset further showed that loss of IRE1 de-represses genes involved in SA biosynthesis, PTI and defense under ER stress. Together, our results identify IRE1 as a key regulator coordinating ER homeostasis with immune signaling by limiting SA-dependent defense activation during ER stress, while simultaneously preventing excessive cell death.

plant biology↗

Loss of PR1 function enhances Arabidopsis resistance to Botrytis cinerea

PATHOGENESIS-RELATED 1 (PR1) is one of the most widely used markers of salicylic acid (SA)-dependent plant immunity, yet its direct functional contribution to pathogen defence remains poorly understood. Here, we investigated the role of PR1 in Arabidopsis thaliana by analyzing a pr1 loss-of-function mutant challenged with bacterial and fungal pathogens and fumonisin B1 (FB1)-induced cell death. Notably, loss of PR1 led to markedly different responses to distinct pathogens; while it moderately increased susceptibility to the pathogenic bacterium Pseudomonas syringae, it substantially enhanced resistance to the necrotrophic fungus Botrytis cinerea, and the responses to the necrotroph Sclerotinia sclerotiorum remained unaltered. The pr1 mutant also displayed reduced spread of FB1-induced cell death, linking PR1 function to the promotion of stress-associated cell death. In line with the susceptibility changes, we observed the strongest PR1 accumulation and cell wall enrichment during B. cinerea infection using mCherry-tagged PR1 expressed under its endogenous promoter. Complementation with full-length PR1 and with a C-terminally truncated PR1 variant lacking the CAPE peptide restored wild-type susceptibility, whereas a non-cleavable PR1 variant did not. These results indicate that proteolytic processing at the CAPE cleavage motif, rather than the CAPE peptide itself, is required for PR1 function. Our data thus strongly suggest that PR1 may act as a susceptibility factor for necrotrophic pathogens by promoting host cell death.

Plant Biology↗

SnRK1.1 Coordinates Organ-Specific Growth-Defense Programs via Transcriptomic Rewiring in Arabidopsis thaliana

SnRK1 (Sucrose non-fermenting-1-Related Kinase 1) is a master regulator of cellular energy homeostasis in plants, coordinating developmental and metabolic responses under environmental and internal stress conditions. Here, we demonstrate that its catalytic subunit, KIN10, orchestrates organ-specific growth-defense programs in Arabidopsis thaliana through transcriptomic rewiring. Using RNA-seq profiling, we reveal that kin10 knockout mutants exhibit extensive transcriptional reprogramming in roots, particularly in pathways linked to signal perception, cell wall remodeling, and intracellular trafficking, which correlates with impaired root growth and reduced root hair elongation upon Pseudomonas syringae infection. In contrast, KIN10 overexpression (KIN10-OE) lines display constitutive defense activation in shoots, including elevated expression of genes associated with reactive oxygen species (ROS) production and salicylic acid (SA) signaling, leading to enhanced ROS accumulation and growth trade-offs. kin10 roots show muted responses to biotic stimuli, while KIN10-OE shoots prioritize defense over growth. These findings position KIN10 as a critical integrator of energy status and immune signaling, enabling fine-tuned, tissue-specific responses essential for optimizing plant adaptation to dynamic environmental challenges.

plant biology↗

Influence Of Salt Stress On The flg22 Induced ROS Production In Arabidopsis thaliana Leaves

In their natural habitats, plants have to cope with multiple stress factors triggering respective response pathways, leading to mutual interference. Our work aimed to study the effect of salt stress in combination with immune response triggered by microbe-associated molecular pattern (MAMP) in Arabidopsis thaliana Col-0 plants. We measured ROS production after treatment with flg22 and the influence of concomitant salt stress (NaCl and Na2CO3).The maximum combined effect of NaCl solution and flg22 on ROS production was achieved at 6 mM salt, which was almost 2 times higher than the single effect of MAMP. A similar maximum combined effect with Na2CO3 was observed at 10 mM concentration. High concentration of NaCl and Na2CO3 was accompanied with declining of ROS production, which was completely inhibited at 150 mM of NaCl and at 50 mM of Na2CO3.The immediate and long term (24 h) effect of NaCl on leaf tissue of Arabidopsis thaliana showed that the impact of salt stress on flg22induced ROS production probably did not affect the genetic aspects of the tissue response, but was associated with ionic and osmotic stresses. Experiments with mannitol, KCl and CaCl2 allowed to conclude that the observed effect was due to the ionic stress of the salt rather than the osmotic one.

physiology↗

Can Actin Depolymerization Actually Result In Increased Plant Resistance To Pathogens?

Introductory paragraphThe integrity of the actin cytoskeleton is essential for plant immune signalling1. Consequently, it is generally assumed that actin disruption reduces plant resistance to pathogen attack2-4. However, in a previous study, it was shown that actin depolymerisation triggers the salicylic acid (SA) signalling pathway5, which is interesting because increased SA is associated with enhanced plant resistance to pathogen attack6,7. Here, we attempt to resolve this seeming inconsistency by showing that the relationship between actin depolymerization and plant resistance is more complex than currently thought. We investigate the precise nature of this relationship using two completely different plant pathosystems: i) a model plant (Arabidopsis thaliana) and a bacterial pathogen (Pseudomonas syringae), and ii) an important crop (Brassica napus) and a fungal pathogen (Leptosphaeria maculans). We demonstrate that actin depolymerization induces a dramatic increase in SA levels and that the increased SA is biosynthesized by the isochorismate synthase pathway. In both pathosystems, this phenomenon leads to increased plant resistance.

plant biology↗