Biology subjects

Kalachova, T.

Publications and source records attributed to Kalachova, T..

6 recordsLinked to original sources

bioRxiv2026

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↗

bioRxiv2026

A plasmodesmata-specific exocyst complex regulates symplastic connectivity by affecting callose turnover

Plasmodesmata are intercellular channels that mediate symplastic communication between plant cells. Molecular transport through these channels is critically regulated by dynamic callose deposition and degradation, yet the secretory mechanisms that deliver regulatory components to plasmodesmata remain poorly understood. Here, we identify and characterize a non-canonical plasmodesmata-associated module of the exocyst, an evolutionarily conserved protein complex involved in secretory vesicle tethering and exocytosis. Exocyst subunits EXO70G1, SEC15A, EXO84C, and SEC10A specifically accumulate at plasmodesmata, whereas the canonical exocyst subunits EXO70A1 and SEC8 do not. Genetic and interaction analyses show that EXO70G1 acts as a landmark for recruiting SEC15A and EXO84C to plasmodesmata, revealing a distinct mode of exocyst targeting at these membrane domains. EXO70G1-dependent exocyst targeting to plasmodesmata depends on phosphoinositides and sphingolipids, consistent with the specialized lipid environment of plasmodesmal membranes. Loss of EXO70G1 results in increased callose accumulation and reduced symplastic transport, and strongly enhances developmental defects of a callose-overproducing mutant. In addition, exo70G1 mutants display enhanced resistance to bacterial pathogen Pseudomonas syringae, linking reduced plasmodesmal permeability to anti-bacterial defense. Cross-species analysis further indicates that plasmodesmata association is a derived feature of the EXO70G clade, present in angiosperms but absent from non-angiosperm EXO70 homologs. Together, our findings show that exocyst diversification in plants has generated a specialized trafficking module - plasmodesmata-associated exocyst - that links vesicle delivery to callose homeostasis at plasmodesmata, thereby regulating intercellular communication, development, and immunity. TeaserA specialized secretion module of the exocyst complex regulates plant cell-to-cell connectivity by controlling callose turnover at plasmodesmata

plant biology↗

bioRxiv2026

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↗

bioRxiv2026

The molecular architecture of the Arabidopsis callose synthase complex

ABSTRACTCallose synthase is responsible for the targeted deposition of the {beta}-1,3-glucan polymer, callose which underlines essential plant developmental processes, including cell division, pathogen defense or cell-cell communication. The architecture of the callose synthase complex (CALSC) as well as the molecular mechanisms of callose synthesis remain unknown. Here we report an integrative characterisation of the Arabidopsis CALS complex, with the most enriched subunits, CALS1, CALS2 and CALS3, forming its core. Structurally, CALSC assembles into a trimer, requiring the plant-specific Bag domain to mediate inter-subunit associations. The biological importance of CALSC assembly is highlighted by the simultaneous loss of CALS1 and CALS3, which abolishes plasmodesmal callose deposition and affects symplastic transport. Site-directed mutagenesis and molecular dynamics simulations depict the topology of the CALS1 active site in detail, including the components of the enzymatic reaction. We pinpoint the translocating tunnel through which the nascent glucan is delivered and mechanistically confirm the role of transmembrane helix 8 in regulating glucan export. Our work provides unprecedented insight into the molecular architecture of the CALSC and the distinct changes from maturation to activity at the plasma membrane, while showcasing the mechanisms involved in callose synthesis at the molecular level.

plant biology↗

bioRxiv2025

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↗

bioRxiv2018

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↗