scholarly journals THESEUS1 modulates cell wall stiffness and abscisic acid production in Arabidopsis thaliana

2021 ◽  
Vol 119 (1) ◽  
pp. e2119258119
Author(s):  
Laura Bacete ◽  
Julia Schulz ◽  
Timo Engelsdorf ◽  
Zdenka Bartosova ◽  
Lauri Vaahtera ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Wall ◽  
Abscisic Acid ◽  
Cell Walls ◽  
Turgor Pressure ◽  
Cell Wall Integrity ◽  
Adaptive Responses ◽  
Maintenance Mechanism ◽  
Cell Wall Damage ◽  
Wall Stiffness

Plant cells can be distinguished from animal cells by their cell walls and high-turgor pressure. Although changes in turgor and the stiffness of cell walls seem coordinated, we know little about the mechanism responsible for coordination. Evidence has accumulated that plants, like yeast, have a dedicated cell wall integrity maintenance mechanism. It monitors the functional integrity of the wall and maintains integrity through adaptive responses induced by cell wall damage arising during growth, development, and interactions with the environment. These adaptive responses include osmosensitive induction of phytohormone production, defense responses, as well as changes in cell wall composition and structure. Here, we investigate how the cell wall integrity maintenance mechanism coordinates changes in cell wall stiffness and turgor in Arabidopsis thaliana. We show that the production of abscisic acid (ABA), the phytohormone-modulating turgor pressure, and responses to drought depend on the presence of a functional cell wall. We find that the cell wall integrity sensor THESEUS1 modulates mechanical properties of walls, turgor loss point, ABA biosynthesis, and ABA-controlled processes. We identify RECEPTOR-LIKE PROTEIN 12 as a component of cell wall integrity maintenance–controlling, cell wall damage–induced jasmonic acid (JA) production. We propose that THE1 is responsible for coordinating changes in turgor pressure and cell wall stiffness.

scholarly journals THESEUS1 modulates cell wall stiffness and abscisic acid production in Arabidopsis thaliana

2021 ◽  
Author(s):  
Laura Bacete ◽  
Julia Schulz ◽  
Timo Engelsdorf ◽  
Zdenka Bartosova ◽  
Lauri Vaahtera ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Wall ◽  
Abscisic Acid ◽  
Cell Walls ◽  
Acid Production ◽  
Turgor Pressure ◽  
Cell Wall Integrity ◽  
Adaptive Responses ◽  
Maintenance Mechanism ◽  
Wall Stiffness

Plant cells can be distinguished from animal cells by their cell walls and high turgor pressure. Although changes in turgor and stiffness of cell walls seem coordinated, we know little about the mechanism responsible for coordination. Evidence has accumulated that plants, like yeast, have a dedicated cell wall integrity maintenance mechanism. This mechanism monitors the functional integrity of the wall and maintains it through adaptive responses when cell wall damage occurs during growth, development, and interactions with the environment. The adaptive responses include osmo-sensitive-induction of phytohormone production, defence responses as well as changes in cell wall composition and structure. Here, we investigate how the cell wall integrity maintenance mechanism coordinates changes in cell wall stiffness and turgor in Arabidopsis thaliana. We show that the production of abscisic acid (ABA), the phytohormone modulating turgor pressure and responses to drought, depends on the presence of a functional cell wall. We find that the cell wall integrity sensor THESEUS1 modulates mechanical properties of walls, turgor loss point and ABA biosynthesis. We identify RECEPTOR-LIKE PROTEIN 12 as a new component of cell wall integrity maintenance controlling cell wall damage-induced jasmonic acid production. Based on the results we propose that THE1 is responsible for coordinating changes in turgor pressure and cell wall stiffness.

scholarly journals Plant cell wall integrity maintenance and pattern-triggered immunity modulate jointly plant stress responses in Arabidopsis thaliana

2017 ◽  
Author(s):  
Timo Engelsdorf ◽  
Nora Gigli-Bisceglia ◽  
Manikandan Veerabagu ◽  
Joseph F. McKenna ◽  
Frauke Augstein ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Wall ◽  
Plant Growth ◽  
Plant Cell ◽  
Stress Responses ◽  
Cell Walls ◽  
Plant Cell Wall ◽  
Cell Wall Integrity ◽  
Maintenance Mechanism ◽  
Signaling Components

AbstractPlant cells are surrounded by walls, which must often meet opposing functional requirements during plant growth and defense. The cells meet them by modifying wall structure and composition in a tightly controlled and adaptive manner. The modifications seem to be mediated by a dedicated cell wall integrity (CWI) maintenance mechanism. Currently the mode of action of the mechanism is not understood and it is unclear how its activity is coordinated with established plant defense signaling. We investigated responses to induced cell wall damage (CWD) impairing CWI and the underlying mechanism in Arabidopsis thaliana. Interestingly inhibitor- and enzyme-derived CWD induced similar, turgor-sensitive stress responses. Genetic analysis showed that the receptor-like kinase (RLK) FEI2 and the mechano-sensitive, plasma membrane-localized Ca2+- channel MCA1 function downstream of the THE1 RLK in CWD perception. Phenotypic clustering with 27 genotypes identified a core group of RLKs and ion channels, required for activation of CWD responses. By contrast, the responses were repressed by pattern-triggered immune (PTI) signaling components including PEPR1 and 2, the receptors for the immune signaling peptide AtPep1. Interestingly AtPep1 application repressed CWD-induced phytohormone accumulation in a PEPR1/2-dependent manner. These results suggest that PTI suppresses CWD-induced defense responses through elicitor peptide-mediated signaling during defense response activation. If PTI is impaired, the suppression of CWD-induced responses is alleviated, thus compensating for defective PTI.Significance statementStress resistance and plant growth determine food crop yield and efficiency of bioenergy production from ligno-cellulosic biomass. Plant cell walls are essential elements of the biological processes, therefore functional integrity of the cell walls must be maintained throughout. Here we investigate the plant cell wall integrity maintenance mechanism. We characterize its mode of action, identify essential signaling components and show that the AtPep1 signaling peptide apparently coordinates pattern triggered immunity (PTI) and cell wall integrity maintenance in plants. These results suggest how PTI and cell wall modification coordinately regulate biotic stress responses with plants possibly compensating for PTI impairment through enhanced activation of stress responses regulated by the CWI maintenance mechanism.

scholarly journals Structure and Biomechanics during Xylem Vessel Transdifferentiation in Arabidopsis thaliana

Plants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1715
Author(s):  
Eleftheria Roumeli ◽  
Leah Ginsberg ◽  
Robin McDonald ◽  
Giada Spigolon ◽  
Rodinde Hendrickx ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Wall ◽  
Cell Walls ◽  
Turgor Pressure ◽  
Plant Cells ◽  
Building Blocks ◽  
Xylem Vessel ◽  
Primary Cell Wall ◽  
Individual Plant ◽  
Vessel Elements

Individual plant cells are the building blocks for all plantae and artificially constructed plant biomaterials, like biocomposites. Secondary cell walls (SCWs) are a key component for mediating mechanical strength and stiffness in both living vascular plants and biocomposite materials. In this paper, we study the structure and biomechanics of cultured plant cells during the cellular developmental stages associated with SCW formation. We use a model culture system that induces transdifferentiation of Arabidopsis thaliana cells to xylem vessel elements, upon treatment with dexamethasone (DEX). We group the transdifferentiation process into three distinct stages, based on morphological observations of the cell walls. The first stage includes cells with only a primary cell wall (PCW), the second covers cells that have formed a SCW, and the third stage includes cells with a ruptured tonoplast and partially or fully degraded PCW. We adopt a multi-scale approach to study the mechanical properties of cells in these three stages. We perform large-scale indentations with a micro-compression system in three different osmotic conditions. Atomic force microscopy (AFM) nanoscale indentations in water allow us to isolate the cell wall response. We propose a spring-based model to deconvolve the competing stiffness contributions from turgor pressure, PCW, SCW and cytoplasm in the stiffness of differentiating cells. Prior to triggering differentiation, cells in hypotonic pressure conditions are significantly stiffer than cells in isotonic or hypertonic conditions, highlighting the dominant role of turgor pressure. Plasmolyzed cells with a SCW reach similar levels of stiffness as cells with maximum turgor pressure. The stiffness of the PCW in all of these conditions is lower than the stiffness of the fully-formed SCW. Our results provide the first experimental characterization of the mechanics of SCW formation at single cell level.

scholarly journals Plant cell wall integrity maintenance in model plants and crop species-relevant cell wall components and underlying guiding principles

2019 ◽  
Vol 77 (11) ◽  
pp. 2049-2077 ◽  
Author(s):  
Nora Gigli-Bisceglia ◽  
Timo Engelsdorf ◽  
Thorsten Hamann
Keyword(s):  
Cell Wall ◽  
Plant Cell ◽  
Cell Walls ◽  
Plant Cell Wall ◽  
Current Knowledge ◽  
Cell Wall Integrity ◽  
Plant Cell Walls ◽  
Maintenance Mechanism ◽  
Regulatory Processes ◽  
Composition And Structure

AbstractThe walls surrounding the cells of all land-based plants provide mechanical support essential for growth and development as well as protection from adverse environmental conditions like biotic and abiotic stress. Composition and structure of plant cell walls can differ markedly between cell types, developmental stages and species. This implies that wall composition and structure are actively modified during biological processes and in response to specific functional requirements. Despite extensive research in the area, our understanding of the regulatory processes controlling active and adaptive modifications of cell wall composition and structure is still limited. One of these regulatory processes is the cell wall integrity maintenance mechanism, which monitors and maintains the functional integrity of the plant cell wall during development and interaction with environment. It is an important element in plant pathogen interaction and cell wall plasticity, which seems at least partially responsible for the limited success that targeted manipulation of cell wall metabolism has achieved so far. Here, we provide an overview of the cell wall polysaccharides forming the bulk of plant cell walls in both monocotyledonous and dicotyledonous plants and the effects their impairment can have. We summarize our current knowledge regarding the cell wall integrity maintenance mechanism and discuss that it could be responsible for several of the mutant phenotypes observed.

scholarly journals Changes in cell ultrastructure and morphology of Arabidopsis thaliana roots after coumarins treatment

2014 ◽  
Vol 70 (3) ◽  
pp. 187-198
Author(s):  
Ewa Kupidłowska
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Wall ◽  
Cell Walls ◽  
Root Elongation ◽  
Inhibitory Effect ◽  
Cell Ultrastructure ◽  
Radial Expansion ◽  
Elongation Zone ◽  
Cortical Cells ◽  
Mother Cell Wall

The ultrastructure and morphology of roots treated with coumarin and umbelliferone as well as the reversibility of the coumarins effects caused by exogenous GA, were studied in <em>Arabidopsis thaliana</em>. Both coumarins suppressed root elongation and appreciably stimulated radial expansion of epidermal and cortical cells in the upper part of the meristem and in the elongation zone. The gibberellic acid applied simultaneously with coumarins decreased their inhibitory effect on root elongation and reduced cells swelling.Microscopic observation showed intensive vacuolization of cells and abnormalities in the structure of the Golgi stacks and the nuclear envelope. The detection of active acid phosphatase in the cytosol of swollen cells indicated increased membrane permeability. Significant abnormalities of newly formed cell walls, e.g. the discontinuity of cellulose layer, uncorrect position of walls and the lack of their bonds with the mother cell wall suggest that coumarins affected the cytoskeleton.

scholarly journals Cell fusion in yeast is negatively regulated by components of the cell wall integrity pathway

2019 ◽  
Vol 30 (4) ◽  
pp. 441-452 ◽  
Author(s):  
Allison E. Hall ◽  
Mark D. Rose
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Death ◽  
Cell Wall ◽  
Yeast Cell ◽  
Cell Fusion ◽  
Cell Walls ◽  
Cell Wall Integrity ◽  
Fusion Genes ◽  
Cell Wall Degradation ◽  
Cell Wall Integrity Pathway

During mating, Saccharomyces cerevisiae cells must degrade the intervening cell wall to allow fusion of the partners. Because improper timing or location of cell wall degradation would cause lysis, the initiation of cell fusion must be highly regulated. Here, we find that yeast cell fusion is negatively regulated by components of the cell wall integrity (CWI) pathway. Loss of the cell wall sensor, MID2, specifically causes “mating-induced death” after pheromone exposure. Mating-induced death is suppressed by mutations in cell fusion genes ( FUS1, FUS2, RVS161, CDC42), implying that mid2Δ cells die from premature fusion without a partner. Consistent with premature fusion, mid2Δ shmoos had thinner cell walls and lysed at the shmoo tip. Normally, Cdc42p colocalizes with Fus2p to form a focus only when mating cells are in contact (prezygotes) and colocalization is required for cell fusion. However, Cdc42p was aberrantly colocalized with Fus2p to form a focus in mid2Δ shmoos. A hyperactive allele of the CWI kinase Pkc1p ( PKC1*) caused decreased cell fusion and Cdc42p localization in prezygotes. In shmoos, PKC1* increased Cdc42p localization; however, it was not colocalized with Fus2p or associated with cell death. We conclude that Mid2p and Pkc1p negatively regulate cell fusion via Cdc42p and Fus2p.

scholarly journals Pectin Biosynthesis Is Critical for Cell Wall Integrity and Immunity in Arabidopsis thaliana

2016 ◽  
Vol 28 (2) ◽  
pp. 537-556 ◽  
Author(s):  
Gerit Bethke ◽  
Amanda Thao ◽  
Guangyan Xiong ◽  
Baohua Li ◽  
Nicole E. Soltis ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Wall ◽  
Cell Wall Integrity

scholarly journals Curcumin Targets Cell Wall Integrity via Calcineurin-Mediated Signaling in Candida albicans

2013 ◽  
Vol 58 (1) ◽  
pp. 167-175 ◽  
Author(s):  
Awanish Kumar ◽  
Sanjiveeni Dhamgaye ◽  
Indresh Kumar Maurya ◽  
Ashutosh Singh ◽  
Monika Sharma ◽  
...  
Keyword(s):  
Cell Wall ◽  
Candida Albicans ◽  
Critical Role ◽  
Pathogenic Fungi ◽  
Cell Wall Integrity ◽  
Ergosterol Biosynthesis ◽  
Ros Generation ◽  
Calcofluor White ◽  
Content Type ◽  
Cell Wall Damage

ABSTRACTCurcumin (CUR) shows antifungal activity against a range of pathogenic fungi, includingCandida albicans. The reported mechanisms of action of CUR include reactive oxygen species (ROS) generation, defects in the ergosterol biosynthesis pathway, decrease in hyphal development, and modulation of multidrug efflux pumps. Reportedly, each of these pathways is independently linked to the cell wall machinery inC. albicans, but surprisingly, CUR has not been previously implicated in cell wall damage. In the present study, we performed transcriptional profiling to identify the yet-unidentified targets of CUR inC. albicans. We found that, among 348 CUR-affected genes, 51 were upregulated and 297 were downregulated. Interestingly, most of the cell wall integrity pathway genes were downregulated. The possibility of the cell wall playing a critical role in the mechanism of CUR required further validation; therefore, we performed specific experiments to establish if there was any link between the two. The fractional inhibitory concentration index values of 0.24 to 0.37 show that CUR interacts synergistically with cell wall-perturbing (CWP) agents (caspofungin, calcofluor white, Congo red, and SDS). Furthermore, we could observe cell wall damage and membrane permeabilization by CUR alone, as well as synergistically with CWP agents. We also found hypersusceptibility in calcineurin and mitogen-activated protein (MAP) kinase pathway mutants against CUR, which confirmed that CUR also targets cell wall biosynthesis inC. albicans. Together, these data provide strong evidence that CUR disrupts cell wall integrity inC. albicans. This new information on the mechanistic action of CUR could be employed in improving treatment strategies and in combinatorial drug therapy.

scholarly journals A Putative MAP Kinase Kinase Kinase, MCK1, Is Required for Cell Wall Integrity and Pathogenicity of the Rice Blast Fungus, Magnaporthe oryzae

2008 ◽  
Vol 21 (5) ◽  
pp. 525-534 ◽  
Author(s):  
Junhyun Jeon ◽  
Jaeduk Goh ◽  
Sungyong Yoo ◽  
Myoung-Hwan Chi ◽  
Jaehyuk Choi ◽  
...  
Keyword(s):  
Cell Wall ◽  
Magnaporthe Oryzae ◽  
Insertional Mutagenesis ◽  
Turgor Pressure ◽  
Cell Wall Integrity ◽  
Mitogen Activated Protein Kinase ◽  
Targeted Disruption ◽  
Disease Symptoms ◽  
Mitogen Activated Protein ◽  
Protein Kinase Kinase

Insertional mutagenesis of Magnaporthe oryzae led to the identification of MCK1, a pathogenicity gene predicted to encode mitogen-activated protein kinase kinase kinase (MAPKKK) homologous to BCK1 in Saccharomyces cerevisiae. Targeted disruption of MCK1 resulted in the fungus undergoing autolysis and showing hypersensitivity to cell-wall-degrading enzyme. The mck1 produced significantly reduced numbers of conidia and developed appressoria in a slightly retarded manner compared with the wild type. Appressorium of the mck1 mutant was unable to penetrate into plant tissues, thereby rendering the mutant nonpathogenic. Cytorrhysis assay and monitoring of lipid mobilization suggested that the appressorial wall was altered, presumably affecting the level of turgor pressure within appressorium. Furthermore, the mck1 mutant failed to grow inside plant tissue. Complementation of the mutated gene restored its ability to cause disease symptoms, demonstrating that MCK1 is required for fungal pathogenicity. Taken together, our results suggest that MCK1 is an MAPKKK involved in maintaining cell wall integrity of M. oryzae, and that remodeling of the cell wall in response to host environments is essential for fungal pathogenesis.

scholarly journals Cytokinesis in fra2 Arabidopsis thaliana p60-katanin Mutant: Defects in Cell Plate/Daughter Wall Formation

2021 ◽  
Author(s):  
Emmanuel Panteris ◽  
Anna Kouskouveli ◽  
Dimitris Pappas ◽  
Ioannis-Dimosthenis S. Adamakis
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Wall ◽  
Cell Walls ◽  
Higher Plants ◽  
Cell Plate ◽  
Wild Type ◽  
Microtubule Organization ◽  
Root Cells ◽  
Wall Formation ◽  
In The Wild

Cytokinesis is accomplished in higher plants by the phragmoplast, creating and conducting the cell plate, to separate daughter nuclei by a new cell wall. The microtubule-severing enzyme p60-katanin plays an important role in the centrifugal expansion and timely disappearance of phragmoplast microtubules. Consequently, aberrant structure and delayed expansion rate of the phragmoplast occur in p60-katanin mutants. Here, the consequences of p60-katanin malfunction in cell plate/daughter wall formation were investigated by transmission electron microscopy (TEM), while deviations in the chemical composition of cell plate/new cell wall were identified by immunolabeling and confocal microscopy, in root cells of the fra2 Arabidopsis thaliana mutant. It was found that, apart from defective phragmoplast microtubule organization, cell plates/new cell walls appeared also faulty in structure, being unevenly thick and perforated by large gaps. In addition, demethylesterified homogalacturonans were prematurely present in fra2 cell plates, while callose content was significantly lower than in the wild-type. Furthermore, KNOLLE syntaxin disappeared from newly formed cell walls in fra2 earlier than in the wild-type. Taken together, these observations indicate that delayed cytokinesis, due to faulty phragmoplast organization and expansion, results in a loss of synchronization between cell plate growth and its chemical maturation.

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