scholarly journals EDS1 Contributes to Nonhost Resistance of Arabidopsis thaliana Against Erwinia amylovora

2012 ◽  
Vol 25 (3) ◽  
pp. 421-430 ◽  
Author(s):  
Manon Moreau ◽  
Alexandre Degrave ◽  
Régine Vedel ◽  
Frédérique Bitton ◽  
Oriane Patrit ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Protein Synthesis ◽  
Erwinia Amylovora ◽  
Gene Activation ◽  
Negative Regulator ◽  
Nonhost Resistance ◽  
Callose Deposition ◽  
In The Wild ◽  
Increased Sensitivity ◽  
Main Components

Erwinia amylovora causes fire blight in rosaceous plants. In nonhost Arabidopsis thaliana, E. amylovora triggers necrotic symptoms associated with transient bacterial multiplication, suggesting either that A. thaliana lacks a susceptibility factor or that it actively restricts E. amylovora growth. Inhibiting plant protein synthesis at the time of infection led to an increase in necrosis and bacterial multiplication and reduced callose deposition, indicating that A. thaliana requires active protein synthesis to restrict E. amylovora growth. Analysis of the callose synthase–deficient pmr4-1 mutant indicated that lack of callose deposition alone did not lead to increased sensitivity to E. amylovora. Transcriptome analysis revealed that approximately 20% of the genes induced following E. amylovora infection are related to defense and signaling. Analysis of mutants affected in NDR1 and EDS1, two main components of the defense-gene activation observed, revealed that E. amylovora multiplied ten times more in the eds1-2 mutant than in the wild type but not in the ndr1-1 mutant. Analysis of mutants affected in three WRKY transcription factors showing EDS1-dependent activation identified WRKY46 and WRKY54 as positive regulators and WRKY70 as a negative regulator of defense against E. amylovora. Altogether, we show that EDS1 is a positive regulator of nonhost resistance against E. amylovora in A. thaliana and hypothesize that it controls the production of several effective defenses against E. amylovora through the action of WRKY46 and WRKY54, while WRKY70 acts as a negative regulator.

scholarly journals Mutations in the EDR1 Gene Alter the Response of Arabidopsis thaliana to Phytophthora infestans and the Bacterial PAMPs flg22 and elf18

2015 ◽  
Vol 28 (2) ◽  
pp. 122-133 ◽  
Author(s):  
Katrin Geissler ◽  
Lennart Eschen-Lippold ◽  
Kai Naumann ◽  
Korbinian Schneeberger ◽  
Detlef Weigel ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Phytophthora Infestans ◽  
Kinase Domain ◽  
Negative Regulator ◽  
Single Amino Acid ◽  
Nonhost Resistance ◽  
Coding Region ◽  
Callose Deposition ◽  
Knock Out

Mechanistically, nonhost resistance of Arabidopsis thaliana against the oomycete Phytophthora infestans is not well understood. Besides PEN2 and PEN3, which contribute to penetration resistance, no further components have been identified so far. In an ethylmethane sulphonate–mutant screen, we mutagenized pen2-1 and screened for mutants with an altered response to infection by P. infestans. One of the mutants obtained, enhanced response to Phytophthora infestans6 (erp6), was analyzed. Whole-genome sequencing of erp6 revealed a single nucleotide polymorphism in the coding region of the kinase domain of At1g08720, which encodes the putative MAPKKK ENHANCED DISEASE RESISTANCE1 (EDR1). We demonstrate that three independent lines with knock-out alleles of edr1 mount an enhanced response to P. infestans inoculation, mediated by increased salicylic acid signaling and callose deposition. Moreover, we show that the single amino acid substitution in erp6 causes the loss of in vitro autophosphorylation activity of EDR1. Furthermore, growth inhibition experiments suggest a so-far-unknown involvement of EDR1 in the response to the pathogen-associated molecular patterns flg22 and elf18. We conclude that EDR1 contributes to the defense response of A. thaliana against P. infestans. Our data position EDR1 as a negative regulator in postinvasive nonhost resistance.

scholarly journals Basic Compatibility of Albugo candida in Arabidopsis thaliana and Brassica juncea Causes Broad-Spectrum Suppression of Innate Immunity

2008 ◽  
Vol 21 (6) ◽  
pp. 745-756 ◽  
Author(s):  
A. J. Cooper ◽  
A. O. Latunde-Dada ◽  
A. Woods-Tör ◽  
J. Lynn ◽  
J. A. Lucas ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Powdery Mildew ◽  
Downy Mildew ◽  
Brassica Juncea ◽  
Broad Spectrum ◽  
Secondary Infection ◽  
Nonhost Resistance ◽  
Susceptible Host ◽  
Albugo Candida ◽  
In The Wild

A biotrophic parasite often depends on an intrinsic ability to suppress host defenses in a manner that will enable it to infect and successfully colonize a susceptible host. If the suppressed defenses otherwise would have been effective against alternative pathogens, it follows that primary infection by the “suppressive” biotroph potentially could enhance susceptibility of the host to secondary infection by avirulent pathogens. This phenomenon previously has been attributed to true fungi such as rust (basidiomycete) and powdery mildew (ascomycete) pathogens. In our study, we observed broad-spectrum suppression of host defense by the oomycete Albugo candida (white blister rust) in the wild crucifer Arabidopsis thaliana and a domesticated relative, Brassica juncea. A. candida subsp. arabidopsis suppressed the “runaway cell death” phenotype of the lesion mimic mutant lsd1 in Arabidopsis thaliana in a sustained manner even after subsequent inoculation with avirulent Hyaloperonospora arabidopsis (Arabidopsis thaliana downy mildew). In sequential inoculation experiments, we show that preinfection by virulent Albugo candida can suppress disease resistance in cotyledons to several downy mildew pathogens, including contrasting examples of genotype resistance to H. arabidopsis in Arabidopsis thaliana that differ in the R protein and modes of defense signaling used to confer the resistance; genotype specific resistance in B. juncea to H. parasitica (Brassica downy mildew; isolates derived from B. juncea); species level (nonhost) resistance in both crucifers to Bremia lactucae (lettuce downy mildew) and an isolate of the H. parasitica race derived from Brassica oleracea; and nonhost resistance in B. juncea to H. arabidopsis. Broad-spectrum powdery mildew resistance conferred by RPW8 also was suppressed in Arabidopsis thaliana to two morphotypes of Erysiphe spp. following pre-infection with A. candida subsp. arabidopsis.

scholarly journals CRK2 enhances salt tolerance in Arabidopsis thaliana by regulating endocytosis and callose deposition in connection with PLDα1

2018 ◽  
Author(s):  
Kerri Hunter ◽  
Sachie Kimura ◽  
Anne Rokka ◽  
Cuong Tran ◽  
Masatsugu Toyota ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Salt Stress ◽  
Salt Tolerance ◽  
Subcellular Localization ◽  
Stress Responses ◽  
Negative Regulator ◽  
Biotic And Abiotic Stress ◽  
Callose Deposition ◽  
Receptor Like Kinase ◽  
Stress Dependent

AbstractHigh salinity has become an increasingly prevalent source of stress to which plants need to adapt. The receptor-like protein kinases (RLKs), including the cysteine-rich receptor-like kinase (CRK) subfamily, are a highly expanded family of transmembrane proteins in plants and are largely responsible for communication between cells and the extracellular environment. Various CRKs have been implicated in biotic and abiotic stress responses, however their functions on a cellular level remain largely uncharacterized. Here we have shown that CRK2 enhances salt tolerance at the germination stage in Arabidopsis thaliana. We identified CRK2 as a negative regulator of endocytosis, under both normal growth conditions and salt stress. We also established that functional CRK2 is required for salt-induced callose deposition. In doing so, we revealed a novel role for callose deposition, in response to increased salinity, and demonstrated its importance for salt tolerance during germination. Using fluorescently tagged proteins we observed specific changes in CRK2’s subcellular localization in response to various stress treatments. Many of CRK2’s cellular functions were dependent on phospholipase D (PLD) activity, as were the subcellular localization changes. Thus we propose that CRK2 acts downstream of PLD during salt stress to regulate endocytosis and promote callose deposition, and that CRK2 adopts specific stress-dependent subcellular localization patterns in order to carry out its functions.One sentence summaryThe receptor-like kinase CRK2 acts in connection with PLDα1 to regulate endocytosis and callose deposition at plasmodesmata, enhancing salt tolerance in Arabidopsis thaliana.

scholarly journals Erwinia amylovora Type Three–Secreted Proteins Trigger Cell Death and Defense Responses in Arabidopsis thaliana

2008 ◽  
Vol 21 (8) ◽  
pp. 1076-1086 ◽  
Author(s):  
A. Degrave ◽  
M. Fagard ◽  
C. Perino ◽  
M. N. Brisset ◽  
S. Gaubert ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Death ◽  
Host Plants ◽  
Erwinia Amylovora ◽  
Disease Process ◽  
Defense Responses ◽  
Secreted Proteins ◽  
Relative Importance ◽  
Callose Deposition ◽  
Ros Accumulation

Erwinia amylovora is the bacterium responsible for fire blight, a necrotic disease affecting plants of the rosaceous family. E. amylovora pathogenicity requires a functional type three secretion system (T3SS). We show here that E. amylovora triggers a T3SS-dependent cell death on Arabidopsis thaliana. The plants respond by inducing T3SS-dependent defense responses, including salicylic acid (SA)-independent callose deposition, activation of the SA defense pathway, reactive oxygen species (ROS) accumulation, and part of the jasmonic acid/ethylene defense pathway. Several of these reactions are similar to what is observed in host plants. We show that the cell death triggered by E. amylovora on A. thaliana could not be simply explained by the recognition of AvrRpt2ea by the resistance gene product RPS2. We then analyzed the role of type three-secreted proteins (T3SPs) DspA/E, HrpN, and HrpW in the induction of cell death and defense reactions in A. thaliana following infection with the corresponding E. amylovora mutant strains. HrpN and DspA/E were found to play an important role in the induction of cell death, activation of defense pathways, and ROS accumulation. None of the T3SPs tested played a major role in the induction of SA-independent callose deposition. The relative importance of T3SPs in A. thaliana is correlated with their relative importance in the disease process on host plants, indicating that A. thaliana can be used as a model to study their role.

scholarly journals Author Correction: ATHB2 is a negative regulator of germination in Arabidopsis thaliana seeds

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Rocío Soledad Tognacca ◽  
Monica Carabelli ◽  
Giorgio Morelli ◽  
Ida Ruberti ◽  
Javier Francisco Botto
Keyword(s):  
Arabidopsis Thaliana ◽  
Negative Regulator

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

scholarly journals Controlled Transcription of Regulator Gene carS by Tet-on or by a Strong Promoter Confirms Its Role as a Repressor of Carotenoid Biosynthesis in Fusarium fujikuroi

2020 ◽  
Vol 9 (1) ◽  
pp. 71
Author(s):  
Julia Marente ◽  
Javier Avalos ◽  
M. Carmen Limón
Keyword(s):  
Wild Strain ◽  
Ring Finger ◽  
Carotenoid Biosynthesis ◽  
Negative Regulator ◽  
Fusarium Fujikuroi ◽  
Structural Genes ◽  
Gene Encoding ◽  
In The Wild ◽  
Set Up

Carotenoid biosynthesis is a frequent trait in fungi. In the ascomycete Fusarium fujikuroi, the synthesis of the carboxylic xanthophyll neurosporaxanthin (NX) is stimulated by light. However, the mutants of the carS gene, encoding a protein of the RING finger family, accumulate large NX amounts regardless of illumination, indicating the role of CarS as a negative regulator. To confirm CarS function, we used the Tet-on system to control carS expression in this fungus. The system was first set up with a reporter mluc gene, which showed a positive correlation between the inducer doxycycline and luminescence. Once the system was improved, the carS gene was expressed using Tet-on in the wild strain and in a carS mutant. In both cases, increased carS transcription provoked a downregulation of the structural genes of the pathway and albino phenotypes even under light. Similarly, when the carS gene was constitutively overexpressed under the control of a gpdA promoter, total downregulation of the NX pathway was observed. The results confirmed the role of CarS as a repressor of carotenogenesis in F. fujikuroi and revealed that its expression must be regulated in the wild strain to allow appropriate NX biosynthesis in response to illumination.

Caffeoyl Shikimate Esterase (CSE) Is an Enzyme in the Lignin Biosynthetic Pathway in Arabidopsis

Science ◽  
2013 ◽  
Vol 341 (6150) ◽  
pp. 1103-1106 ◽  
Author(s):  
Ruben Vanholme ◽  
Igor Cesarino ◽  
Katarzyna Rataj ◽  
Yuguo Xiao ◽  
Lisa Sundin ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Walls ◽  
Metabolite Profiling ◽  
Biosynthetic Pathway ◽  
Wild Type ◽  
Secondary Cell Walls ◽  
Phenolic Metabolite ◽  
In The Wild ◽  
Lignin Biosynthetic Pathway

Lignin is a major component of plant secondary cell walls. Here we describe caffeoyl shikimate esterase (CSE) as an enzyme central to the lignin biosynthetic pathway. Arabidopsis thaliana cse mutants deposit less lignin than do wild-type plants, and the remaining lignin is enriched in p-hydroxyphenyl units. Phenolic metabolite profiling identified accumulation of the lignin pathway intermediate caffeoyl shikimate in cse mutants as compared to caffeoyl shikimate levels in the wild type, suggesting caffeoyl shikimate as a substrate for CSE. Accordingly, recombinant CSE hydrolyzed caffeoyl shikimate into caffeate. Associated with the changes in lignin, the conversion of cellulose to glucose in cse mutants increased up to fourfold as compared to that in the wild type upon saccharification without pretreatment. Collectively, these data necessitate the revision of currently accepted models of the lignin biosynthetic pathway.

scholarly journals Aspergillus nidulans Protein O-Mannosyltransferases Play Roles in Cell Wall Integrity and Developmental Patterning

2009 ◽  
Vol 8 (10) ◽  
pp. 1475-1485 ◽  
Author(s):  
Thanyanuch Kriangkripipat ◽  
Michelle Momany
Keyword(s):  
Cell Wall ◽  
Aspergillus Nidulans ◽  
Double Mutant ◽  
Elevated Temperatures ◽  
Cell Wall Integrity ◽  
Wild Type ◽  
Spatial Cues ◽  
Developmental Patterning ◽  
In The Wild ◽  
Increased Sensitivity

ABSTRACT Protein O-mannosyltransferases (Pmts) initiate O-mannosyl glycan biosynthesis from Ser and Thr residues of target proteins. Fungal Pmts are divided into three subfamilies, Pmt1, -2, and -4. Aspergillus nidulans possesses a single representative of each Pmt subfamily, pmtA (subfamily 2), pmtB (subfamily 1), and pmtC (subfamily 4). In this work, we show that single Δpmt mutants are viable and have unique phenotypes and that the ΔpmtA ΔpmtB double mutant is the only viable double mutant. This makes A. nidulans the first fungus in which all members of individual Pmt subfamilies can be deleted without loss of viability. At elevated temperatures, all A. nidulans Δpmt mutants show cell wall-associated defects and increased sensitivity to cell wall-perturbing agents. The Δpmt mutants also show defects in developmental patterning. Germ tube emergence is early in ΔpmtA and more frequent in ΔpmtC mutants than in the wild type. In ΔpmtB mutants, intrahyphal hyphae develop. All Δpmt mutants show distinct conidiophore defects. The ΔpmtA strain has swollen vesicles and conidiogenous cells, the ΔpmtB strain has swollen conidiophore stalks, and the ΔpmtC strain has dramatically elongated conidiophore stalks. We also show that AN5660, an ortholog of Saccharomyces cerevisiae Wsc1p, is modified by PmtA and PmtC. The Δpmt phenotypes at elevated temperatures, increased sensitivity to cell wall-perturbing agents and restoration to wild-type growth with osmoticum suggest that A. nidulans Pmts modify proteins in the cell wall integrity pathway. The altered developmental patterns in Δpmt mutants suggest that A. nidulans Pmts modify proteins that serve as spatial cues.

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