Synergistic Activation of Defense Responses in <i>Arabidopsis</i> by Simultaneous Loss of the GSL5 Callose Synthase and the EDR1 Protein Kinase

Wawrzyńska, Anna; Rodibaugh, Natalie; Innes, Roger W.

doi:10.1094/mpmi-23-5-0578

Cited by 29 publications

(15 citation statements)

References 43 publications

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“…These phenotypic characteristics are, however, not present in the edr1 and pmr4 single mutants. When inoculated with G. cichoracearum, the edr1 pmr4 double mutant displayed enhanced resistance, compared with edr1 in the absence of callose depositions, accompanied by enhanced cell death (Wawrzynska et al 2010). Data obtained in our infection experiments with P. infestans revealed an enhancement of cell death at the infection sites, without the intense callose depositions seen in the mesophyll of the edr1 single mutants (Fig.…”

Section: Discussionmentioning

confidence: 62%

“…The edr1 pmr4 double mutant was identified in a screen for mutations enhancing the edr1 phenotype. The plants are dwarfed, show a spontaneous formation of necrosis, and constitutive expression of SA-and JA-related genes (Wawrzynska et al 2010). These phenotypes are reminiscent of the lesion-simulating disease or accelerated cell death mutants, which exhibit a deregulated SA signaling (Dietrich et Fig.…”

Section: Discussionmentioning

confidence: 99%

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

Geißler¹,

Eschen‐Lippold²,

Naumann³

et al. 2015

MPMI

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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.

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Section: Discussionmentioning

confidence: 62%

Section: Discussionmentioning

confidence: 99%

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

Geißler¹,

Eschen‐Lippold²,

Naumann³

et al. 2015

MPMI

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“…Different GSL genes exhibit partially redundant roles in plant growth, development and defences (Chen and Kim 2009). It has been shown that the GSL5 enzyme is responsible for the synthesis of wound-and pathogeninducible callose in leaf tissue (Jacobs et al 2003;Nishimura et al 2003;Wawrzynska et al 2010). GSL5 also plays an important role in exine formation and pollen wall patterning (Dong et al 2005b;Enns et al 2005).…”

Section: Discussionmentioning

confidence: 99%

“…Based on analyses of mutations made by knocking out the individual GSL genes, it is found that the genes exhibit partially redundant roles in plant growth and development; a single GSL gene can also have diverse functions (Chen and Kim 2009). For example, GSL5 is responsible for the synthesis of wound-inducible and pathogen-inducible callose in leaf tissue (Jacobs et al 2003;Nishimura et al 2003;Wawrzynska et al 2010); it also plays an important role in exine formation and pollen wall patterning (Dong et al 2005b;Enns et al 2005). However, genetic evidence is incomplete regarding functions of the different GSL genes; so far, evidence is available only for AtGSL1, 2, 5, 6, 8 and 10 (Kaliff et al 2007;Dong et al 2008;Huang et al 2008;Töller et al 2008;Chen et al 2009a;Consonni et al 2009;Xie et al 2009).…”

Section: Introductionmentioning

confidence: 99%

HrpNEa-induced deterrent effect on phloem feeding of the green peach aphid Myzus persicae requires AtGSL5 and AtMYB44 genes in Arabidopsis thaliana

et al. 2011

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In Arabidopsis thaliana (Arabidopsis) treated with the harpin protein HrpN Ea, resistance to the green peach aphid Myzus persicae, a generalist phloem-feeding insect, develops with induced expression of the AtMYB44 gene. Special GLUCAN SYNTHESIS-LIKE (GSL) genes and beta-1,3-glucan callose play an important role in plant defence responses to attacks by phloem-feeding insects. Here we report that AtGLS5 and AtMYB44 are both required for Hrp Ea-induced repression of M. persicae feeding from the phloem of Arabidopsis leaves. In 24 h successive surveys on large-scale aphid populations, the proportion of feeding aphids was much smaller in HrpN Ea-treated plants than in control plants, and aphids preferred to feed from the 37 tested atgsl mutants rather than the wild-type plant. The atgsl mutants were generated previously by mutagenesis in 12 identified AtGSL genes (AtGSL1 through AtGSL12); in the 24 h survey, both atgsl5 and atgsl6 tolerated aphid feeding, and atgsl5 was the most tolerant. Consistently, atgsl5 was also most inhibitive to the deterrent effect of HrpN Ea on the phloem-feeding activity of aphids as monitored by the electrical penetration graph technique. These results suggested an important role of the AtGSL5 gene in the effect of HrpN Ea. In response to HrpN Ea, AtGSL5 expression and callose deposition were induced in the wild-type plant but not in atgsl5. In response to HrpN Ea, moreover, the AtMYB44 gene known to be required for repression of aphid reproduction on the plant was also required for repression of the phloem-feeding activity. Small amounts of the AtGSL5 transcript and callose deposition were detected in the atmyb44 mutant, as in atgsl5. Both mutants performed similarly in tolerating the phloem-feeding activity and impairing the deterrent effect of HrpN Ea, suggesting that AtGSL5 and AtMYB44 both contributed to the effect.

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“…In addition to EDR2, several genes in Arabidopsis have been shown to play negative roles in disease resistance to powdery mildew, such as EDR1, PMR4, MLO2, and ATG2 (Frye et al, 2001;Nishimura et al, 2003;Consonni et al, 2006;Vorwerk et al, 2007). Previously, it has been shown that PMR4, EDR1, and MLO2 define different genetic pathways in plant immunity (Frye et al, 2001;Nishimura et al, 2003;Consonni et al, 2006;Wawrzynska et al, 2010). The observation that bsk1-1 suppressed all edr1, mlo2, and pmr4-mediated powdery mildew resistance phenotypes indicates that BSK1 may play a general but important role in plant defense responses.…”

Section: Bsk1 Plays An Important Role In Defense Responsesmentioning

confidence: 99%

BR-SIGNALING KINASE1 Physically Associates with FLAGELLIN SENSING2 and Regulates Plant Innate Immunity in Arabidopsis

et al. 2013

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Pathogen-associated molecular pattern (PAMP)-trigged immunity (PTI) is the first defensive line of plant innate immunity and is mediated by pattern recognition receptors. Here, we show that a mutation in BR-SIGNALING KINASE1 (BSK1), a substrate of the brassinosteroid (BR) receptor BRASSINOSTEROID INSENSITIVE1, suppressed the powdery mildew resistance caused by a mutation in ENHANCED DISEASE RESISTANCE2, which negatively regulates powdery mildew resistance and programmed cell death, in Arabidopsis thaliana. A loss-of-function bsk1 mutant displayed enhanced susceptibility to virulent and avirulent pathogens, including Golovinomyces cichoracearum, Pseudomonas syringae, and Hyaloperonospora arabidopsidis. The bsk1 mutant also accumulated lower levels of salicylic acid upon infection with G. cichoracearum and P. syringae. BSK1 belongs to a receptor-like cytoplasmic kinase family and displays kinase activity in vitro; this kinase activity is required for its function. BSK1 physically associates with the PAMP receptor FLAGELLIN SENSING2 and is required for a subset of flg22-induced responses, including the reactive oxygen burst, but not for mitogen-activated protein kinase activation. Our data demonstrate that BSK1 is involved in positive regulation of PTI. Together with previous findings, our work indicates that BSK1 represents a key component directly involved in both BR signaling and plant immunity.

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Synergistic Activation of Defense Responses in Arabidopsis by Simultaneous Loss of the GSL5 Callose Synthase and the EDR1 Protein Kinase

Cited by 29 publications

References 43 publications

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

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

HrpNEa-induced deterrent effect on phloem feeding of the green peach aphid Myzus persicae requires AtGSL5 and AtMYB44 genes in Arabidopsis thaliana

BR-SIGNALING KINASE1 Physically Associates with FLAGELLIN SENSING2 and Regulates Plant Innate Immunity in Arabidopsis

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