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Redundancy among phospholipase D isoforms in resistance triggered by recognition of the Pseudomonas syringae effector AvrRpm1 in Arabidopsis thaliana.

Johansson ON, Fahlberg P, Karimi E, Nilsson AK, Ellerström M, Andersson MX - Front Plant Sci (2014)

Bottom Line: Recognition of microbial effectors or their activity by plant resistance (R)-proteins triggers a second line of defense resulting in effector triggered immunity (ETI).However, repression of PLD dependent PA production by n-butanol strongly inhibited the HR following Pseudomonas syringae effector recognition.Thus, the effect of mutations of PLDs could become detectable, and the corresponding genes can be proposed to be involved in the HR.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology and Environmental Sciences, University of Gothenburg Gothenburg, Sweden.

ABSTRACT
Plants possess a highly sophisticated system for defense against microorganisms. So called MAMP (microbe-associated molecular patterns) triggered immunity (MTI) prevents the majority of non-adapted pathogens from causing disease. Adapted plant pathogens use secreted effector proteins to interfere with such signaling. Recognition of microbial effectors or their activity by plant resistance (R)-proteins triggers a second line of defense resulting in effector triggered immunity (ETI). The latter usually comprises the hypersensitive response (HR) which includes programmed cell death at the site of infection. Phospholipase D (PLD) mediated production of phosphatidic acid (PA) has been linked to both MTI and ETI in plants. Inhibition of PLD activity has been shown to attenuate MTI as well as ETI. In this study, we systematically tested single and double knockouts in all 12 genes encoding PLDs in Arabidopsis thaliana for effects on ETI and MTI. No single PLD could be linked to ETI triggered by recognition of effectors secreted by the bacterium Pseudomonas syringae. However, repression of PLD dependent PA production by n-butanol strongly inhibited the HR following Pseudomonas syringae effector recognition. In addition some pld mutants were more sensitive to n-butanol than wild type. Thus, the effect of mutations of PLDs could become detectable, and the corresponding genes can be proposed to be involved in the HR. Only knockout of PLDδ caused a loss of MTI-induced cell wall based defense against the non-host powdery mildew Erysiphe pisi. This is thus in stark contrast to the involvement of a multitude of PLD isoforms in the HR triggered by AvrRpm1 recognition.

No MeSH data available.


Related in: MedlinePlus

Involvement of PLDδ in microbe-associated molecular pattern (MAMP) triggered cell wall based defense against pea powdery mildew. The indicated wild type (Col-0) and mutant lines were inoculated with Ep spores and trypan blue stained at 2 dpi. The rate of successful penetration of the epidermal cell wall was calculated from counting of at least 50 germinated spores on three independent leaves. Average and SD is shown. An asterisk indicates statistically significant difference from wild type (Col-0), p < 0.05, one way ANOVA.
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Figure 7: Involvement of PLDδ in microbe-associated molecular pattern (MAMP) triggered cell wall based defense against pea powdery mildew. The indicated wild type (Col-0) and mutant lines were inoculated with Ep spores and trypan blue stained at 2 dpi. The rate of successful penetration of the epidermal cell wall was calculated from counting of at least 50 germinated spores on three independent leaves. Average and SD is shown. An asterisk indicates statistically significant difference from wild type (Col-0), p < 0.05, one way ANOVA.

Mentions: We previously reported that PLDδ was the only isoform involved in PLD-dependent cell wall based defense against the non-host powdery mildew Bgh and that the pldδ mutant also demonstrated a loss of penetration resistance toward pea powdery mildew Ep (Pinosa et al., 2013). We thus tested the response of the full panel of PLD mutants to Ep (Figure 7). To this end plants were inoculated with Ep, leaves stained with trypan blue 2 days post infection and scored for disease progress. The pen1-1 mutant was included as a control as it has a severely deficient cell wall based resistance response against non-host powdery mildews (Collins et al., 2003). The number of germinated spores that successfully penetrated the epidermal cell wall was about 15% in wild type (Col-0), whereas pen1-1 allowed about 70% of the germinated spores to penetrate the epidermal cell wall. Among the tested PLD single mutants, only pld δ displayed any increase in penetration rate compared to wild type. Higher order mutants containing the pldδ displayed the same phenotype as the single mutant. There was no change in frequency of single epidermal cell death following successful penetration in any of the tested mutants compared to wild type.


Redundancy among phospholipase D isoforms in resistance triggered by recognition of the Pseudomonas syringae effector AvrRpm1 in Arabidopsis thaliana.

Johansson ON, Fahlberg P, Karimi E, Nilsson AK, Ellerström M, Andersson MX - Front Plant Sci (2014)

Involvement of PLDδ in microbe-associated molecular pattern (MAMP) triggered cell wall based defense against pea powdery mildew. The indicated wild type (Col-0) and mutant lines were inoculated with Ep spores and trypan blue stained at 2 dpi. The rate of successful penetration of the epidermal cell wall was calculated from counting of at least 50 germinated spores on three independent leaves. Average and SD is shown. An asterisk indicates statistically significant difference from wild type (Col-0), p < 0.05, one way ANOVA.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4230166&req=5

Figure 7: Involvement of PLDδ in microbe-associated molecular pattern (MAMP) triggered cell wall based defense against pea powdery mildew. The indicated wild type (Col-0) and mutant lines were inoculated with Ep spores and trypan blue stained at 2 dpi. The rate of successful penetration of the epidermal cell wall was calculated from counting of at least 50 germinated spores on three independent leaves. Average and SD is shown. An asterisk indicates statistically significant difference from wild type (Col-0), p < 0.05, one way ANOVA.
Mentions: We previously reported that PLDδ was the only isoform involved in PLD-dependent cell wall based defense against the non-host powdery mildew Bgh and that the pldδ mutant also demonstrated a loss of penetration resistance toward pea powdery mildew Ep (Pinosa et al., 2013). We thus tested the response of the full panel of PLD mutants to Ep (Figure 7). To this end plants were inoculated with Ep, leaves stained with trypan blue 2 days post infection and scored for disease progress. The pen1-1 mutant was included as a control as it has a severely deficient cell wall based resistance response against non-host powdery mildews (Collins et al., 2003). The number of germinated spores that successfully penetrated the epidermal cell wall was about 15% in wild type (Col-0), whereas pen1-1 allowed about 70% of the germinated spores to penetrate the epidermal cell wall. Among the tested PLD single mutants, only pld δ displayed any increase in penetration rate compared to wild type. Higher order mutants containing the pldδ displayed the same phenotype as the single mutant. There was no change in frequency of single epidermal cell death following successful penetration in any of the tested mutants compared to wild type.

Bottom Line: Recognition of microbial effectors or their activity by plant resistance (R)-proteins triggers a second line of defense resulting in effector triggered immunity (ETI).However, repression of PLD dependent PA production by n-butanol strongly inhibited the HR following Pseudomonas syringae effector recognition.Thus, the effect of mutations of PLDs could become detectable, and the corresponding genes can be proposed to be involved in the HR.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology and Environmental Sciences, University of Gothenburg Gothenburg, Sweden.

ABSTRACT
Plants possess a highly sophisticated system for defense against microorganisms. So called MAMP (microbe-associated molecular patterns) triggered immunity (MTI) prevents the majority of non-adapted pathogens from causing disease. Adapted plant pathogens use secreted effector proteins to interfere with such signaling. Recognition of microbial effectors or their activity by plant resistance (R)-proteins triggers a second line of defense resulting in effector triggered immunity (ETI). The latter usually comprises the hypersensitive response (HR) which includes programmed cell death at the site of infection. Phospholipase D (PLD) mediated production of phosphatidic acid (PA) has been linked to both MTI and ETI in plants. Inhibition of PLD activity has been shown to attenuate MTI as well as ETI. In this study, we systematically tested single and double knockouts in all 12 genes encoding PLDs in Arabidopsis thaliana for effects on ETI and MTI. No single PLD could be linked to ETI triggered by recognition of effectors secreted by the bacterium Pseudomonas syringae. However, repression of PLD dependent PA production by n-butanol strongly inhibited the HR following Pseudomonas syringae effector recognition. In addition some pld mutants were more sensitive to n-butanol than wild type. Thus, the effect of mutations of PLDs could become detectable, and the corresponding genes can be proposed to be involved in the HR. Only knockout of PLDδ caused a loss of MTI-induced cell wall based defense against the non-host powdery mildew Erysiphe pisi. This is thus in stark contrast to the involvement of a multitude of PLD isoforms in the HR triggered by AvrRpm1 recognition.

No MeSH data available.


Related in: MedlinePlus