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Yeast cell wall extract induces disease resistance against bacterial and fungal pathogens in Arabidopsis thaliana and Brassica crop.

Narusaka M, Minami T, Iwabuchi C, Hamasaki T, Takasaki S, Kawamura K, Narusaka Y - PLoS ONE (2015)

Bottom Line: HM reduced the severity of bacterial leaf spot and anthracnose on A. thaliana and Brassica crop leaves with protective effects.In addition, HM-induced resistance conferred chitin-independent disease resistance to bacterial pathogens in A. thaliana.These results suggest that HM contains multiple microbe-associated molecular patterns that activate defense responses in plants.

View Article: PubMed Central - PubMed

Affiliation: Research Institute for Biological Sciences Okayama, Okayama, Japan.

ABSTRACT
Housaku Monogatari (HM) is a plant activator prepared from a yeast cell wall extract. We examined the efficacy of HM application and observed that HM treatment increased the resistance of Arabidopsis thaliana and Brassica rapa leaves to bacterial and fungal infections. HM reduced the severity of bacterial leaf spot and anthracnose on A. thaliana and Brassica crop leaves with protective effects. In addition, gene expression analysis of A. thaliana plants after treatment with HM indicated increased expression of several plant defense-related genes. HM treatment appears to induce early activation of jasmonate/ethylene and late activation of salicylic acid (SA) pathways. Analysis using signaling mutants revealed that HM required SA accumulation and SA signaling to facilitate resistance to the bacterial pathogen Pseudomonas syringae pv. maculicola and the fungal pathogen Colletotrichum higginsianum. In addition, HM-induced resistance conferred chitin-independent disease resistance to bacterial pathogens in A. thaliana. These results suggest that HM contains multiple microbe-associated molecular patterns that activate defense responses in plants. These findings suggest that the application of HM is a useful tool that may facilitate new disease control methods.

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Induction of resistance to P. syringae pv. maculicola by HM application in Arabidopsis defense signaling-defective mutants.The 35-day-old A. thaliana mutants were sprayed with water (control) or 1250 ppm HM at 2 days prior to spray inoculation with a bacterial suspension (108 cfu mL−1) of P. syringae pv. maculicola. Pathogen growth was determined 3 days after inoculation by assessing P. syringae pv. maculicola-rpoD mRNA by qRT-PCR. Bars indicate the standard error (SE). The asterisk indicates a significant difference compared with the control (Dunnett’s method [35], P < 0.05). The experiment was repeated at least three times with similar results.
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pone.0115864.g003: Induction of resistance to P. syringae pv. maculicola by HM application in Arabidopsis defense signaling-defective mutants.The 35-day-old A. thaliana mutants were sprayed with water (control) or 1250 ppm HM at 2 days prior to spray inoculation with a bacterial suspension (108 cfu mL−1) of P. syringae pv. maculicola. Pathogen growth was determined 3 days after inoculation by assessing P. syringae pv. maculicola-rpoD mRNA by qRT-PCR. Bars indicate the standard error (SE). The asterisk indicates a significant difference compared with the control (Dunnett’s method [35], P < 0.05). The experiment was repeated at least three times with similar results.

Mentions: We investigated whether the defense-related hormone SA plays a role in HM-induced activation of SAR using NahG transgenic Arabidopsis, which fails to accumulate SA [14]; eds16–1, which does not produce SA [15]; and npr1–1, which fails to activate PR gene expression [16]. Both JA and ET have been suggested to play important roles in plant defense against pathogen infection. To determine the roles of JA and ET in HM-induced resistance, we tested A. thaliana mutants that varied in their ability to respond to methyl jasmonate (jar1–1 is insensitive to JA [17]) or ET (ein2–12 is insensitive to ET [18]). HM was applied to these plants, and their resistance levels to Psm were determined. These mutants were treated with 1250 ppm HM at 2 days prior to bacterial inoculation. At 3 dpi, mutants deficient in the SA signaling pathways exhibited decreased induced resistance to Psm infection, whereas mutants deficient in the JA or ET signaling pathways were protected in a manner similar to the wild-type Col-0 (Fig. 3). The water-pretreated controls exhibited increased bacterial growth. Thus, HM appears to activate disease resistance to Psm via a pathway that is dependent on SA. In addition, HM has no direct toxic effect on bacteria.


Yeast cell wall extract induces disease resistance against bacterial and fungal pathogens in Arabidopsis thaliana and Brassica crop.

Narusaka M, Minami T, Iwabuchi C, Hamasaki T, Takasaki S, Kawamura K, Narusaka Y - PLoS ONE (2015)

Induction of resistance to P. syringae pv. maculicola by HM application in Arabidopsis defense signaling-defective mutants.The 35-day-old A. thaliana mutants were sprayed with water (control) or 1250 ppm HM at 2 days prior to spray inoculation with a bacterial suspension (108 cfu mL−1) of P. syringae pv. maculicola. Pathogen growth was determined 3 days after inoculation by assessing P. syringae pv. maculicola-rpoD mRNA by qRT-PCR. Bars indicate the standard error (SE). The asterisk indicates a significant difference compared with the control (Dunnett’s method [35], P < 0.05). The experiment was repeated at least three times with similar results.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4286235&req=5

pone.0115864.g003: Induction of resistance to P. syringae pv. maculicola by HM application in Arabidopsis defense signaling-defective mutants.The 35-day-old A. thaliana mutants were sprayed with water (control) or 1250 ppm HM at 2 days prior to spray inoculation with a bacterial suspension (108 cfu mL−1) of P. syringae pv. maculicola. Pathogen growth was determined 3 days after inoculation by assessing P. syringae pv. maculicola-rpoD mRNA by qRT-PCR. Bars indicate the standard error (SE). The asterisk indicates a significant difference compared with the control (Dunnett’s method [35], P < 0.05). The experiment was repeated at least three times with similar results.
Mentions: We investigated whether the defense-related hormone SA plays a role in HM-induced activation of SAR using NahG transgenic Arabidopsis, which fails to accumulate SA [14]; eds16–1, which does not produce SA [15]; and npr1–1, which fails to activate PR gene expression [16]. Both JA and ET have been suggested to play important roles in plant defense against pathogen infection. To determine the roles of JA and ET in HM-induced resistance, we tested A. thaliana mutants that varied in their ability to respond to methyl jasmonate (jar1–1 is insensitive to JA [17]) or ET (ein2–12 is insensitive to ET [18]). HM was applied to these plants, and their resistance levels to Psm were determined. These mutants were treated with 1250 ppm HM at 2 days prior to bacterial inoculation. At 3 dpi, mutants deficient in the SA signaling pathways exhibited decreased induced resistance to Psm infection, whereas mutants deficient in the JA or ET signaling pathways were protected in a manner similar to the wild-type Col-0 (Fig. 3). The water-pretreated controls exhibited increased bacterial growth. Thus, HM appears to activate disease resistance to Psm via a pathway that is dependent on SA. In addition, HM has no direct toxic effect on bacteria.

Bottom Line: HM reduced the severity of bacterial leaf spot and anthracnose on A. thaliana and Brassica crop leaves with protective effects.In addition, HM-induced resistance conferred chitin-independent disease resistance to bacterial pathogens in A. thaliana.These results suggest that HM contains multiple microbe-associated molecular patterns that activate defense responses in plants.

View Article: PubMed Central - PubMed

Affiliation: Research Institute for Biological Sciences Okayama, Okayama, Japan.

ABSTRACT
Housaku Monogatari (HM) is a plant activator prepared from a yeast cell wall extract. We examined the efficacy of HM application and observed that HM treatment increased the resistance of Arabidopsis thaliana and Brassica rapa leaves to bacterial and fungal infections. HM reduced the severity of bacterial leaf spot and anthracnose on A. thaliana and Brassica crop leaves with protective effects. In addition, gene expression analysis of A. thaliana plants after treatment with HM indicated increased expression of several plant defense-related genes. HM treatment appears to induce early activation of jasmonate/ethylene and late activation of salicylic acid (SA) pathways. Analysis using signaling mutants revealed that HM required SA accumulation and SA signaling to facilitate resistance to the bacterial pathogen Pseudomonas syringae pv. maculicola and the fungal pathogen Colletotrichum higginsianum. In addition, HM-induced resistance conferred chitin-independent disease resistance to bacterial pathogens in A. thaliana. These results suggest that HM contains multiple microbe-associated molecular patterns that activate defense responses in plants. These findings suggest that the application of HM is a useful tool that may facilitate new disease control methods.

Show MeSH
Related in: MedlinePlus