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Gaseous 3-pentanol primes plant immunity against a bacterial speck pathogen, Pseudomonas syringae pv. tomato via salicylic acid and jasmonic acid-dependent signaling pathways in Arabidopsis.

Song GC, Choi HK, Ryu CM - Front Plant Sci (2015)

Bottom Line: We performed quantitative real-time PCR to investigate the 3-pentanol-mediated Arabidopsis immune responses by determining Pathogenesis-Related (PR) gene expression levels associated with defense signaling through salicylic acid (SA), jasmonic acid (JA), and ethylene signaling pathways.Selected Arabidopsis mutants confirmed that the 3-pentanol-mediated immune response involved SA and JA signaling pathways and the NPR1 gene.Taken together, this study indicates that gaseous 3-pentanol triggers induced resistance in Arabidopsis by priming SA and JA signaling pathways.

View Article: PubMed Central - PubMed

Affiliation: Molecular Phytobacteriology Laboratory, Korea Research Institute of Bioscience and Biotechnology , Daejeon, South Korea.

ABSTRACT
3-Pentanol is an active organic compound produced by plants and is a component of emitted insect sex pheromones. A previous study reported that drench application of 3-pentanol elicited plant immunity against microbial pathogens and an insect pest in crop plants. Here, we evaluated whether 3-pentanol and the derivatives 1-pentanol and 2-pentanol induced plant systemic resistance using the in vitro I-plate system. Exposure of Arabidopsis seedlings to 10 μM and 100 nM 3-pentanol evaporate elicited an immune response to Pseudomonas syringae pv. tomato DC3000. We performed quantitative real-time PCR to investigate the 3-pentanol-mediated Arabidopsis immune responses by determining Pathogenesis-Related (PR) gene expression levels associated with defense signaling through salicylic acid (SA), jasmonic acid (JA), and ethylene signaling pathways. The results show that exposure to 3-pentanol and subsequent pathogen challenge upregulated PDF1.2 and PR1 expression. Selected Arabidopsis mutants confirmed that the 3-pentanol-mediated immune response involved SA and JA signaling pathways and the NPR1 gene. Taken together, this study indicates that gaseous 3-pentanol triggers induced resistance in Arabidopsis by priming SA and JA signaling pathways. To our knowledge, this is the first report that a volatile compound of an insect sex pheromone triggers plant systemic resistance against a bacterial pathogen.

No MeSH data available.


Related in: MedlinePlus

Effects of gaseous 1-pentanol, 2-pentanol, and 3-pentanol on Arabidopsis systemic resistance. (A,B)Arabidopsis seedlings were planted in an I-plate, which contains two physically separated compartments that share the same headspace. Plants are exposed to volatile 3-pentanol and its isoforms (or sterile distilled water control), which evaporates from solutions in the other compartment. All plants were drop-inoculated with P. syringae pv. tomato DC3000 (Pto) 7 days after exposure to volatiles from 1 nM, 100 nM, 10 μM, and 1 mM 1-pentanol, 2-pentanol, and 3-pentanol. Disease severity (B) was measured 7 days after pathogen inoculation. The asterisk in (B) indicates significant differences (P = 0.05 by LSD) between treatment and control. Error bars represent means ± SEM; N = 12 plants per treatment.
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Figure 1: Effects of gaseous 1-pentanol, 2-pentanol, and 3-pentanol on Arabidopsis systemic resistance. (A,B)Arabidopsis seedlings were planted in an I-plate, which contains two physically separated compartments that share the same headspace. Plants are exposed to volatile 3-pentanol and its isoforms (or sterile distilled water control), which evaporates from solutions in the other compartment. All plants were drop-inoculated with P. syringae pv. tomato DC3000 (Pto) 7 days after exposure to volatiles from 1 nM, 100 nM, 10 μM, and 1 mM 1-pentanol, 2-pentanol, and 3-pentanol. Disease severity (B) was measured 7 days after pathogen inoculation. The asterisk in (B) indicates significant differences (P = 0.05 by LSD) between treatment and control. Error bars represent means ± SEM; N = 12 plants per treatment.

Mentions: Plant and bacterial preparations were conducted as described previously (Ryu et al., 2003a, 2004; Lee et al., 2012). Briefly, Arabidopsis thaliana ecotype Columbia (Col-0) seedlings that had been lowed to germinate and grow for at least 2 days were transferred to one compartment of an I-plate (SPL Lifesciences Co., Pocheon, Gyeonggi-do, South Korea) containing 1/2 Murashige and Skoog medium supplemented with 0.6% (w/v) agar and 1.5% (w/v) sucrose. Plants were cultivated in the I-plates in a growth chamber for 14 days at 21°C under a 16 h light/8 h dark cycle before collecting samples for gene expression analysis. Bacterial pathogens were cultured overnight at 30°C in LB medium supplemented with 100 μg/ml rifampicin. Arabidopsis thaliana ecotype Columbia (Col-0) plants were prepared as described previously (Lee et al., 2012). The I-plate system was employed to assess induced resistance mediated by 1-pentanol, 2-pentanol, and 3-pentanol; 30 μl of 1 nM, 100 nM, 10 μM, and 1 mM of each C5 amyl alcohol (or sterile distilled water control) was added to one compartment of an I-plate (the a-compartment in Figure 1A) containing Arabidopsis plants in the other compartment, and the plate was tightly sealed with Parafilm. For the induced resistance assay, 2 μL of freshly prepared suspension of P. syringae pv. tomato DC3000 (Pto) in sterile distilled water [107 colony-forming units (CFUs) per mL] was drop-inoculated on leaves 7 days after exposure to each C5 amyl alcohol. Sterile distilled water was mock-inoculated as a negative control. Inoculated plants were placed in a dew chamber (100% humidity) under darkness for 1 d at 25°C. Disease severity was measured 5–7 days after pathogen challenge. The disease rate (0–5) of each plant was measured by recording the percentage of total plant leaf surface showing symptoms as follows: 0 = no symptoms, 1 = mild chlorosis at the inoculated site, 2 = chlorosis covering half of the leaf, 3 = chlorosis covering the whole leaf, 4 = severe chlorosis and mild necrosis, and 5 = most severe symptoms with necrosis (Lee et al., 2012). This was designed as a completely randomized experiment with 12 replications and one plant per replication. The entire experiment was repeated three times. For long-term storage, bacterial cultures were maintained at –80°C in King’s B medium containing 20% glycerol.


Gaseous 3-pentanol primes plant immunity against a bacterial speck pathogen, Pseudomonas syringae pv. tomato via salicylic acid and jasmonic acid-dependent signaling pathways in Arabidopsis.

Song GC, Choi HK, Ryu CM - Front Plant Sci (2015)

Effects of gaseous 1-pentanol, 2-pentanol, and 3-pentanol on Arabidopsis systemic resistance. (A,B)Arabidopsis seedlings were planted in an I-plate, which contains two physically separated compartments that share the same headspace. Plants are exposed to volatile 3-pentanol and its isoforms (or sterile distilled water control), which evaporates from solutions in the other compartment. All plants were drop-inoculated with P. syringae pv. tomato DC3000 (Pto) 7 days after exposure to volatiles from 1 nM, 100 nM, 10 μM, and 1 mM 1-pentanol, 2-pentanol, and 3-pentanol. Disease severity (B) was measured 7 days after pathogen inoculation. The asterisk in (B) indicates significant differences (P = 0.05 by LSD) between treatment and control. Error bars represent means ± SEM; N = 12 plants per treatment.
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Related In: Results  -  Collection

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Figure 1: Effects of gaseous 1-pentanol, 2-pentanol, and 3-pentanol on Arabidopsis systemic resistance. (A,B)Arabidopsis seedlings were planted in an I-plate, which contains two physically separated compartments that share the same headspace. Plants are exposed to volatile 3-pentanol and its isoforms (or sterile distilled water control), which evaporates from solutions in the other compartment. All plants were drop-inoculated with P. syringae pv. tomato DC3000 (Pto) 7 days after exposure to volatiles from 1 nM, 100 nM, 10 μM, and 1 mM 1-pentanol, 2-pentanol, and 3-pentanol. Disease severity (B) was measured 7 days after pathogen inoculation. The asterisk in (B) indicates significant differences (P = 0.05 by LSD) between treatment and control. Error bars represent means ± SEM; N = 12 plants per treatment.
Mentions: Plant and bacterial preparations were conducted as described previously (Ryu et al., 2003a, 2004; Lee et al., 2012). Briefly, Arabidopsis thaliana ecotype Columbia (Col-0) seedlings that had been lowed to germinate and grow for at least 2 days were transferred to one compartment of an I-plate (SPL Lifesciences Co., Pocheon, Gyeonggi-do, South Korea) containing 1/2 Murashige and Skoog medium supplemented with 0.6% (w/v) agar and 1.5% (w/v) sucrose. Plants were cultivated in the I-plates in a growth chamber for 14 days at 21°C under a 16 h light/8 h dark cycle before collecting samples for gene expression analysis. Bacterial pathogens were cultured overnight at 30°C in LB medium supplemented with 100 μg/ml rifampicin. Arabidopsis thaliana ecotype Columbia (Col-0) plants were prepared as described previously (Lee et al., 2012). The I-plate system was employed to assess induced resistance mediated by 1-pentanol, 2-pentanol, and 3-pentanol; 30 μl of 1 nM, 100 nM, 10 μM, and 1 mM of each C5 amyl alcohol (or sterile distilled water control) was added to one compartment of an I-plate (the a-compartment in Figure 1A) containing Arabidopsis plants in the other compartment, and the plate was tightly sealed with Parafilm. For the induced resistance assay, 2 μL of freshly prepared suspension of P. syringae pv. tomato DC3000 (Pto) in sterile distilled water [107 colony-forming units (CFUs) per mL] was drop-inoculated on leaves 7 days after exposure to each C5 amyl alcohol. Sterile distilled water was mock-inoculated as a negative control. Inoculated plants were placed in a dew chamber (100% humidity) under darkness for 1 d at 25°C. Disease severity was measured 5–7 days after pathogen challenge. The disease rate (0–5) of each plant was measured by recording the percentage of total plant leaf surface showing symptoms as follows: 0 = no symptoms, 1 = mild chlorosis at the inoculated site, 2 = chlorosis covering half of the leaf, 3 = chlorosis covering the whole leaf, 4 = severe chlorosis and mild necrosis, and 5 = most severe symptoms with necrosis (Lee et al., 2012). This was designed as a completely randomized experiment with 12 replications and one plant per replication. The entire experiment was repeated three times. For long-term storage, bacterial cultures were maintained at –80°C in King’s B medium containing 20% glycerol.

Bottom Line: We performed quantitative real-time PCR to investigate the 3-pentanol-mediated Arabidopsis immune responses by determining Pathogenesis-Related (PR) gene expression levels associated with defense signaling through salicylic acid (SA), jasmonic acid (JA), and ethylene signaling pathways.Selected Arabidopsis mutants confirmed that the 3-pentanol-mediated immune response involved SA and JA signaling pathways and the NPR1 gene.Taken together, this study indicates that gaseous 3-pentanol triggers induced resistance in Arabidopsis by priming SA and JA signaling pathways.

View Article: PubMed Central - PubMed

Affiliation: Molecular Phytobacteriology Laboratory, Korea Research Institute of Bioscience and Biotechnology , Daejeon, South Korea.

ABSTRACT
3-Pentanol is an active organic compound produced by plants and is a component of emitted insect sex pheromones. A previous study reported that drench application of 3-pentanol elicited plant immunity against microbial pathogens and an insect pest in crop plants. Here, we evaluated whether 3-pentanol and the derivatives 1-pentanol and 2-pentanol induced plant systemic resistance using the in vitro I-plate system. Exposure of Arabidopsis seedlings to 10 μM and 100 nM 3-pentanol evaporate elicited an immune response to Pseudomonas syringae pv. tomato DC3000. We performed quantitative real-time PCR to investigate the 3-pentanol-mediated Arabidopsis immune responses by determining Pathogenesis-Related (PR) gene expression levels associated with defense signaling through salicylic acid (SA), jasmonic acid (JA), and ethylene signaling pathways. The results show that exposure to 3-pentanol and subsequent pathogen challenge upregulated PDF1.2 and PR1 expression. Selected Arabidopsis mutants confirmed that the 3-pentanol-mediated immune response involved SA and JA signaling pathways and the NPR1 gene. Taken together, this study indicates that gaseous 3-pentanol triggers induced resistance in Arabidopsis by priming SA and JA signaling pathways. To our knowledge, this is the first report that a volatile compound of an insect sex pheromone triggers plant systemic resistance against a bacterial pathogen.

No MeSH data available.


Related in: MedlinePlus