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The F-box protein MAX2 contributes to resistance to bacterial phytopathogens in Arabidopsis thaliana.

Piisilä M, Keceli MA, Brader G, Jakobson L, Jõesaar I, Sipari N, Kollist H, Palva ET, Kariola T - BMC Plant Biol. (2015)

Bottom Line: Interestingly, max2 mutant plants showed increased susceptibility to the bacterial necrotroph Pectobacterium carotovorum as well as to the hemi-biotroph Pseudomonas syringae but not to the fungal necrotroph Botrytis cinerea. max2 mutant phenotype was associated with constitutively increased stomatal conductance and decreased tolerance to apoplastic ROS but also with alterations in hormonal balance.We conclude that the increased susceptibility to P. syringae and P. carotovorum is due to increased stomatal conductance in max2 mutants promoting pathogen entry into the plant apoplast.Additional factors contributing to pathogen susceptibility in max2 plants include decreased tolerance to pathogen-triggered apoplastic ROS and alterations in hormonal signaling.

View Article: PubMed Central - PubMed

ABSTRACT

Background: The Arabidopsis thaliana F-box protein MORE AXILLARY GROWTH2 (MAX2) has previously been characterized for its role in plant development. MAX2 appears essential for the perception of the newly characterized phytohormone strigolactone, a negative regulator of polar auxin transport in Arabidopsis.

Results: A reverse genetic screen for F-box protein mutants altered in their stress responses identified MAX2 as a component of plant defense. Here we show that MAX2 contributes to plant resistance against pathogenic bacteria. Interestingly, max2 mutant plants showed increased susceptibility to the bacterial necrotroph Pectobacterium carotovorum as well as to the hemi-biotroph Pseudomonas syringae but not to the fungal necrotroph Botrytis cinerea. max2 mutant phenotype was associated with constitutively increased stomatal conductance and decreased tolerance to apoplastic ROS but also with alterations in hormonal balance.

Conclusions: Our results suggest that MAX2 previously characterized for its role in regulation of polar auxin transport in Arabidopsis, and thus plant development also significantly influences plant disease resistance. We conclude that the increased susceptibility to P. syringae and P. carotovorum is due to increased stomatal conductance in max2 mutants promoting pathogen entry into the plant apoplast. Additional factors contributing to pathogen susceptibility in max2 plants include decreased tolerance to pathogen-triggered apoplastic ROS and alterations in hormonal signaling.

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max2plants are highly susceptible to ozone. Soil grown four weeks old wild-type Col-0, max2 point mutation (max2-1), Salk (max2-4) and rcd1-4 (as an ozone sensitive control) lines were exposed to 350 ppb ozone (O3) for 6 h in a controlled O3 chamber. The plants were photographed before and 1 day after O3 exposure in order to show cell death on the leaves. A) Non-treated Col-0, max2-1, max2-4 and rcd1-4 lines grown in clean air. B) O3 phenotype of Col-0, max2-1, max2-4 and rcd1-4 lines 1 day after 6 h O3 exposure. C) Ion leakage in Col-0, max2-1, max2-4 and rcd1-4 lines measured at different time points after O3 exposure indicating the amount of cell death. The result is presented as ratio of ion leakage of total ion concentration. Data represent the means ± SE of 3 independent experiments with 5 plants/line in every time point in each experiment. **P < 0.01; two-tailed t test.
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Fig1: max2plants are highly susceptible to ozone. Soil grown four weeks old wild-type Col-0, max2 point mutation (max2-1), Salk (max2-4) and rcd1-4 (as an ozone sensitive control) lines were exposed to 350 ppb ozone (O3) for 6 h in a controlled O3 chamber. The plants were photographed before and 1 day after O3 exposure in order to show cell death on the leaves. A) Non-treated Col-0, max2-1, max2-4 and rcd1-4 lines grown in clean air. B) O3 phenotype of Col-0, max2-1, max2-4 and rcd1-4 lines 1 day after 6 h O3 exposure. C) Ion leakage in Col-0, max2-1, max2-4 and rcd1-4 lines measured at different time points after O3 exposure indicating the amount of cell death. The result is presented as ratio of ion leakage of total ion concentration. Data represent the means ± SE of 3 independent experiments with 5 plants/line in every time point in each experiment. **P < 0.01; two-tailed t test.

Mentions: After 6 h exposure to 300 ppb of ozone rcd1-4 plants had developed distinct lesions while wild-type plants did not show any signs of damage (Figure 1). Of the tested F-box T-DNA lines, approximately 10 displayed varying degree of lesion formation. The line with the most distinct increase in ozone sensitivity, max2-4 (SALK_028336), harbored a T-DNA insertion in a gene encoding the F-box protein MAX2 (MORE AXILLARY GROWTH2), previously well characterized as a negative regulator of polar auxin transport [29]. Interestingly, in response to ozone, the max2-4 plants developed clearly visible and spreading lesions (Figure 1A and B). Increased ozone sensitivity was observed also for max2-1 point mutation line [28] confirming that the phenotype was indeed a result from mutation in the MAX2 gene (Figure 1A and B). The observed ozone sensitivity was further confirmed by measuring the ion leakage from the max2 mutants and wild-type plants at time points 0, 8 and 24 h after beginning of ozone exposure (Figure 1C). In max2 mutants the ion leakage was clearly higher compared to wild-type plants. These results strongly indicate that MAX2 contributes to ozone tolerance in Arabidopsis.Figure 1


The F-box protein MAX2 contributes to resistance to bacterial phytopathogens in Arabidopsis thaliana.

Piisilä M, Keceli MA, Brader G, Jakobson L, Jõesaar I, Sipari N, Kollist H, Palva ET, Kariola T - BMC Plant Biol. (2015)

max2plants are highly susceptible to ozone. Soil grown four weeks old wild-type Col-0, max2 point mutation (max2-1), Salk (max2-4) and rcd1-4 (as an ozone sensitive control) lines were exposed to 350 ppb ozone (O3) for 6 h in a controlled O3 chamber. The plants were photographed before and 1 day after O3 exposure in order to show cell death on the leaves. A) Non-treated Col-0, max2-1, max2-4 and rcd1-4 lines grown in clean air. B) O3 phenotype of Col-0, max2-1, max2-4 and rcd1-4 lines 1 day after 6 h O3 exposure. C) Ion leakage in Col-0, max2-1, max2-4 and rcd1-4 lines measured at different time points after O3 exposure indicating the amount of cell death. The result is presented as ratio of ion leakage of total ion concentration. Data represent the means ± SE of 3 independent experiments with 5 plants/line in every time point in each experiment. **P < 0.01; two-tailed t test.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
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getmorefigures.php?uid=PMC4340836&req=5

Fig1: max2plants are highly susceptible to ozone. Soil grown four weeks old wild-type Col-0, max2 point mutation (max2-1), Salk (max2-4) and rcd1-4 (as an ozone sensitive control) lines were exposed to 350 ppb ozone (O3) for 6 h in a controlled O3 chamber. The plants were photographed before and 1 day after O3 exposure in order to show cell death on the leaves. A) Non-treated Col-0, max2-1, max2-4 and rcd1-4 lines grown in clean air. B) O3 phenotype of Col-0, max2-1, max2-4 and rcd1-4 lines 1 day after 6 h O3 exposure. C) Ion leakage in Col-0, max2-1, max2-4 and rcd1-4 lines measured at different time points after O3 exposure indicating the amount of cell death. The result is presented as ratio of ion leakage of total ion concentration. Data represent the means ± SE of 3 independent experiments with 5 plants/line in every time point in each experiment. **P < 0.01; two-tailed t test.
Mentions: After 6 h exposure to 300 ppb of ozone rcd1-4 plants had developed distinct lesions while wild-type plants did not show any signs of damage (Figure 1). Of the tested F-box T-DNA lines, approximately 10 displayed varying degree of lesion formation. The line with the most distinct increase in ozone sensitivity, max2-4 (SALK_028336), harbored a T-DNA insertion in a gene encoding the F-box protein MAX2 (MORE AXILLARY GROWTH2), previously well characterized as a negative regulator of polar auxin transport [29]. Interestingly, in response to ozone, the max2-4 plants developed clearly visible and spreading lesions (Figure 1A and B). Increased ozone sensitivity was observed also for max2-1 point mutation line [28] confirming that the phenotype was indeed a result from mutation in the MAX2 gene (Figure 1A and B). The observed ozone sensitivity was further confirmed by measuring the ion leakage from the max2 mutants and wild-type plants at time points 0, 8 and 24 h after beginning of ozone exposure (Figure 1C). In max2 mutants the ion leakage was clearly higher compared to wild-type plants. These results strongly indicate that MAX2 contributes to ozone tolerance in Arabidopsis.Figure 1

Bottom Line: Interestingly, max2 mutant plants showed increased susceptibility to the bacterial necrotroph Pectobacterium carotovorum as well as to the hemi-biotroph Pseudomonas syringae but not to the fungal necrotroph Botrytis cinerea. max2 mutant phenotype was associated with constitutively increased stomatal conductance and decreased tolerance to apoplastic ROS but also with alterations in hormonal balance.We conclude that the increased susceptibility to P. syringae and P. carotovorum is due to increased stomatal conductance in max2 mutants promoting pathogen entry into the plant apoplast.Additional factors contributing to pathogen susceptibility in max2 plants include decreased tolerance to pathogen-triggered apoplastic ROS and alterations in hormonal signaling.

View Article: PubMed Central - PubMed

ABSTRACT

Background: The Arabidopsis thaliana F-box protein MORE AXILLARY GROWTH2 (MAX2) has previously been characterized for its role in plant development. MAX2 appears essential for the perception of the newly characterized phytohormone strigolactone, a negative regulator of polar auxin transport in Arabidopsis.

Results: A reverse genetic screen for F-box protein mutants altered in their stress responses identified MAX2 as a component of plant defense. Here we show that MAX2 contributes to plant resistance against pathogenic bacteria. Interestingly, max2 mutant plants showed increased susceptibility to the bacterial necrotroph Pectobacterium carotovorum as well as to the hemi-biotroph Pseudomonas syringae but not to the fungal necrotroph Botrytis cinerea. max2 mutant phenotype was associated with constitutively increased stomatal conductance and decreased tolerance to apoplastic ROS but also with alterations in hormonal balance.

Conclusions: Our results suggest that MAX2 previously characterized for its role in regulation of polar auxin transport in Arabidopsis, and thus plant development also significantly influences plant disease resistance. We conclude that the increased susceptibility to P. syringae and P. carotovorum is due to increased stomatal conductance in max2 mutants promoting pathogen entry into the plant apoplast. Additional factors contributing to pathogen susceptibility in max2 plants include decreased tolerance to pathogen-triggered apoplastic ROS and alterations in hormonal signaling.

Show MeSH
Related in: MedlinePlus