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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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MAX2 controls the basal level of stomatal conductance. Effects of 3 h 350 nmol/mol O3 exposure on stomatal conductance were measured on wild-type Col-0 and max2 mutants with a custom made whole-rosette gas exchange measurement device. A) Stomatal conductance before, during and after 3 h O3 exposure of Col-0 and max2 plants. B) CO2 uptake rate of max2 mutants and Col-0 before, during and after 3 h O3 exposure. C) Cumulative dose of O3 absorbed by max2 and Col-0 plants before, during and after 3 h O3 exposure. D) Stomatal O3 uptake rate of max2 mutants and Col-0. For each line 4 plants were used in the experiment and the results are shown as means ± SE. Experiments were repeated twice with similar results.
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Fig4: MAX2 controls the basal level of stomatal conductance. Effects of 3 h 350 nmol/mol O3 exposure on stomatal conductance were measured on wild-type Col-0 and max2 mutants with a custom made whole-rosette gas exchange measurement device. A) Stomatal conductance before, during and after 3 h O3 exposure of Col-0 and max2 plants. B) CO2 uptake rate of max2 mutants and Col-0 before, during and after 3 h O3 exposure. C) Cumulative dose of O3 absorbed by max2 and Col-0 plants before, during and after 3 h O3 exposure. D) Stomatal O3 uptake rate of max2 mutants and Col-0. For each line 4 plants were used in the experiment and the results are shown as means ± SE. Experiments were repeated twice with similar results.

Mentions: The enhanced stomatal conductance of max2 mutants was verified by measuring stomatal conductance of non-treated and ozone exposed max2 plants with a custom made gas-exchange device [50]. In agreement with the porometer measurement, the basal level of stomatal conductance before the ozone exposure was two times higher in the max2 mutant lines than that observed in wild-type plants (Figure 4A). However, the application of O3 (in time point 0 min) induced rapid stomatal closure in both max2 mutant and wild-type plants. Interestingly, a slight recovery of stomatal conductance was observed after the closure in wild-type plants, but not in max2 plants (Figure 4A). This could be explained by the rapid, O3-triggered induction of cell death in max2 mutants, further supported by the quick decrease of general photosynthesis (CO2 uptake, μmol/m2s) in these plants (Figure 4B). While the ozone-induced stomatal closure of max2 plants was as rapid as that detected in wild-type plants (Figure 4A), the intake of ozone still remained higher (Figure 4C) due to the higher stomatal conductance at the beginning of the ozone exposure. Stomatal O3 uptake rate of max2 mutants was higher compared to Col-0 (Figure 4D) probably due to more open stomata.Figure 4


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)

MAX2 controls the basal level of stomatal conductance. Effects of 3 h 350 nmol/mol O3 exposure on stomatal conductance were measured on wild-type Col-0 and max2 mutants with a custom made whole-rosette gas exchange measurement device. A) Stomatal conductance before, during and after 3 h O3 exposure of Col-0 and max2 plants. B) CO2 uptake rate of max2 mutants and Col-0 before, during and after 3 h O3 exposure. C) Cumulative dose of O3 absorbed by max2 and Col-0 plants before, during and after 3 h O3 exposure. D) Stomatal O3 uptake rate of max2 mutants and Col-0. For each line 4 plants were used in the experiment and the results are shown as means ± SE. Experiments were repeated twice with similar results.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Fig4: MAX2 controls the basal level of stomatal conductance. Effects of 3 h 350 nmol/mol O3 exposure on stomatal conductance were measured on wild-type Col-0 and max2 mutants with a custom made whole-rosette gas exchange measurement device. A) Stomatal conductance before, during and after 3 h O3 exposure of Col-0 and max2 plants. B) CO2 uptake rate of max2 mutants and Col-0 before, during and after 3 h O3 exposure. C) Cumulative dose of O3 absorbed by max2 and Col-0 plants before, during and after 3 h O3 exposure. D) Stomatal O3 uptake rate of max2 mutants and Col-0. For each line 4 plants were used in the experiment and the results are shown as means ± SE. Experiments were repeated twice with similar results.
Mentions: The enhanced stomatal conductance of max2 mutants was verified by measuring stomatal conductance of non-treated and ozone exposed max2 plants with a custom made gas-exchange device [50]. In agreement with the porometer measurement, the basal level of stomatal conductance before the ozone exposure was two times higher in the max2 mutant lines than that observed in wild-type plants (Figure 4A). However, the application of O3 (in time point 0 min) induced rapid stomatal closure in both max2 mutant and wild-type plants. Interestingly, a slight recovery of stomatal conductance was observed after the closure in wild-type plants, but not in max2 plants (Figure 4A). This could be explained by the rapid, O3-triggered induction of cell death in max2 mutants, further supported by the quick decrease of general photosynthesis (CO2 uptake, μmol/m2s) in these plants (Figure 4B). While the ozone-induced stomatal closure of max2 plants was as rapid as that detected in wild-type plants (Figure 4A), the intake of ozone still remained higher (Figure 4C) due to the higher stomatal conductance at the beginning of the ozone exposure. Stomatal O3 uptake rate of max2 mutants was higher compared to Col-0 (Figure 4D) probably due to more open stomata.Figure 4

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