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. 2022 Apr 29;27(9):2833.
doi: 10.3390/molecules27092833.

Abscisic Acid-Defensive Player in Flax Response to Fusarium culmorum Infection

Aleksandra Boba  1 , Kamil Kostyn  2 , Yelyzaveta Kochneva  1 , Wioleta Wojtasik  1 , Justyna Mierziak  1 , Anna Prescha  3 , Beata Augustyniak  1 , Magdalena Grajzer  3 , Jan Szopa  1 , Anna Kulma  1
Affiliations

Abscisic Acid-Defensive Player in Flax Response to Fusarium culmorum Infection

Aleksandra Boba et al. Molecules. .

Abstract

Fusarium culmorum is a ubiquitous soil pathogen with a wide host range. In flax (Linum ussitatissimum), it causes foot and root rot and accumulation of mycotoxins in flax products. Fungal infections lead to huge losses in the flax industry. Moreover, due to mycotoxin accumulation, flax products constitute a potential threat to the consumers. We discovered that the defense against this pathogen in flax is based on early oxidative burst among others. In flax plants infected with F. culmorum, the most affected genes are connected with ROS production and processing, callose synthesis and ABA production. We hypothesize that ABA triggers defense mechanism in flax and is a significant player in a successful response to infection.

Keywords: Fusarium culmorum; abscisic acid; flax; infection; terpenoids.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Amounts of H2O2 measured in 14 days old flax seedlings infected with F. culmorum at 6 hpi, 12 hpi, 24 hpi, 36 hpi and 48 hpi. C—untreated control, Fc—Fusarium culmorum treated. Results are presented as means of three biological repeats ± sd.
Figure 2
Figure 2
Transcript levels of genes involved in ROS production and processing (RboHD—NADPH oxidase D, RboHF—NADPH oxidase F, APx—ascorbate peroxidase, CAT—catalase, SOD—superoxide dismutase) in flax seedlings treated with F. culmorum measured at five time-points after the infection. Results (means of three biological repeats ± sd) are presented as fold of the control (equal to 1). Statistically significant changes are marked with asterisks.
Figure 3
Figure 3
Heatmap of terpenoid pathway key gene expression in flax after F. culmorum infection (x—fold of the control). (A)—terpenoid backbone synthesis genes; (B)—phytosterol synthesis genes; (C)—tocopherol synthesis genes; (D)—carotenoid synthesis genes; (E)—apocarotenoid and ABA synthesis genes. Detailed results on the expression can be found in Supplementary File S3.
Figure 4
Figure 4
Heatmap of terpenoid metabolites in flax after F. culmorum infection (x–fold of the control). (A)—phytosterols; (B)—carotenoids; (C)—ABA. Detailed results on the expression can be found in Supplementary File S4.
Figure 5
Figure 5
Transcript levels of callose synthase genes (CALS1, CALS2, CALS3, CALS4) in flax seedlings treated with F. culmorum measured at five timepoints after the infection. Results are presented as a fold of the control (means of three biological repeats ± sd). Statistically significant changes are marked with asterisks.
Figure 6
Figure 6
Amounts of callose measured in 14 days old flax seedlings infected with F. culmorum at 6 hpi, 12 hpi, 24 hpi, 36 hpi and 48 hpi. C—untreated control, Fc—Fusarium culmorum treated. Results are presented as means of three biological repeats ± sd. Statistically significant changes are marked with asterisks.
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References

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