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Camalexin contributes to the partial resistance of Arabidopsis thaliana to the biotrophic soilborne protist Plasmodiophora brassicae.

Lemarié S, Robert-Seilaniantz A, Lariagon C, Lemoine J, Marnet N, Levrel A, Jubault M, Manzanares-Dauleux MJ, Gravot A - Front Plant Sci (2015)

Bottom Line: This induction correlated with slower P. brassicae growth in Bur-0 compared to Col-0, thus suggesting a relationship between the levels of camalexin biosynthesis and the different levels of resistance.The Bur/Col allelic substitution in the region of the previously identified clubroot resistance QTL PbAt5.2 (Chromosome 5) was associated with both the enhanced clubroot-triggered induction of camalexin biosynthesis and the reduced P. brassicae development.Altogether, our results suggest that high levels of clubroot-triggered camalexin biosynthesis play a role in the quantitative control of partial resistance of Arabidopsis to clubroot.

View Article: PubMed Central - PubMed

Affiliation: UMR1349 IGEPP, INRA Le Rheu, France.

ABSTRACT
Camalexin has been reported to play defensive functions against several pathogens in Arabidopsis. In this study, we investigated the possible role of camalexin accumulation in two Arabidopsis genotypes with different levels of basal resistance to the compatible eH strain of the clubroot agent Plasmodiophora brassicae. Camalexin biosynthesis was induced in infected roots of both Col-0 (susceptible) and Bur-0 (partially resistant) accessions during the secondary phase of infection. However, the level of accumulation was four-to-seven times higher in Bur-0 than Col-0. This was associated with the enhanced transcription of a set of camalexin biosynthetic P450 genes in Bur-0: CYP71A13, CYP71A12, and CYP79B2. This induction correlated with slower P. brassicae growth in Bur-0 compared to Col-0, thus suggesting a relationship between the levels of camalexin biosynthesis and the different levels of resistance. Clubroot-triggered biosynthesis of camalexin may also participate in basal defense in Col-0, as gall symptoms and pathogen development were enhanced in the pad3 mutant (Col-0 genetic background), which is defective in camalexin biosynthesis. Clubroot and camalexin responses were then studied in Heterogeneous Inbred Families (HIF) lines derived from a cross between Bur-0 and Col-0. The Bur/Col allelic substitution in the region of the previously identified clubroot resistance QTL PbAt5.2 (Chromosome 5) was associated with both the enhanced clubroot-triggered induction of camalexin biosynthesis and the reduced P. brassicae development. Altogether, our results suggest that high levels of clubroot-triggered camalexin biosynthesis play a role in the quantitative control of partial resistance of Arabidopsis to clubroot.

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(A,B) Clubroot symptoms and (C), quantification of Plasmodiophora brassicae DNA in infected roots of the partially resistant accession Bur-0 and the susceptible accession Col-0. (A) Clubroot symptoms were evaluated using the GA/LA disease index calculated by image analysis at 17 and 21 dpi. GA/LA was calculated from gall area (GA in cm2) divided by an estimation of the rosette extent (LA in cm2). Error bars represent standard error (Four biological replicate, 18 plants analyzed per biological replicate). Asterisks indicate statistically significant differences according to the (P < 0.05) (B) Illustration of clubroot symptoms. The scale bar indicates 1 cm. (C) Pathogen DNA quantification (Pb) by qPCR, expressed as a ratio relative to the expression level of the plant Fbox gene at 10, 14, and 17 dpi (Three biological replicates, 12–54 plants per biological replicate). Asterisks indicate statistically significant differences according to the Wald tests applied on a linear mixed model (P < 0.05).
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Figure 5: (A,B) Clubroot symptoms and (C), quantification of Plasmodiophora brassicae DNA in infected roots of the partially resistant accession Bur-0 and the susceptible accession Col-0. (A) Clubroot symptoms were evaluated using the GA/LA disease index calculated by image analysis at 17 and 21 dpi. GA/LA was calculated from gall area (GA in cm2) divided by an estimation of the rosette extent (LA in cm2). Error bars represent standard error (Four biological replicate, 18 plants analyzed per biological replicate). Asterisks indicate statistically significant differences according to the (P < 0.05) (B) Illustration of clubroot symptoms. The scale bar indicates 1 cm. (C) Pathogen DNA quantification (Pb) by qPCR, expressed as a ratio relative to the expression level of the plant Fbox gene at 10, 14, and 17 dpi (Three biological replicates, 12–54 plants per biological replicate). Asterisks indicate statistically significant differences according to the Wald tests applied on a linear mixed model (P < 0.05).

Mentions: We then compared symptom development and pathogen growth with the time-course of camalexin accumulation in both genotypes. Disease symptoms were quantified at 17 and 21 dpi and showed a two-fold increase in the severity of clubroot symptoms in Col-0 compared to Bur-0 at both time points (Figures 5A,B). The ratio between pathogen and plant DNA content was determined in infected Col-0 and Bur-0 roots. At 10 dpi, no significant difference in relative pathogen DNA content between the two genotypes was observed (P = 0.134). At 14 and 17 dpi, the relative pathogen DNA content increased in both genotypes, but to a higher degree in Col-0 than in Bur-0. Thus, pathogen DNA content was two-times higher in Col-0 than in Bur-0 infected roots at 14 and 17 dpi (Figure 5C).


Camalexin contributes to the partial resistance of Arabidopsis thaliana to the biotrophic soilborne protist Plasmodiophora brassicae.

Lemarié S, Robert-Seilaniantz A, Lariagon C, Lemoine J, Marnet N, Levrel A, Jubault M, Manzanares-Dauleux MJ, Gravot A - Front Plant Sci (2015)

(A,B) Clubroot symptoms and (C), quantification of Plasmodiophora brassicae DNA in infected roots of the partially resistant accession Bur-0 and the susceptible accession Col-0. (A) Clubroot symptoms were evaluated using the GA/LA disease index calculated by image analysis at 17 and 21 dpi. GA/LA was calculated from gall area (GA in cm2) divided by an estimation of the rosette extent (LA in cm2). Error bars represent standard error (Four biological replicate, 18 plants analyzed per biological replicate). Asterisks indicate statistically significant differences according to the (P < 0.05) (B) Illustration of clubroot symptoms. The scale bar indicates 1 cm. (C) Pathogen DNA quantification (Pb) by qPCR, expressed as a ratio relative to the expression level of the plant Fbox gene at 10, 14, and 17 dpi (Three biological replicates, 12–54 plants per biological replicate). Asterisks indicate statistically significant differences according to the Wald tests applied on a linear mixed model (P < 0.05).
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Figure 5: (A,B) Clubroot symptoms and (C), quantification of Plasmodiophora brassicae DNA in infected roots of the partially resistant accession Bur-0 and the susceptible accession Col-0. (A) Clubroot symptoms were evaluated using the GA/LA disease index calculated by image analysis at 17 and 21 dpi. GA/LA was calculated from gall area (GA in cm2) divided by an estimation of the rosette extent (LA in cm2). Error bars represent standard error (Four biological replicate, 18 plants analyzed per biological replicate). Asterisks indicate statistically significant differences according to the (P < 0.05) (B) Illustration of clubroot symptoms. The scale bar indicates 1 cm. (C) Pathogen DNA quantification (Pb) by qPCR, expressed as a ratio relative to the expression level of the plant Fbox gene at 10, 14, and 17 dpi (Three biological replicates, 12–54 plants per biological replicate). Asterisks indicate statistically significant differences according to the Wald tests applied on a linear mixed model (P < 0.05).
Mentions: We then compared symptom development and pathogen growth with the time-course of camalexin accumulation in both genotypes. Disease symptoms were quantified at 17 and 21 dpi and showed a two-fold increase in the severity of clubroot symptoms in Col-0 compared to Bur-0 at both time points (Figures 5A,B). The ratio between pathogen and plant DNA content was determined in infected Col-0 and Bur-0 roots. At 10 dpi, no significant difference in relative pathogen DNA content between the two genotypes was observed (P = 0.134). At 14 and 17 dpi, the relative pathogen DNA content increased in both genotypes, but to a higher degree in Col-0 than in Bur-0. Thus, pathogen DNA content was two-times higher in Col-0 than in Bur-0 infected roots at 14 and 17 dpi (Figure 5C).

Bottom Line: This induction correlated with slower P. brassicae growth in Bur-0 compared to Col-0, thus suggesting a relationship between the levels of camalexin biosynthesis and the different levels of resistance.The Bur/Col allelic substitution in the region of the previously identified clubroot resistance QTL PbAt5.2 (Chromosome 5) was associated with both the enhanced clubroot-triggered induction of camalexin biosynthesis and the reduced P. brassicae development.Altogether, our results suggest that high levels of clubroot-triggered camalexin biosynthesis play a role in the quantitative control of partial resistance of Arabidopsis to clubroot.

View Article: PubMed Central - PubMed

Affiliation: UMR1349 IGEPP, INRA Le Rheu, France.

ABSTRACT
Camalexin has been reported to play defensive functions against several pathogens in Arabidopsis. In this study, we investigated the possible role of camalexin accumulation in two Arabidopsis genotypes with different levels of basal resistance to the compatible eH strain of the clubroot agent Plasmodiophora brassicae. Camalexin biosynthesis was induced in infected roots of both Col-0 (susceptible) and Bur-0 (partially resistant) accessions during the secondary phase of infection. However, the level of accumulation was four-to-seven times higher in Bur-0 than Col-0. This was associated with the enhanced transcription of a set of camalexin biosynthetic P450 genes in Bur-0: CYP71A13, CYP71A12, and CYP79B2. This induction correlated with slower P. brassicae growth in Bur-0 compared to Col-0, thus suggesting a relationship between the levels of camalexin biosynthesis and the different levels of resistance. Clubroot-triggered biosynthesis of camalexin may also participate in basal defense in Col-0, as gall symptoms and pathogen development were enhanced in the pad3 mutant (Col-0 genetic background), which is defective in camalexin biosynthesis. Clubroot and camalexin responses were then studied in Heterogeneous Inbred Families (HIF) lines derived from a cross between Bur-0 and Col-0. The Bur/Col allelic substitution in the region of the previously identified clubroot resistance QTL PbAt5.2 (Chromosome 5) was associated with both the enhanced clubroot-triggered induction of camalexin biosynthesis and the reduced P. brassicae development. Altogether, our results suggest that high levels of clubroot-triggered camalexin biosynthesis play a role in the quantitative control of partial resistance of Arabidopsis to clubroot.

No MeSH data available.


Related in: MedlinePlus