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. 2017 Oct 19;17(1):167.
doi: 10.1186/s12870-017-1116-1.

Different genetic architectures underlie crop responses to the same pathogen: the {Helianthus annuus * Phoma macdonaldii} interaction case for black stem disease and premature ripening

Amandine Bordat  1   2 , Gwenaëlle Marchand  1   3 , Nicolas B Langlade  1 , Nicolas Pouilly  1 , Stéphane Muños  1 , Grégory Dechamp-Guillaume  4   5 , Patrick Vincourt  1 , Emmanuelle Bret-Mestries  6
Affiliations

Different genetic architectures underlie crop responses to the same pathogen: the {Helianthus annuus * Phoma macdonaldii} interaction case for black stem disease and premature ripening

Amandine Bordat et al. BMC Plant Biol. .

Abstract

Background: Phoma macdonaldii has been reported as the causal agent of black stem disease (BS) and premature ripening (PR) on sunflower. PR is considered as the most widespread and detrimental disease on sunflower in France. While genetic variability and QTL mapping for partial resistance of sunflower to stem, collar and roots attacks have been reported on plantlets in controlled conditions, this work aims to describe the genetic variability in a subset of a sunflower lines, and for the first time to map QTL involved in PR resistance evaluated in field conditions using controlled inoculation.

Results: An efficient and reliable method for inoculation used in field experiments induced stem base necrosis on up to 98% of all plants. A significant genetic variability for PR resistance in the field was detected among the 20 inbred lines of the core collection tested across the two years. For QTL mapping, the PR resistance evaluation was performed on two recombinant inbred lines (RIL) populations derived from the crosses XRQxPSC8 and FUxPAZ2 in two different years. QTL analyses were based on a newly developed consensus genetic map comprising 1007 non-redundant molecular markers. In each of the two RIL populations, different QTL involved in PR partial sunflower resistance were detected. The most significant QTL were detected 49 days post infection (DPI) on LG10 (LOD 7.7) and on LG7 (LOD 12.1) in the XRQxPSC8 and FUxPAZ2 RIL population, respectively. In addition, different QTL were detected on both populations for PR resistance measured between 14 and 35 DPI. In parallel, the incidence of natural attack of P. macdonaldii resulting in BS disease was recorded, showing that in these populations, the genetic of resistance to both diseases is not governed by the same factors.

Conclusion: This work provides the first insights on the genetic architecture of sunflower PR resistance in the field. Moreover, the separate studies of symptoms on different organs and in time series allowed the identification of a succession of genetic components involved in the sunflower resistance to PR and BS diseases caused by Phoma macdonaldii along the development of the {plant * pathogen} interaction.

Keywords: Black stem; Phoma macdonaldii; Premature ripening; QTL mapping; Sunflower.

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Conflict of interest statement

Ethics approval and consent to participate

Sunflower plant material used in this study was grown from seeds made available by INRA as parts of INRA sunflower genetic resources. The two RIL populations were created by INRA from sunflower parental inbred lines created by INRA. Most of the lines belonging to the INRA core collection (Table 1) were also created by INRA from cultivated or wild, publicly available sources. The lines SF085 (CD) and Tub-1709-1-1-6A (TUB) were obtained by selfing from USDA sources.

All field experiments were conducted in accordance with local legislation and did not involve endangered or protected species.

Consent for publication

Not applicable.

Competing interests

The authors declare that they have no competing interests.

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Figures

Fig. 1
Fig. 1
Correspondence between the scoring of Phoma macdonaldii PR disease and the symptoms observed on sunflower (a: score 0; b: score 1; c: score 2; d: score 3; e: score 4)
Fig. 2
Fig. 2
Phenotypic variability of the symptoms of Phoma macdonaldii at the stem base observed on the sunflower core-collection trial in 2010 (a: SF061; b: SF057; c: SF334; d: SF110)
Fig. 3
Fig. 3
Evolution of the Phoma macdonaldii PR plants percentage (disease score ≥ 3) for a subset of the 20 sunflower inbred lines of the core-collection trial (2010) between the end of flowering (F4) and the complete maturity (M4) developmental stages
Fig. 4
Fig. 4
Variability of AUDPC for premature ripening observed on the 20 core-collection lines screened in 2010. The size of the errors bars equals to one standard deviation
Fig. 5
Fig. 5
Evolution of the Phoma macdonaldii BS disease (score 2 = percentage of plants with coalescent spots on the stem) for a subset of the 20 sunflower inbred lines of the core-collection trial (2010)
Fig. 6
Fig. 6
Frequency distributions of mean disease score for PR resistance in the XRQxPSC8 (a) at 49DPI and FUxPAZ2 (b) at 42 DPI RIL populations. Phenotypic values of parental lines are indicated
Fig. 7
Fig. 7
Mapping of QTL detected for all the traits in the “INEDI” RIL population. Premature Ripening Traits (Pm_PR_dpiN for Phoma macdonaldii PR score N days post inoculation, AUDPC_PR), Black Stem Disease Traits (Pm_BS_dpiN for P.macdonaldii BS score N days post inoculation), Alternaria for susceptibility score to Alternaria helianthi
Fig. 8
Fig. 8
Mapping of QTL detected for all the traits in the FU x PAZ2 RIL population. Premature Ripening Traits (Pm_PR_dpiN for Phoma macdonaldii PR score N days post inoculation, AUDPC_PR), Black Stem Disease Traits (Pm_BS_dpiN for P.macdonaldii BS score N days post inoculation, AUDPC_BS) and, according to Additional file 4: Developmental traits (F1, M0, M3), morphological traits (Nb_leaves, Leaf_Rk for the rank of the biggest leaf, Leaf_Length, Leaf_width, Height, Collar_diam for base stem diameter), Yield per se
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References

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