Abstract
BackgroundPhoma 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.ResultsAn 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.ConclusionThis 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.
Highlights
Phoma macdonaldii has been reported as the causal agent of black stem disease (BS) and premature ripening (PR) on sunflower
In 2009, the resistance level to PR of 42 genotypes was evaluated in a field trial in Auzeville-Tolosane: 40 lines were selected from the Helianthus annuus core collection of 48 lines [16] and two additional lines were included due to their high level of resistance in 2007 preliminary observations: (Tub-1709-1)-1-6A is derived by selfing from the USDA accession TUB-1709-1 which results from an introgression of H. tuberosus [17], and 97B7 is an INRA line derived from a cross involving H. argophyllus
Disease development in the four experiments BS and PR development data were obtained on 1086 plants for 20 lines of the core collection in 2010, 2919 plants in the recombinant inbred lines (RIL) population XRQxPSC8 and 3153 plants in the RIL population FUxPAZ2
Summary
Phoma macdonaldii has been reported as the causal agent of black stem disease (BS) and premature ripening (PR) on sunflower. Candidate genes could be identified through transcriptomic studies of the sunflower * P. macdonaldii interaction (e.g. sunflower-likelipase, MYB-related transcription factor regulating PAL2, a key enzyme involved in the phenylpropanoid pathway) [13] In these studies, the pathosystem was developed on two-leaf-stage plantlets that is not fully representative of natural attacks. We showed that artificial inoculation at the stem base with pycniospores or mycelium of P. macdonaldii could be used for screening genotypes showing a substantial level of resistance to PR Using this phenotyping protocol in field, we investigated in this study the phenotypical variability and the genetic architecture of premature ripening and black stem resistance along plant development in Helianthus
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