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

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.

A cDNA microarray approach to decipher sunflower (Helianthus annuus) responses to the necrotrophic fungus Phoma macdonaldii.

To identify the genes involved in the partial resistance of sunflower (Helianthus annuus) to the necrotrophic fungus Phoma macdonaldii, we developed a 1000-element cDNA microarray containing carefully chosen genes putatively involved in primary metabolic pathways, signal transduction and biotic stress responses. A two-pass general linear model was used to normalize the data and then to detect differentially expressed genes. This method allowed us to identify 38 genes differentially expressed among genotypes, treatments and times, mainly belonging to plant defense, signaling pathways and amino acid metabolism. Based on a set of genes whose differential expression was highly significant, we propose a model in which negative regulation of a dual-specificity MAPK phosphatase could be implicated in sunflower defense mechanisms against the pathogen. The resulting activation of the MAP kinase cascade could subsequently trigger defense responses (e.g. thaumatin biosynthesis and phenylalanine ammonia lyase activation), under the control of transcription factors belonging to MYB and WRKY families. Concurrently, the activation of protein phosphatase 2A (PP2A), which is implicated in cell death inhibition, could limit pathogen development. The results reported here provide a valuable first step towards the understanding and analysis of the P. macdonaldii-sunflower interaction.