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Δευτέρα 6 Μαρτίου 2017

Key metabolic traits of Pisum sativum maintain cell vitality during Didymella pinodes infection: cultivar resistance and the microsymbionts' influence

Publication date: Available online 6 March 2017
Source:Journal of Proteomics
Author(s): Reinhard Turetschek, Getinet Desalegn, Tamara Epple, Hans-Peter Kaul, Stefanie Wienkoop
Ascochyta blight causes severe losses in field pea production and the search for resistance traits towards the causal agent Didymella pinodes is of particular importance for farmers. Various microsymbionts were reported to shape the plants' immune response. However, regardless their contribution to resistance, they are hardly included in experimental designs. Here, we first delineate the bi-directional effect of the symbionts' (rhizobia, mycorrhiza) and the leaf proteome/metabolome of two field pea cultivars with varying resistance levels towards D. pinodes. The pathogen infection showed higher influence on the interaction with the microsymbionts in the susceptible cultivar which was reflected in decreased nodule weight and root mycorrhiza colonisation. Vice versa, symbionts induced variation in the pathogen infection response, which, however, appeared to be overruled by the genotypic characteristics such as maintenance of photosynthesis and provision of sugars and carbon back bones to fuel secondary metabolism. An active sulphur metabolism, functionality of the glutathione-ascorbate hub and fine adjustment of hormone synthesis to suppress induced cell death appeared to support resistance. Thus, we conclude that sustainment of cell vitality through these complex metabolic traits is substantial for a more efficient infection response of the tolerant cultivar.SignificanceThe infection response of two Pisum sativum cultivars with varying resistance levels towards Didymella pinodes was analysed most comprehensively at a proteomic and metabolomic level. Enhanced tolerance was linked to newly discovered cultivar specific metabolic traits such as hormone synthesis and presumably suppression of cell death.

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