Abstract

AimsThis study aims the detection of proteins associated with increased resistance of tubers to necrotrophic bacteria Dickeya solani in tetraploid and diploid potato plants.MethodsComparative analysis of differently expressed proteins in tuber tissue of potato cultivars and diploid interspecific hybrids of Solanum, differing in resistance to Dickeya solani, was performed using nano-liquid chromatography coupled with tandem mass spectrometry (LC-MS-MS/MS). Two highly resistant (Bea and Humalda) and three susceptible (Irys, Katahdin, Ulster Supreme) potato cultivars, and the highly resistant (DG 00–270) and the susceptible (DG 08–305) diploid clones, were studied. Proteins were extracted from wounded potato tubers inoculated with bacteria at an early symptomatic phase of infection and from controls, i.e., intact tubers and wounded mock-inoculated tubers. Data are available via ProteomeXchange with identifier PXD013009.ResultsEight constitutive differentially expressed proteins with fold changes ≥1.9 and q-value ≤0.1 between the resistant and susceptible cultivar groups after D. solani infection were selected. Probable inactive patatin-03-Kuras 1 and the proteinase inhibitor PTI exhibited significantly increased protein abundances after bacterial inoculation in both resistant cultivars compared to the susceptible cultivars. In the diploid clones, only metallocarboxypeptidase and metallocarboxypeptidase-like inhibitors exhibited much higher fold changes following pathogenic invasion (274.4- and 368.6-fold, respectively) than after mock inoculation (165.5- and 130.7-fold, respectively).ConclusionsThese results show that different proteins indicating significant fold changes between the resistant and susceptible potato cultivars and diploid clones are induced at an early phase of symptomatic D. solani infection.

Highlights

  • Among the several soft rot enterobacterial necrotrophic pathogens of the two genera Pectobacterium and Dickeya, which cause blackleg in potato plants and soft rot of potato tubers, Dickeya solani has received the most attention due to highly aggressive infection caused by this pathogen in potato plants and the ability of this species to initiate disease occurrence at low inoculum levels (Czajkowski et al 2009; Toth et al 2011)

  • Only metallocarboxypeptidase and metallocarboxypeptidase-like inhibitors exhibited much higher fold changes following pathogenic invasion (274.4- and 368.6-fold, respectively) than after mock inoculation (165.5- and 130.7-fold, respectively). These results show that different proteins indicating significant fold changes between the resistant and susceptible potato cultivars and diploid clones are induced at an early phase of symptomatic D. solani infection

  • Mapping studies in a diploid population originating from hybrids of Solanum chacoense and Solanum yungasense have shown the complexity of the inheritance of resistance to Pectobacterium atrosepticum (Zimnoch-Guzowska et al 2000)

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Summary

Introduction

Among the several soft rot enterobacterial necrotrophic pathogens of the two genera Pectobacterium and Dickeya, which cause blackleg in potato plants and soft rot of potato tubers, Dickeya solani has received the most attention due to highly aggressive infection caused by this pathogen in potato plants and the ability of this species to initiate disease occurrence at low inoculum levels (Czajkowski et al 2009; Toth et al 2011). Potato tubers can be infected by bacteria through wounds, natural openings (stomata, lenticels), or stolons. Seed tubers infected with bacteria are the main sources of inocula. Bacteria can move throughout the plant via the water-conducting tissues and can infect growing plants and progeny tubers through stolons. Infected seed tubers may rot in the soil and reinfect growing potato plants (through roots) and progeny tubers (directly through wounds and lenticels or through stolons). Potato tubers can be contaminated with pectinolytic bacteria and infected through wounds during harvest, transport and grading. Elphinstone and Perombelon (1986) stated that a single rotting tuber contaminated c. Tuber infection occurs in two phases: an asymptomatic phase, in which bacteria do not express genes encoding plant cell walldegrading enzymes (Toth and Birch 2005), and a late

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