Increased ferritin and iron accumulation in tubers of thaxtomin A-habituated potato var. Yukon Gold somaclones with enhanced resistance to common scab

The principal causal agent of potato common scab is Streptomyces scabiei. This pathogen induces the formation of scabby lesions on the tuber surface, decreasing their value and marketability. The best approach to reduce disease incidence and severity is to cultivate resistant potato varieties. However, potato breeding for varietal resistance to common scab has faced several challenges. The main pathogenicity factor of S. scabiei is thaxtomin A (TA). Two somaclones, YG8 and YG32, were regenerated from TA-habituated potato var. Yukon Gold calli and infected with S. scabiei in controlled conditions. Severity of common scab and lesion depth were significantly decreased in both somaclones compared to the original variety, indicating increased resistance to the disease. Proteomic analysis comparing YG8 and YG32 tuber proteomes with that of Yukon Gold tubers showed changes in the abundance of proteins involved in various processes, including response to oxidative stress and iron homeostasis. The abundance of the iron storage protein ferritin was considerably enhanced in YG8 and YG32 tubers, correlating with increased iron accumulation in tubers. Ferritin gene expression was induced in response to S. scabiei in YG32 minitubers but not in YGP tubers, suggesting the reprogramming of ferritin gene expression in TA-habituated somaclone minitubers. Treatment of S. scabiei-infected YG32 minitubers with the iron chelator deferoxamine restored their susceptibility to the disease. These results suggest that changes in the regulation of iron homeostasis are involved in increasing resistance to common scab in the Yukon Gold TA-habituated somaclones.