Cu/ZnSOD involved in tolerance to dehydration in cut rose (Rosa hybrida)

• DDTC, a Cu/ZnSOD activity inhibitor, accelerates the adverse effects of dehydration on flower opening quality.
• Five SOD genes were isolated and their expression was investigated during dehydration and rehydration.
• Transcript abundance of the Cu/ZnSOD genes was elevated when Cu/ZnSOD activity was inhibited with DDTC suggesting negative feedback regulation.

Dehydration results in abnormal flower opening and quality loss during the marketing of cut rose flowers. Our previous studies have revealed that changes in superoxide dismutase (SOD) activity are related to the dehydration tolerance of cut roses. Here, we demonstrate that cut roses were adversely influenced by dehydration conditions, which affected the normal flower opening process, suppressing the increase in flower diameter and shortening vase life. Pretreatment with sodium diethyldithiocarbamate (DDTC), an inhibitor of Cu/ZnSOD activity, accelerated the adverse effects of dehydration on flower opening quality. Compared to flowers placed in water continuously, in dehydrated flowers superoxide anion (SOA) production and SOD activities were enhanced during dehydration and decreased during subsequent rehydration. DDTC pretreatment diminished SOA production and inhibited Cu/ZnSOD activities during both dehydration and subsequent rehydration. Five SOD genes, RhMnSOD1, RhCu/ZnSOD1, RhCu/ZnSOD2, RhCu/ZnSOD3 and RhFeSOD1, were isolated and their expression was analyzed in petals. Dehydration reduced the expression of RhMnSOD1 and RhCu/ZnSOD1/2/3 genes; during rehydration, expression levels recovered. DDTC pretreatment delayed the reduction and recovery of gene expression during dehydration and rehydration, respectively. In conclusion, our results suggest that SOD enzymes, especially Cu/ZnSODs, are involved in the dehydration tolerance of cut rose flowers and that the inhibition of Cu/ZnSOD activities may increase the expression of RhCu/ZnSOD genes in cut rose flower petals via a negative feedback mechanism.