Silicon-moderated K-deficiency-induced leaf chlorosis by decreasing putrescine accumulation in sorghum.

BACKGROUND AND

aimsAlthough silicon (Si) has been widely reported to alleviate plant nutrient deficiency, the alleviating effect of Si on potassium (K) deficiency and its underlying mechanism are poorly understood. Here, we examined whether Si-regulated putrescine (Put) metabolisms are involved in Si-alleviated K deficiency.

methodsSorghum seedlings were grown in K deficiency solution with and without Si for 15 d. The influence of K deficiency and Si on leaf chlorosis symptoms, K(+) concentration, polyamine (PA) levels, amine oxidase activities, the transcription of Put synthesis genes, antioxidant enzyme activities and H2O2 accumulation were measured. KEY

resultsUnder K-sufficient conditions, plant growth was not affected by Si application. Si application significantly alleviated the growth inhibition induced by K-deficient stress, however. K deficiency induced leaf chlorosis and reduction in several leaf chlorosis-related metrics, including photosynthesis, efficiency of photosystem II photochemistry, chlorophyll content and chlorophyll a/b ratio; all of these changes were moderated by Si application. Si application did not influence the K(+) concentration in leaves under K-sufficient or K-deficient conditions. It did, however, decrease the excessive accumulation of Put that was otherwise induced by K deficiency. Simultaneously, Put synthesis gene transcription and activation of amine oxidases were down-regulated by Si application under K-deficient conditions. In addition, Si reduced K-deficiency-enhanced antioxidant enzyme activities and decreased K-deficiency-induced H2O2 accumulation.

conclusionsThese results indicate that Si application could reduce K-deficiency-induced Put accumulation by inhibiting Put synthesis and could decrease H2O2 production via PA oxidation. Decreased H2O2 accumulation contributes to the alleviation of cell death, thereby also alleviating K-deficiency-induced leaf chlorosis and necrosis.