Iron deficiency specifically activated anthocyanin accumulation in out pericarp of red-fleshed kiwifruit (Actinidia chinensis)

The typical feature of red-fleshed Actinidia chinensis is the radical redness of the locules in the inner pericarp. However, in commercial orchards, we observed that kiwifruit on vines exhibiting leaf chlorosis symptoms also showed an extension of reddish flesh to the outer pericarp. The mechanisms linking anthocyanin accumulation in the outer pericarp of kiwifruit with leaf chlorosis remain poorly understood. Through establishment of the field and callus treatment experiments under iron deficiency, we analyzed element contents, fruit quality and differentially expressed genes, and confirmed that iron deficiency contributes to both the anthocyanin accumulation in the outer pericarp and the chlorosis symptoms in the leaves and fruit. Additionally, we found that genes involved in anthocyanin biosynthesis, as well as MYB75 , were significantly activated, with MYB75 playing a key role in activating many of these genes. Two DELLA proteins of GA pathway were significantly induced, while LBD37like, a repressor of anthocyanin pathway, was inhibited by iron deficiency. A lot of iron transporters and storage proteins related to iron deficiency responses were identified in the over-reddened fruit. These discoveries enhance our understanding of anthocyanin regulation under iron deprivation and provide insights into how fruit responds to iron deficiency. • The reddening of the outer pericarp was induced by iron deficiency in the kiwifruit cultivar ‘Hongyang’. • Element analysis confirmed that the anthocyanin accumulation and chlorosis result from iron deficiency. • Anthocyanin biosynthesis and Fe homeostasis genes were induced in the over-reddened outer pericarp.