Cd2+ uptake inhibited by MhNCED3 from Malus hupehensis alleviates Cd-induced cell death

Abstract Abscisic acid (ABA) is a plant hormone induced by cadmium (Cd) stress. This study discusses the role of ABA biosynthesis mediated by 9- cis -epoxycarotenoid dioxygenase ( MhNCED3 ) in cell death caused by Cd. Results show that ABA application to Cd-stressed Malus hupehensis reduced the Cd 2+ influx to roots and Cd accumulation. The apoptosis rate of root cells was also decreased after ABA application, and the expression of vacuolar processing enzyme ( MhγVPE ) and VPE activity was down-regulated. Transgenic Arabidopsis and apple calli with ectopic-expressed MhNCED3 had lower Cd 2+ influx, lower Cd contents, as well as lower expression of genes (NRAMP and IRT) that control Cd 2+ uptake under Cd stress. The cell death in overexpressed MhNCED3 apple calli was lower than that in the wild type. The expression of γVPE and VPE activity also showed a lower level in transgenic plants. The growth of transgenic apple calli that had a higher endogenous ABA level was expectedly better than that of the wild type under Cd stress. Additionally, ABA restricted the upward-translocation of Cd, with evidence of a lower translocation factor and expression of the gene involved in Cd delivery ( AtHMA2 ). Our results suggested that MhNCED3 regulated Cd-induced cell death via VPE, which was probably accomplished through the Cd uptake inhibited by ABA.