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

Abstract

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 Cd2+ 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 Cd2+ influx, lower Cd contents, as well as lower expression of genes (NRAMP and IRT) that control Cd2+ 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.