Critical role of LdZIP7 in enhancing cadmium tolerance of Lymantria dispar larvae: Functional identification at both the individual and cellular levels.

Abstract

Heavy metals are prevalent environmental pollutants in habitats of phytophagous insects. This study investigates the tolerance of Lymantria dispar larvae to cadmium (Cd) and the associated mechanisms involving the ZIP family. Cd stress reduced larval body weight and extended the development duration without causing significant mortality. A significantly up-regulated expression of apoptosis genes Caspase-1, Caspase-3 and Caspase-7 was observed in Cd-exposed larvae. In Cd-exposed larvae, the expression of the apoptosis-inhibitory factor Bcl-2 in the mitochondrial pathway decreased, while apoptosis-inducing factors Bax and AIFM increased. Cd stress markedly elevated the expression of CHOP and Bip, key genes in the endoplasmic reticulum stress pathway. Among the ZIP family genes, LdZIP7 showed the highest up-regulation in response to Cd treatment. Silencing LdZIP7 intensified the negative impacts of Cd stress on L. dispar larvae and significantly reduced the tolerance of L. dispar larvae to Cd. The main manifestations were a further significant decrease in larval body weight, a further significant extension of developmental duration, and the further activation of the mitochondrial pathway and the endoplasmic reticulum stress pathway-triggered apoptosis in Cd-treated larvae. At the Sf9 cell level, LdZIP7 predominantly localises in the nuclear membrane and cell membrane. Overexpression of LdZIP7 mitigates Cd-induced cytotoxicity by inhibiting the Ca²⁺-MPTP opening degree-mitochondrial membrane potential-apoptosis pathway. Overall, LdZIP7 plays a pivotal role in alleviating the biotoxic effects of Cd and is a significant regulatory gene for Cd tolerance in L. dispar larvae.