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

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, 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 localizes 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.