Role of c‐Jun NH2‐terminal kinase‐mediated mitogen‐activated protein kinase pathway in response to pesticides in Apis cerana cerana

摘要

Abstract The mitogen‐activated protein kinase (MAPK) cascade pathway plays an important role in regulating stress responses. The function of the c‐Jun NH2‐terminal kinase (JNK), a component of the MAPK cascade pathway, in Apis cerana cerana (Acc) remains unclear. Here, JNK was isolated and identified from Acc. Bioinformatics analyses revealed there is a typical serine/threonine protein kinase catalytic domain in the AccJNK protein. An expression profile analysis showed that AccJNK was significantly induced by pesticide treatments. To further explore the functional mechanisms of AccJNK, a yeast 2‐hybrid screen was performed, activator protein‐1 (AP‐1) was screened as the interaction partner of AccJNK, and the interaction relationship was further verified by pull‐down assay. Quantitative real‐time polymerase chain reaction showed the expression pattern of AccAP‐1 was similar to that of AccJNK. After a knockdown of AccJNK or AccAP‐1 by RNA interference, the survival rate of Acc after pesticide treatments increased. Additionally, the expression levels of antioxidant‐related genes and the activities of antioxidant enzymes increased, suggesting that the knockdown of AccJNK or AccAP‐1 increased the antioxidant capacity of bees. Our study revealed that the JNK‐mediated MAPK pathway responds to pesticide stress by altering the antioxidant capacity of Acc.