Deciphering the molecular mechanisms underlying insect resistance to Cry toxins produced by Bacillus thuringiensis (Bt) is pivotal for the sustainable utilization of Bt biopesticides and transgenic Bt crops. Previously, we identified that mitogen-activated protein kinase (MAPK)-mediated reduced expression of the gene is associated with Bt Cry1Ac resistance in the diamondback moth, Plutella xylostella (L.). However, the underlying transcriptional regulation mechanism remains enigmatic. Here, the promoter in Cry1Ac-susceptible and Cry1Ac-resistant strains was cloned and analyzed and found to contain a putative Jun binding site (JBS). A dual-luciferase reporter assay and yeast one-hybrid assay demonstrated that the transcription factor PxJun repressed expression by interacting with this JBS. The expression levels of were increased in the midguts of all resistant strains compared to the susceptible strain. Silencing of expression significantly elevated expression and Cry1Ac susceptibility in the resistant NIL-R strain, and silencing of expression decreased expression and also increased expression. These results indicate that MAPK-activated PxJun suppresses expression to confer Cry1Ac resistance in , deepening our understanding of the transcriptional regulation of midgut Cry receptor genes and the molecular basis of insect resistance to Bt Cry toxins. The transcriptional regulation mechanisms underlying reduced expression of Bt toxin receptor genes in Bt-resistant insects remain elusive. This study unveils that a transcription factor PxJun activated by the MAPK signaling pathway represses expression and confers Cry1Ac resistance in . Our results provide new insights into the transcriptional regulation mechanisms of midgut Cry receptor genes and deepen our understanding of the molecular basis of insect resistance to Bt Cry toxins. To our knowledge, this study identified the first transcription factor that can be involved in the transcriptional regulation mechanisms of midgut Cry receptor genes in Bt-resistant insects.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8315950PMC
http://dx.doi.org/10.1128/AEM.00466-21DOI Listing

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