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A long non-coding RNA regulates cadherin transcription and susceptibility to Bt toxin Cry1Ac in pink bollworm, Pectinophora gossypiella

Shengyun Li, Fiaz Hussain, Gopalan C. Unnithan, Shuanglin Dong, Zain UlAbdin, Shaohua Gu, Lolita G. Mathew, Jeffrey A. Fabrick, Xinzhi Ni, Yves Carrière, Bruce E. Tabashnik, Xianchun Li
Pesticide biochemistry and physiology 2019 v.158 pp. 54-60
Bacillus thuringiensis, Pectinophora gossypiella, alleles, cadherins, cotton, crystal proteins, evolution, insecticidal proteins, introns, larvae, messenger RNA, midgut, mutation, neonates, non-coding RNA, pests, planting, reverse transcriptase polymerase chain reaction, small interfering RNA, toxins, transcription (genetics), transgenic plants
Extensive planting of transgenic crops producing insecticidal proteins from the bacterium Bacillus thuringiensis (Bt) has spurred increasingly rapid evolution of resistance in pests. In the pink bollworm, Pectinophora gossypiella, a devastating global pest, resistance to Bt toxin Cry1Ac produced by transgenic cotton is linked with mutations in a gene (PgCad1) encoding a cadherin protein that binds Cry1Ac in the larval midgut. We previously reported a long non-coding RNA (lncRNA) in intron 20 of cadherin alleles associated with both resistance and susceptibility to Cry1Ac. Here we tested the hypothesis that reducing expression of this lncRNA decreases transcription of PgCad1 and susceptibility to Cry1Ac. Quantitative RT-PCR showed that feeding susceptible neonates small interfering RNAs (siRNAs) targeting this lncRNA but not PgCad1 decreased the abundance of transcripts of both the lncRNA and PgCad1. Moreover, neonates fed the siRNAs had lower susceptibility to Cry1Ac. The results imply that the lncRNA increases transcription of PgCad1 and susceptibility of pink bollworm to Cry1Ac. The results suggest that disruption of lncRNA expression could be a novel mechanism of pest resistance to Bt toxins.