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10-Minute Presentation

Physiology, Biochemistry, and Toxicology

10-min: PBT, Genetics

Genetics of insect resistance to Vip3Aa

Wednesday, November 13, 2024
2:18 PM – 2:30 PM MST
Location: Phoenix Convention Center, 121 C, PCC
Oral Presentation

    Presenting Author(s)

  • DH

    David G. Heckel

    Director Emeritus
    Max Planck Institute for Chemical Ecology
    Jena, Thuringen, Germany

    • Co-Author(s)

  • Bruce E. Tabashnik (he/him/his)

    Regents Professor & Department Head
    University of Arizona
    Tucson, Arizona

  • YX

    Yutao Xiao

    Chinese Academy of Agricultural Sciences
    Shenzhen, Guangdong, China (People's Republic)

  • KL

    Kaiyu Liu

    Central China Normal University
    Wuhan, Hubei, China (People's Republic)

  • KW

    Kongming Wu

    Chinese Academy of Agricultural Sciences
    Beijing, Beijing, China (People's Republic)

  • CL

    Chongyu Liao

    Chinese Academy of Agricultural Sciences
    Shenzhen, Guangdong, China (People's Republic)

  • ZL

    Zhenxing Liu

    Chinese Academy of Agricultural Sciences
    Shenzhen, Guangdong, China (People's Republic)

  • MJ

    Minghui Jin

    Chinese Academy of Agricultural Sciences
    Shenzhen, Guangdong, China (People's Republic)

  • LZ

    Luming Zou

    Chinese Academy of Agricultural Sciences
    Shenzhen, Guangdong, China (People's Republic)

The VIP (vegetative insecticidal proteins) toxins from Bacillus thuringiensis kill insects via different pathways compared with the Cry toxins. Vip3Aa is deployed in transgenic crops as a backup against pest evolution of Cry toxin resistance, and is currently effective against the fall armyworm, Spodoptera frugiperda. However, Vip3Aa-resistant strains of several pest species are now known. Two different mutations associated with resistance to Vip3Aa have been reported from lab-selected strains of invasive S. frugiperda from China. One is a change in the promoter sequence of SfMyb, a transcription factor that apparently controls the expression of protein binding targets of Vip3A in the midgut. Another is insertion of a transposable element that alters transcripts of SfCHS2, the chitin synthase responsible for production of chitin of the peritrophic matrix in the midgut. Knockouts of the chitin synthase gene conferred resistance to Vip3Aa in S. frugiperda and two other lepidopteran pests. We expect that mutations conferring S. frugiperda resistance to Vip3Aa occur in loci other than SfMyb and SfCHS2. Anticipating and managing Vip3Aa resistance is important for sustainable pest control, especially with field-evolved resistance to Cry toxins conferred by a dominant mutation affecting tetraspanin and associated with increased protease activity.