SfVipR2 edition confirms caterpillar resistance to Vip3Aa

Inactivation of the SfVipR2 gene conferred over 2.500 times greater resistance to the Vip3Aa protein in Spodoptera frugiperda. Researchers obtained this result through gene editing with CRISPR/Cas9. The resistance showed autosomal and completely recessive inheritance.

The study also evaluated strains with inactivation of SfVipR1, SfVipR2, and SfCHS2 (doi 10.1016/j.pestbp.2026.107294). All shared the same YJ-19 genetic background. Each isolated mutation produced high resistance to Vip3Aa. The researchers observed no relevant alteration in susceptibility to the Cry1Fa protein.

Susceptible descendants

Reciprocal crosses between the three resistant lines generated offspring susceptible to Vip3Aa. The result demonstrated complete genetic complementarity between the mutations. It also indicated an absence of epistasis between the three non-allelic loci.

The loss of any one of the genes compromised the action of Vip3Aa. However, the molecular and biochemical mechanisms involved remain undefined. Scientists hypothesize that all three genes participate in a common toxicological process.

Evolution of resistance

Genetic architecture increases the risk of resistance evolution in field populations. Three independent genes can give rise to the same resistant phenotype. This work recommends monitoring alleles in SfVipR1, SfVipR2, and SfCHS2 using molecular markers or tests with resistant strains.

Researchers also advocate for suitable refuges with non-Bt host plants. Another measure involves pyramided hybrids with Vip and Cry proteins of different modes of action. These strategies may delay the selection for resistance to Vip3Aa.