Resistance selection of triflumezopyrim in Laodelphax striatellus (fallén): Resistance risk, cross-resistance and metabolic mechanism

Abstract

The risk assessment and resistance mechanisms of insecticide resistance are critical for resistance management strategy before a new insecticide is widely used. Triflumezopyrim (TFM) is the first commercialized mesoionic insecticide, which can inhibit nicotinic acetylcholine receptor with high-performance against the small brown planthopper (SBPH), Laodelphax striatellus (Fallén). In our study, the resistance of SBPH to TFM increased 26.29-fold, and the actual heritability of resistance was 0.09 after 21 generations of continuous selection by TFM. After five generations of constant feeding under insecticide-free conditions from F16 generation, the resistance level decreased 2.05-fold, and the average resistance decline rate per generation was 0.01, but there were no statistical decline. The TFM resistant strains had no cross-resistance to imidacloprid, nitenpyram, thiamethoxam, dinotefuran, flonicamid, pymetrozine, and chlorfenapyr. The third and fifth nymphal stage duration, pre-adult stage, adult preoviposition period, longevity, emergence rate, and hatchability of the resistant strain were significantly lower than those of the susceptible strain, while the female-male ratio was considerably increased. The fitness cost was 0.89. Further, cytochrome P450 monooxygenase (P450) and carboxylesterase (CarE) activities were markedly increased, but only the enzyme inhibitor piperonyl butoxide (PBO) had a significant synergistic effect on the resistant strain. The expression of CYP303A1, CYP4CE2, and CYP419A1v2 of P450 genes was significantly increased. SBPH has a certain risk of resistance to TFM with continuous application. The TFM resistance may be due to the increased activity of P450 enzyme regulated by the overexpression of P450 genes.

MicroRNA PC‐5p‐3991_515 mediates triflumezopyrim susceptibility in the small brown planthopper through regulating the post‐transcriptional expression of P450 CYP417A2

“…The results suggested that CYP417A2 could positively regulate the tolerance of SBPH to triflumezopyrim. Previous researchers have not found the cross‐resistance between triflumezopyrim and other neonicotinoid insecticides 9,38 . But CYP417A2 protein can effectively degrade imidacloprid in SBPH 18 .…”

“…Previous researchers have not found the cross-resistance between triflumezopyrim and other neonicotinoid insecticides. 9,38 But CYP417A2 protein can effectively degrade imidacloprid in SBPH. 18 Therefore, there is a risk of cross-resistance between triflumezopyrim and imidacloprid through CYP417A2 protein in SBPH.…”