Determination of resistance levels, cross resistance and resistance mechanisms of abamectin + spiromesifen mixture of Panonychus ulmi Koch (Acari: Tetranychidae) populations collected from apple orchards in isparta province

The presence of resistance to S+A mixture formulation in Panonychus ulmi populations collected from apple orchards in Isparta province and selected with S+A mixture, the presence of cross-resistance for spiromesifen, spirodiclofen, abamectin, milbemectin and spirodiclofen+abamectin in resistant populations and S+A resistance mechanisms were determined by biochemical and molecular methods. The resistance ratios of the orchards populations for S+A were 3.12, 4.44 and 7.66 fold. The LC50 value of the IR population was 23.24 times higher than the HS population. In G-2, M-1 and T-2, spiromesifen and spirodiclofen were 3.92 and 2.82; 1.03 and 2.90; 1.40 and 3.20 times, respectively. The cross-resistance rates of the IR population to spiromesifen, spirodiclofen, spirodiclofen+abamectin, abamectin and milbemectin were 19.16, 13.84, 10.58, 32.21 and 61.06 fold, respectively. LC10 values in M-1, IR and HS were 96.93, 94.15 and 92.40; 69.76, 76.74 and 83.72; 37.93, 42.19 and 53.45 % effect in DEM+S+A, TPP+S+A and PBO+S+A synergists, respectively. Esterase was highest in the G-2 population, GST in the IR population and P450 enzyme in the M-1 population. G314D mutation in GIuCI 1 and I321T and G326E point mutations in GluCl 3 were screened in HS and all resistant populations. The G314D point mutation in GIuCI 1 was identified in IR and M-1; the I321T point mutation in GIuCI 3 was identified in all orchards and IR populations. The G326E mutation was made by classic PCR and analyzed with the Genius program but was not detected in any population. In BC domain, N41Y and R87M mutations were found in IR, Y29D, R87M, A174S in T-2, Y29D and R87M in M-1, and R87M in G-2 according to HS population. In the CT domain, P1877S mutations in G-2, I1862M, E1864V, S1865P, S1889N and T2030K mutations in T-2, T2030K mutations in M-1 were determined in the HS population. No mutation was found in the IR population in the CT domain.