Realized heritability, inheritance and cross‐resistance patterns in imidacloprid‐resistant strain of Dysdercus koenigii (Fabricius) (Hemiptera: Pyrrhocoridae)

Abstract

BACKGROUNDImidacloprid, a neonicotinoid insecticide, is widely sprayed alone or mixed with other insecticides against Dysdercus koenigii, a potential pest of cotton in Pakistan. Recently, resistance to imidacloprid in field populations of D. koenigii has developed because of its overuse. Herein, we have investigated inheritance of imidacloprid resistance in D. koenigii and its cross‐resistance to other insecticides.RESULTSThe imidacloprid‐selected population had a 91 421‐fold increase in resistance to imidacloprid after six generations. Overlapping 95% fiducial limits of LC50s of the F1 (Imida‐Sel ♂ × Sus‐ST ♀) and F1† (Imida‐Sel ♀ × Sus‐ST ♂) suggested an autosomal and incomplete dominant resistance to imidacloprid (DLC = 0.84 for F1 and 0.86 for F1†). Reciprocal backcrosses of the F1 and F1† with Sus‐ST predicted a polygenic inheritance. Realized heritability of imidacloprid resistance was 0.38. When mean slope = 1.74 and h2 = 0.38, then 3–13 generations would be required for a ten‐fold increase in LC50s at 90–20% intensity of selection. Very high cross‐resistance to emamectin benzoate (143‐fold), deltamethrin (1675‐fold) and lambda‐cyhalothrin (140‐fold), and moderate cross‐resistance to acetamiprid (37‐fold) in the imidacloprid‐selected strain compared to the field population were observed.CONCLUSIONImidacloprid resistance developed very quickly under continuous selection pressure in the laboratory. These factors might lead to an increasing likelihood of resistance development in field populations, if imidacloprid is used continuously without insecticide rotation for prolonged periods. The present results would be supportive for better management of D. koenigii by devising an effective resistance management strategy. © 2020 Society of Chemical Industry

Inheritance mode and metabolic mechanism of the sulfoximine insecticide sulfoxaflor resistance in Oxycarenus hyalinipennis (Costa)

“…comm.). Similar to our results, higher resistance levels have previously been reported following laboratory selections in DCB to chlorfenapyr (RR = 149.07‐fold), imidacloprid (RR = 104‐fold), 41,50 N. lugens to sulfoxaflor (RR =123.6‐fold), 42 P. solenopsis to acetamiprid (RR = 315‐fold) 81 and Dysdercus koenigii (Fabricius) to imidacloprid and emamectin benzoate 82,83 . However, the results of this study show that DCB has strong potential for the development of resistance to sulfoxaflor in the field (Fig.…”

“…In the current study, the nonsignificant difference in LC 50 values of F 1 and F 1 ' reciprocal crosses among resistant and susceptible populations revealed that no maternal effects were involved in controlling sulfoxaflor resistance in selected populations of DCB, rather its mode of inheritance was autosomal. The autosomal mode of resistance inheritance has also been reported in different insects to various insecticides like O. hyalinipennis to imidacloprid 41 and chlorfenapyr, 50 D. koenigii to imidacloprid and emamectin benzoate, 82,83 and M. domestica to fipronil 84 . However, in contrast to the present results, sex‐linked inheritance of lambda‐cyhalothrin resistance in Tetranychus urticae (Koch) (laboratory selected) has been reported 85 …”

“…Our results indicate the 0.2 value of h 2 in the Sulfo‐Sel strain and it is expected that DCB would need 6.6 generations for a 10‐fold increase in sulfoxaflor resistance. Other findings with different values of h 2 were reported in different cotton insect pests against various insecticides, for example O. hyalinipennis to fipronil was 0.24, 9 D. koenigii to imidacloprid and emamectin benzoate was 0.38 and 0.59, respectively, 82,83 P. solenopsis to spinosad and chlorpyrifos was 0.94 and 0.59, respectively, 93,103 and Spodoptera litura to imidacloprid was 0.15 21 . Although laboratory experiments are not a replica of field conditions, the estimated h 2 and projected rate ( G ) of resistance through laboratory selection could be used in devising resistance management strategy.…”

Realized Heritability, Risk Assessment, and Inheritance Pattern in Earias vittella (Lepidoptera: Noctuidae) Resistant to Dipel (Bacillus thuringiensis Kurstaki)

“…Higher phenotypic variance may come from gene mutations and laboratory selection pressure, but in field environments it may come from migration of individuals, insecticide alternation, and ecological factors [ 23 , 25 , 26 ]. The h 2 estimation is a useful variable in proactive and effective resistance management of insect pests [ 27 , 28 ]. The h 2 estimation of resistance through laboratory selection predicts the rate of phenotypic and genetic variations due to insecticide resistance [ 28 , 29 ].…”

First Evaluation of Field Evolved Resistance to Commonly Used Insecticides in House Fly Populations from Saudi Arabian Dairy Farms

“…Overuse of insecticides has also resulted in environmental pollution, increased the cost of preventive control, and caused destruction of non-target organisms [12,13]. These issues emphasize the necessity to employ an integrated pest management program against insect pests, including the house fly [14][15][16]. To overcome the development of resistance, excessive applications of insecticides at increasing dose rates and more frequent intervals have been used, but these practices have escalated the problem and rendered the control of house fly even more difficult all over the world, particularly in areas where most suitable insecticides have lost their efficacy [17].…”