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Genetics and evidence for an esterase‐associated mechanism of resistance to indoxacarb in a field population of diamondback moth (Lepidoptera: Plutellidae)
Author(s) -
Sayyed Ali H,
Wright Denis J
Publication year - 2006
Publication title -
pest management science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.296
H-Index - 125
eISSN - 1526-4998
pISSN - 1526-498X
DOI - 10.1002/ps.1270
Subject(s) - indoxacarb , diamondback moth , spinosad , biology , plutellidae , population , fipronil , plutella , toxicology , deltamethrin , lepidoptera genitalia , botany , pesticide , agronomy , medicine , environmental health
Bioassays (at generation G 2 ) with a newly collected field population (designated CH3) of Plutella xylostella L. from farmers' fields in the Cameron Highlands, Malaysia, indicated resistance ratios of 813‐, 79‐, 171‐, 498‐ and 1285‐fold for indoxacarb, fipronil, spinosad, deltamethrin and Bacillus thuringiensis toxin Cry1Ac respectively compared with a laboratory susceptible population (Lab‐UK). At G 2 the field‐derived population was divided into two subpopulations: one was selected (G 2 to G 7 ) with indoxacarb (indoxa‐SEL), while the second was left unselected (UNSEL). A significant reduction in the resistance ratio for each compound was observed in UNSEL at G 8 . For indoxa‐SEL, bioassays at G 8 found that selection with indoxacarb gave a resistance ratio of 2594 compared with Lab‐UK and of 90 compared with UNSEL. The toxicity of fipronil, spinosad and deltamethrin was not significantly different in indoxa‐SEL at G 8 compared with G 2 but was significantly greater than UNSEL at G 8 . The toxicity of Cry1Ac was significantly reduced in indoxa‐SEL at G 8 compared with G 2 but was also significantly greater than UNSEL at G 8 . This suggests that indoxacarb selection maintained resistance to these compounds in the indoxa‐SEL population. Synergist studies indicated that resistance to indoxacarb in indoxa‐SEL was esterase associated. Logit regression analysis of F 1 reciprocal crosses between indoxa‐SEL and Lab‐UK indicated that resistance to indoxacarb was inherited as an autosomal, incompletely recessive ( D LC = 0.35) trait. Tests of monogenic inheritance suggested that resistance to indoxacarb was controlled by a single locus. Copyright © 2006 Society of Chemical Industry