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Characterisation of abamectin resistance in a field‐evolved multiresistant population of Plutella xylostella
Author(s) -
Pu Xin,
Yang Yihua,
Wu Shuwen,
Wu Yidong
Publication year - 2010
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.1885
Subject(s) - abamectin , piperonyl butoxide , plutella , spinosad , population , biology , plutellidae , biopesticide , avermectin , cross resistance , toxicology , diamondback moth , genetics , pesticide , botany , larva , agronomy , medicine , environmental health , anatomy
BACKGROUND: Plutella xylostella (L.) has evolved resistance to various kinds of insecticide in the field. Reversion and selection, cross‐resistance, inheritance and mechanisms of abamectin resistance were characterised in a field‐derived multiresistant population of P. xylostella from China. RESULTS: Compared with a susceptible Roth strain, the field‐derived TH population showed ∼5000‐fold resistance to abamectin. Rapid reversion of abamectin resistance was observed in the TH population when kept without insecticide selection. The TH‐Abm strain, selected from the TH population with abamectin, developed 23 670‐fold resistance to abamectin, a high level of cross‐resistance to emamectin benzoate and low levels of cross‐resistance to spinosad and fipronil. Genetic analyses indicated that abamectin resistance in the TH‐Abm strain was autosomal, incompletely dominant and polygenic. P450 monooxygenase activities in the TH‐Abm strain were significantly elevated compared with the TH strain. Piperonyl butoxide (PBO) inhibited a small part of abamectin resistance in the TH‐Abm strain. CONCLUSION: Field‐evolved high‐level resistance to abamectin in the TH population was not stable. Selection of the TH population with abamectin resulted in an extremely high level of cross‐resistance to emamectin benzoate and low levels of cross‐resistance to spinosad and fipronil. Enhanced oxidative metabolism was involved in, but may not be the major mechanism of, polygenic abamectin resistance in the TH‐Abm strain. Copyright © 2009 Society of Chemical Industry