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A point mutation in a glutamate‐gated chloride channel confers abamectin resistance in the two‐spotted spider mite, Tetranychus urticae Koch
Author(s) -
Kwon D. H.,
Yoon K. S.,
Clark J. M.,
Lee S. H.
Publication year - 2010
Publication title -
insect molecular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.955
H-Index - 93
eISSN - 1365-2583
pISSN - 0962-1075
DOI - 10.1111/j.1365-2583.2010.01017.x
Subject(s) - tetranychus urticae , abamectin , biology , spider mite , genetics , gene , backcrossing , point mutation , botany , mutation , mite , pesticide , agronomy
The molecular mechanisms and genetics of abamectin resistance mediated by target site insensitivity in the two‐spotted spider mite, Tetranychus urticae , were investigated by comparing two isogenic abamectin‐susceptible (AbaS) and abamectin‐resistant (AbaR) strains. Cloning and sequencing of full‐length cDNA fragments of γ‐amino butyric acid (GABA)‐gated chloride channel genes revealed no polymorphisms between the two strains. However, sequence comparison of the full‐length cDNA fragment of a T. urticae glutamate‐gated chloride channel gene ( TuGluCl ) identified a G323D point mutation as being tentatively related with abamectin resistance. In individual F 2 progenies obtained by backcrossing, the G323D genotype was confirmed to correlate with abamectin resistance. Bioassays using progeny from reciprocal crossings revealed that the abamectin resistance trait resulting from TuGluCl insensitivity is incompletely recessive.