A point mutation in a glutamate-gated chloride channel confers abamectin resistance in the two-spotted spider mite, Tetranychus urticae Koch

被引：176

作者：

Kwon, D. H. ^{[1
]}

Yoon, K. S. ^{[2
]}

Clark, J. M. ^{[2
]}

Lee, S. H. ^{[1
]}

机构：

[1] Seoul Natl Univ, Dept Agr Biotechnol, Seoul 151742, South Korea

[2] Univ Massachusetts, Dept Vet & Anim Sci, Amherst, MA 01003 USA

来源：

INSECT MOLECULAR BIOLOGY | 2010年 / 19卷 / 04期

关键词：

glutamate-gated chloride channel; target site insensitivity; macrocyclic lactone; abamectin; Tetranychus urticae; ACARI; SUSCEPTIBILITY; POPULATIONS; AVERMECTINS; GENETICS;

D O I：

10.1111/j.1365-2583.2010.01017.x

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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 gamma-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.

引用

页码：583 / 591

页数：9

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