Mutations in the Bemisia tabaci para sodium channel gene associated with resistance to a pyrethroid plus organophosphate mixture

S. Morin; M. S. Williamson; S. J. Goodson; J. K. Brown; B. E. Tabashnik; T. J. Dennehy

doi:10.1016/S0965-1748(02)00137-6

Mutations in the Bemisia tabaci para sodium channel gene associated with resistance to a pyrethroid plus organophosphate mixture

S. Morin^*, M. S. Williamson, S. J. Goodson, J. K. Brown, B. E. Tabashnik, T. J. Dennehy

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

113 Scopus citations

Abstract

The voltage-gated sodium channel is the primary target site of pyrethroid insecticides. In some insects, super knockdown resistance (super-kdr) to pyrethroids is caused by point mutations in the linker fragment between transmembrane segments 4 and 5 of the para-type sodium channel protein domain II (IIS4-5). Here, we identify two mutations in the IIS4-5 linker of the para-type sodium channel of the whitefly, Bemisia tabaci: methionine to valine at position 918 (M918V) and leucine to isoleucine at position 925 (L925I). Although each mutation was isolated independently from strains >100-fold resistant to a pyrethroid (fenpropathrin) plus organophosphate (acephate) mixture, only L925I was associated with resistance in strains derived from the field in 2000 and 2001. The L925I mutation occurred in all individuals from nine different field collections that survived exposure to a discriminating concentration of fenpropathrin plus acephate. Linkage analysis of hemizygous male progeny of unmated heterozygous F1 females (L925Ixwild-type) shows that the observed resistance is tightly linked to the voltage-gated sodium channel locus. The results provide a molecular tool for better understanding, monitoring and managing pyrethroid resistance in B. tabaci.

Original language	English
Pages (from-to)	1781-1791
Number of pages	11
Journal	Insect Biochemistry and Molecular Biology
Volume	32
Issue number	12
DOIs	https://doi.org/10.1016/S0965-1748(02)00137-6
State	Published - 1 Dec 2002
Externally published	Yes

Bibliographical note

Funding Information:
We thank Dr Ian Denholm for critical reading of the manuscript, and Marni Zaborac, Ben DeGain and Daniel Holley for their excellent technical support in running the bioassays. The work was supported by the Vaadia-BARD Postdoctoral Fellowship No. FI-300-2000. We thank the Arizona Cotton Growers Association (Project No. 00-81AZ) and Cotton Incorporated (Project No. 00-810) for ongoing support of the monitoring, selection and phenotypic characterization of resistance in Arizona whiteflies, conducted by the University of Arizona Extension Arthropod Resistance Management Laboratory, and for partial support for the molecular biological studies described herein. IACR-Rothamsted receives grant-aided support from the Biotechnology and Biological Sciences Research Council of the United Kingdom.

Keywords

Bemisia tabaci
Insecticide
Pyrethroid
Resistance
Voltage-gated sodium channel

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10.1016/S0965-1748(02)00137-6

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title = "Mutations in the Bemisia tabaci para sodium channel gene associated with resistance to a pyrethroid plus organophosphate mixture",

abstract = "The voltage-gated sodium channel is the primary target site of pyrethroid insecticides. In some insects, super knockdown resistance (super-kdr) to pyrethroids is caused by point mutations in the linker fragment between transmembrane segments 4 and 5 of the para-type sodium channel protein domain II (IIS4-5). Here, we identify two mutations in the IIS4-5 linker of the para-type sodium channel of the whitefly, Bemisia tabaci: methionine to valine at position 918 (M918V) and leucine to isoleucine at position 925 (L925I). Although each mutation was isolated independently from strains >100-fold resistant to a pyrethroid (fenpropathrin) plus organophosphate (acephate) mixture, only L925I was associated with resistance in strains derived from the field in 2000 and 2001. The L925I mutation occurred in all individuals from nine different field collections that survived exposure to a discriminating concentration of fenpropathrin plus acephate. Linkage analysis of hemizygous male progeny of unmated heterozygous F1 females (L925Ixwild-type) shows that the observed resistance is tightly linked to the voltage-gated sodium channel locus. The results provide a molecular tool for better understanding, monitoring and managing pyrethroid resistance in B. tabaci.",

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author = "S. Morin and Williamson, {M. S.} and Goodson, {S. J.} and Brown, {J. K.} and Tabashnik, {B. E.} and Dennehy, {T. J.}",

note = "Funding Information: We thank Dr Ian Denholm for critical reading of the manuscript, and Marni Zaborac, Ben DeGain and Daniel Holley for their excellent technical support in running the bioassays. The work was supported by the Vaadia-BARD Postdoctoral Fellowship No. FI-300-2000. We thank the Arizona Cotton Growers Association (Project No. 00-81AZ) and Cotton Incorporated (Project No. 00-810) for ongoing support of the monitoring, selection and phenotypic characterization of resistance in Arizona whiteflies, conducted by the University of Arizona Extension Arthropod Resistance Management Laboratory, and for partial support for the molecular biological studies described herein. IACR-Rothamsted receives grant-aided support from the Biotechnology and Biological Sciences Research Council of the United Kingdom. ",

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AU - Williamson, M. S.

AU - Goodson, S. J.

AU - Brown, J. K.

AU - Tabashnik, B. E.

AU - Dennehy, T. J.

N1 - Funding Information: We thank Dr Ian Denholm for critical reading of the manuscript, and Marni Zaborac, Ben DeGain and Daniel Holley for their excellent technical support in running the bioassays. The work was supported by the Vaadia-BARD Postdoctoral Fellowship No. FI-300-2000. We thank the Arizona Cotton Growers Association (Project No. 00-81AZ) and Cotton Incorporated (Project No. 00-810) for ongoing support of the monitoring, selection and phenotypic characterization of resistance in Arizona whiteflies, conducted by the University of Arizona Extension Arthropod Resistance Management Laboratory, and for partial support for the molecular biological studies described herein. IACR-Rothamsted receives grant-aided support from the Biotechnology and Biological Sciences Research Council of the United Kingdom.

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N2 - The voltage-gated sodium channel is the primary target site of pyrethroid insecticides. In some insects, super knockdown resistance (super-kdr) to pyrethroids is caused by point mutations in the linker fragment between transmembrane segments 4 and 5 of the para-type sodium channel protein domain II (IIS4-5). Here, we identify two mutations in the IIS4-5 linker of the para-type sodium channel of the whitefly, Bemisia tabaci: methionine to valine at position 918 (M918V) and leucine to isoleucine at position 925 (L925I). Although each mutation was isolated independently from strains >100-fold resistant to a pyrethroid (fenpropathrin) plus organophosphate (acephate) mixture, only L925I was associated with resistance in strains derived from the field in 2000 and 2001. The L925I mutation occurred in all individuals from nine different field collections that survived exposure to a discriminating concentration of fenpropathrin plus acephate. Linkage analysis of hemizygous male progeny of unmated heterozygous F1 females (L925Ixwild-type) shows that the observed resistance is tightly linked to the voltage-gated sodium channel locus. The results provide a molecular tool for better understanding, monitoring and managing pyrethroid resistance in B. tabaci.

AB - The voltage-gated sodium channel is the primary target site of pyrethroid insecticides. In some insects, super knockdown resistance (super-kdr) to pyrethroids is caused by point mutations in the linker fragment between transmembrane segments 4 and 5 of the para-type sodium channel protein domain II (IIS4-5). Here, we identify two mutations in the IIS4-5 linker of the para-type sodium channel of the whitefly, Bemisia tabaci: methionine to valine at position 918 (M918V) and leucine to isoleucine at position 925 (L925I). Although each mutation was isolated independently from strains >100-fold resistant to a pyrethroid (fenpropathrin) plus organophosphate (acephate) mixture, only L925I was associated with resistance in strains derived from the field in 2000 and 2001. The L925I mutation occurred in all individuals from nine different field collections that survived exposure to a discriminating concentration of fenpropathrin plus acephate. Linkage analysis of hemizygous male progeny of unmated heterozygous F1 females (L925Ixwild-type) shows that the observed resistance is tightly linked to the voltage-gated sodium channel locus. The results provide a molecular tool for better understanding, monitoring and managing pyrethroid resistance in B. tabaci.

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ER -

Mutations in the Bemisia tabaci para sodium channel gene associated with resistance to a pyrethroid plus organophosphate mixture

Abstract

Bibliographical note

Keywords

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