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Resistance mechanisms to chlorpyrifos and F392W mutation frequencies in the acetylcholine esterase ace1 allele of field populations of the tobacco whitefly, Bemisia tabaci in China.

Zhang NN, Liu CF, Yang F, Dong SL, Han ZJ - J. Insect Sci. (2012)

Bottom Line: However, the resistance dropped significantly to about 18-fold in only 4 generations without selection pressure.F392W mutations in acel were prevalent in NJ-S and NJ-R strains and 6 field-collected populations of both B and Q-biotype from locations that cover a wide geographical area of China.These findings provide important information about tobacco whitefly chlorpyrifos resistance mechanisms and guidance to combat resistance and optimize use patterns of chlorpyrifos and other organophosphate and carbamate insecticides.

View Article: PubMed Central - PubMed

Affiliation: College of Plant Protection, Education Ministry Key Laboratory of Integrated Management of Crop Diseases and Pests, Nanjing Agricultural University, Nanjing 210095, China. skyning456@163.com

ABSTRACT
The tobacco whitefly B-biotype Bemisia tabaci Gennadius (Hemiptera: Aleyrodidae) is a worldwide pest of many crops. In China, chlorpyrifos has been used to control this insect for many years and is still being used despite the fact that some resistance has been reported. To combat resistance and maintain good control efficiency of chlorpyrifos, it is essential to understand resistance mechanisms. A chlorpyrifos resistant tobacco whitefly strain (NJ-R) and a susceptible strain (NJ-S) were derived from a field-collected population in Nanjing, China, and the resistance mechanisms were investigated. More than 30-fold resistance was achieved after selected by chlorpyrifos for 13 generations in the laboratory. However, the resistance dropped significantly to about 18-fold in only 4 generations without selection pressure. Biochemical assays indicated that increased esterase activity was responsible for this resistance, while acetylcholine esterase, glutathione S-transferase, and microsomal-O-demethylase played little or no role. F392W mutations in acel were prevalent in NJ-S and NJ-R strains and 6 field-collected populations of both B and Q-biotype from locations that cover a wide geographical area of China. These findings provide important information about tobacco whitefly chlorpyrifos resistance mechanisms and guidance to combat resistance and optimize use patterns of chlorpyrifos and other organophosphate and carbamate insecticides.

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Related in: MedlinePlus

Examination of F392W point mutation in 10 NJ-S Bemisia tabaci (from S-1 to S-10) and 10 NJ-R tobacco whiteflies (from R-1 to R-10) by cloning a 211 bp-acel gene fragment. SUD-S (ncbi protein: ABV45413.1) and R-CK (ncbi protein: ABV45421.1) served as susceptible and resistant references. All 10 NJ-R individuals and 9 out of 10 NJ-S individuals carried the F392W mutation. High quality figures are available online.
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f02_01: Examination of F392W point mutation in 10 NJ-S Bemisia tabaci (from S-1 to S-10) and 10 NJ-R tobacco whiteflies (from R-1 to R-10) by cloning a 211 bp-acel gene fragment. SUD-S (ncbi protein: ABV45413.1) and R-CK (ncbi protein: ABV45421.1) served as susceptible and resistant references. All 10 NJ-R individuals and 9 out of 10 NJ-S individuals carried the F392W mutation. High quality figures are available online.

Mentions: To confirm this result, a PCR assay of individual tobacco whitefly was conducted using primers that are able to amplify a 221 bp fragment across the F392W mutation site in acel specifically. One out of 10 NJ-S individuals showed the sensitive genotype (F392) and the other nine had the F392W mutation, whereas all 10 individuals from NJR strain displayed the F392W mutation (Figure 2). The results indicated that F392W mutation was not responsible for the chlorpyrifos susceptibility difference between NJ-S and NJ-R stains, and that both NJ-S and NJ-R strains had a similar level of target resistance.


Resistance mechanisms to chlorpyrifos and F392W mutation frequencies in the acetylcholine esterase ace1 allele of field populations of the tobacco whitefly, Bemisia tabaci in China.

Zhang NN, Liu CF, Yang F, Dong SL, Han ZJ - J. Insect Sci. (2012)

Examination of F392W point mutation in 10 NJ-S Bemisia tabaci (from S-1 to S-10) and 10 NJ-R tobacco whiteflies (from R-1 to R-10) by cloning a 211 bp-acel gene fragment. SUD-S (ncbi protein: ABV45413.1) and R-CK (ncbi protein: ABV45421.1) served as susceptible and resistant references. All 10 NJ-R individuals and 9 out of 10 NJ-S individuals carried the F392W mutation. High quality figures are available online.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3472965&req=5

f02_01: Examination of F392W point mutation in 10 NJ-S Bemisia tabaci (from S-1 to S-10) and 10 NJ-R tobacco whiteflies (from R-1 to R-10) by cloning a 211 bp-acel gene fragment. SUD-S (ncbi protein: ABV45413.1) and R-CK (ncbi protein: ABV45421.1) served as susceptible and resistant references. All 10 NJ-R individuals and 9 out of 10 NJ-S individuals carried the F392W mutation. High quality figures are available online.
Mentions: To confirm this result, a PCR assay of individual tobacco whitefly was conducted using primers that are able to amplify a 221 bp fragment across the F392W mutation site in acel specifically. One out of 10 NJ-S individuals showed the sensitive genotype (F392) and the other nine had the F392W mutation, whereas all 10 individuals from NJR strain displayed the F392W mutation (Figure 2). The results indicated that F392W mutation was not responsible for the chlorpyrifos susceptibility difference between NJ-S and NJ-R stains, and that both NJ-S and NJ-R strains had a similar level of target resistance.

Bottom Line: However, the resistance dropped significantly to about 18-fold in only 4 generations without selection pressure.F392W mutations in acel were prevalent in NJ-S and NJ-R strains and 6 field-collected populations of both B and Q-biotype from locations that cover a wide geographical area of China.These findings provide important information about tobacco whitefly chlorpyrifos resistance mechanisms and guidance to combat resistance and optimize use patterns of chlorpyrifos and other organophosphate and carbamate insecticides.

View Article: PubMed Central - PubMed

Affiliation: College of Plant Protection, Education Ministry Key Laboratory of Integrated Management of Crop Diseases and Pests, Nanjing Agricultural University, Nanjing 210095, China. skyning456@163.com

ABSTRACT
The tobacco whitefly B-biotype Bemisia tabaci Gennadius (Hemiptera: Aleyrodidae) is a worldwide pest of many crops. In China, chlorpyrifos has been used to control this insect for many years and is still being used despite the fact that some resistance has been reported. To combat resistance and maintain good control efficiency of chlorpyrifos, it is essential to understand resistance mechanisms. A chlorpyrifos resistant tobacco whitefly strain (NJ-R) and a susceptible strain (NJ-S) were derived from a field-collected population in Nanjing, China, and the resistance mechanisms were investigated. More than 30-fold resistance was achieved after selected by chlorpyrifos for 13 generations in the laboratory. However, the resistance dropped significantly to about 18-fold in only 4 generations without selection pressure. Biochemical assays indicated that increased esterase activity was responsible for this resistance, while acetylcholine esterase, glutathione S-transferase, and microsomal-O-demethylase played little or no role. F392W mutations in acel were prevalent in NJ-S and NJ-R strains and 6 field-collected populations of both B and Q-biotype from locations that cover a wide geographical area of China. These findings provide important information about tobacco whitefly chlorpyrifos resistance mechanisms and guidance to combat resistance and optimize use patterns of chlorpyrifos and other organophosphate and carbamate insecticides.

Show MeSH
Related in: MedlinePlus