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G D Moores - One of the best experts on this subject based on the ideXlab platform.
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identification of mutations conferring insecticide insensitive ache in the cotton melon aphid aphis gossypii glover
Insect Molecular Biology, 2004Co-Authors: M. C. Andrews, L M Field, Martin S. Williamson, Amanda Callaghan, G D MooresAbstract:We have identified two mutations in the ace1 gene of Aphis gossypii that are associated with insensitivity of acetylcholinesterase (AChE) to carbamate and organophosphate insecticides. The first of these, S431F (equivalent to F331 in Torpedo californica), is associated with insensitivity to the carbamate insecticide Pirimicarb in a range of A. gossypii clones. The S431F mutation is also found in the peach-potato aphid, Myzus persicae (Sulzer), and a rapid RFLP diagnostic allows the identification of individuals of both aphid species with a resistant genotype. This diagnostic further revealed the presence of S431 in several other Pirimicarb-susceptible aphid species. The serine at this position in the wild-type enzyme has only been reported for aphids and provides a molecular explanation of why Pirimicarb has a specific aphicidal action. A less specific insensitivity to a wide range of carbamates and organophosphates is associated with a second mutation, A302S (A201 in T. californica).
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association between biochemical markers and insecticide resistance in the cotton aphid aphis gossypii glover
Pesticide Biochemistry and Physiology, 1998Co-Authors: G D Moores, I Denholm, Alan L DevonshireAbstract:Abstract The activity and electrophoretic mobility of nonspecific esterases, and the sensitivity of acetylcholinesterase (AChE) to organophosphate and carbamate insecticides, was determined for 21 strains or clones of Aphis gossypii of worldwide origin and related to patterns of insecticide resistance disclosed by diagnostic dose bioassays with demeton-S-methyl, Pirimicarb, and permethrin. Results confirmed previous work showing the occurrence of two forms of mutant AChE, both conferring insensitivity to Pirimicarb and representing the primary mechanism of resistance to this insecticide. One of these mutant AChE enzymes also caused resistance to demeton- S -methyl in its own right, whereas the other only conferred resistance in combination with moderate or high levels of nonspecific esterase activity. Lack of any correlation between permethrin resistance and quantitative or qualitative changes in esterases implied a distinct, as yet uncharacterised, mechanism of resistance to pyrethroids, possibly based on insensitivity in the target protein for these pesticides.
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association between biochemical markers and insecticide resistance in the cotton aphid aphis gossypiiglover
Pesticide Biochemistry and Physiology, 1998Co-Authors: Zhaojun Han, G D Moores, I Denholm, Alan L DevonshireAbstract:Abstract The activity and electrophoretic mobility of nonspecific esterases, and the sensitivity of acetylcholinesterase (AChE) to organophosphate and carbamate insecticides, was determined for 21 strains or clones of Aphis gossypii of worldwide origin and related to patterns of insecticide resistance disclosed by diagnostic dose bioassays with demeton-S-methyl, Pirimicarb, and permethrin. Results confirmed previous work showing the occurrence of two forms of mutant AChE, both conferring insensitivity to Pirimicarb and representing the primary mechanism of resistance to this insecticide. One of these mutant AChE enzymes also caused resistance to demeton- S -methyl in its own right, whereas the other only conferred resistance in combination with moderate or high levels of nonspecific esterase activity. Lack of any correlation between permethrin resistance and quantitative or qualitative changes in esterases implied a distinct, as yet uncharacterised, mechanism of resistance to pyrethroids, possibly based on insensitivity in the target protein for these pesticides.
Marcelo L Larramendy - One of the best experts on this subject based on the ideXlab platform.
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lethal and sublethal effects of the Pirimicarb based formulation aficida on boana pulchella dumeril and bibron 1841 tadpoles anura hylidae
Ecotoxicology and Environmental Safety, 2018Co-Authors: Guillermo Sebastian Natale, Josefina Veracandioti, Ruiz C De Arcaute, Sonia Soloneski, Marcelo L LarramendyAbstract:Abstract Acute lethal and sublethal toxicity of the Pirimicarb-based commercial formulation Aficida ® were evaluated on Boana pulchella tadpoles. Whereas mortality was used as end point for lethality, frequency of micronuclei and other nuclear abnormalities as well as alterations in the frequency of erythroblasts in circulating blood as biomarkers for genotoxicity and cytotoxicity, respectively. Swimming, growth, developmental and morphological abnormalities were also employed as sublethal end points. Results show that the species is within the 13th percentile of the distribution of acute sensitivity of species to Pirimicarb for aquatic vertebrates. Results revealed values of 23.78 and 101.45 mg/L Pirimicarb as LC50 96 h for GS25 and GS36 tadpoles, respectively. The most evident effects were related with the swimming activity with NOEC and LOEC values within the 0.005–0.39 mg/L Pirimicarb concentration range. Aficida ® induced DNA damage at the chromosomal level by increasing micronuclei frequency and other nuclear abnormalities, i.e. , lobbed and notched nuclei and binucleated cells. Cellular cytotoxicity was found after Aficida ® treatment. The presence of abdominal oedemas in exposed organisms and thus flotation response of organisms could be proposed as a new sensitive exposure parameter. The multiple end point assessment approach used allowed a complete understanding the multi level of effects occurring by exposure to Pirimicarb, at least in B. pulchella .
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lethal and sublethal effects of the Pirimicarb based formulation aficida on boana pulchella dumeril and bibron 1841 tadpoles anura hylidae
Ecotoxicology and Environmental Safety, 2018Co-Authors: Guillermo Sebastian Natale, Josefina Veracandioti, Ruiz C De Arcaute, Sonia Soloneski, Marcelo L LarramendyAbstract:Abstract Acute lethal and sublethal toxicity of the Pirimicarb-based commercial formulation Aficida ® were evaluated on Boana pulchella tadpoles. Whereas mortality was used as end point for lethality, frequency of micronuclei and other nuclear abnormalities as well as alterations in the frequency of erythroblasts in circulating blood as biomarkers for genotoxicity and cytotoxicity, respectively. Swimming, growth, developmental and morphological abnormalities were also employed as sublethal end points. Results show that the species is within the 13th percentile of the distribution of acute sensitivity of species to Pirimicarb for aquatic vertebrates. Results revealed values of 23.78 and 101.45 mg/L Pirimicarb as LC50 96 h for GS25 and GS36 tadpoles, respectively. The most evident effects were related with the swimming activity with NOEC and LOEC values within the 0.005–0.39 mg/L Pirimicarb concentration range. Aficida ® induced DNA damage at the chromosomal level by increasing micronuclei frequency and other nuclear abnormalities, i.e. , lobbed and notched nuclei and binucleated cells. Cellular cytotoxicity was found after Aficida ® treatment. The presence of abdominal oedemas in exposed organisms and thus flotation response of organisms could be proposed as a new sensitive exposure parameter. The multiple end point assessment approach used allowed a complete understanding the multi level of effects occurring by exposure to Pirimicarb, at least in B. pulchella .
Grant A Herron - One of the best experts on this subject based on the ideXlab platform.
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can resistance management strategies recover insecticide susceptibility in pests a case study with cotton aphid aphis gossypii aphididae hemiptera in australian cotton
Australian Journal of Entomology, 2017Co-Authors: Grant A Herron, Lewis J WilsonAbstract:Cotton pest management in the Australian cotton industry was highly pesticide reliant from its inception in the early 1960s until the late 1990s. Aphids were controlled effectively over this period either co-incidentally by compounds applied against Helicoverpa spp. or by targeted applications of dimethoate/omethoate or Pirimicarb in the late 1990s. By cotton season 1999–2000, after this prolonged period of selection, the cotton aphid Aphis gossypii Glover showed resistance to Pirimicarb and cross resistance to dimethoate/omethoate as well as resistance to older organophosphates (profenofos, chlorpyrifos-methyl, chlorpyrifos-ethyl) targeted against Helicoverpa spp.. No new chemical controls were available so effective control required development of an insecticide resistance management (IRM) strategy incorporated with integrated pest management (IPM) strategies designed to maximalise any known selective disadvantage for resistant individuals. The IRM component emphasised rotation between insecticide mode of action (MOA) groups and limited the number of applications of any MOA. The IPM component incorporated farm hygiene to reduce overwinter hosts for resistant aphids, conserved natural enemies and incorporated effective use of pest sampling and thresholds. The aphid management strategy was fluid, evolving and adapting as new knowledge, new resistance and further IPM or IRM tactics became available. For instance, in 2007–2008 resistance was detected in aphids to the neonicotinoids resulting in field failures. Detection of neonicotinoid resistance required modifications to the aphid management strategy to address prolonged selection by both neonicotinoid seed treatments and foliar applications. The strategy also considered the need to manage concurrent pest species to mitigate the risk that insecticides sprayed against those pests would coincidently cause aphid outbreaks or select for resistance in aphids. The integrated strategy has now almost completely recovered susceptibility to IPM friendly Pirimicarb and resistance to neonicotinoid insecticides has declined dramatically.
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baseline susceptibility and cross resistance in aphis gossypii glover aphididae hemiptera to phorate and sulfoxaflor
Australian Journal of Entomology, 2014Co-Authors: Grant A Herron, Brendan J Langfield, Daniel R Bogema, Yizhou ChenAbstract:Susceptible discriminating doses of phorate (0.2 g/L) and sulfoxaflor (0.01 g/L) against cotton aphid Aphis gossypii Glover were determined by laboratory bioassay where aphids were sprayed with insecticide with the aid of a Potter spray tower. All of the populations tested were susceptible to sulfoxaflor, and only a Pirimicarb resistant strain had cross-resistance to phorate. If phorate is used as a side dressing in Australian cotton for insect control, neither Pirimicarb, or any other chemical associated with insensitive acetylcholinesterase type one resistance, should be used as the first foliar spray for any subsequent aphid control.
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Field isolates of Aphis gossypii collected during the 2011/2012 season showing Pirimicarb resistance status determined by individual PCR-RFLP.
2014Co-Authors: Yizhou Chen, Daniel R Bogema, I M Barchia, Grant A HerronAbstract:R: Resistant to Pirimicarb.S: Susceptible to Pirimicar.
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evidence of superclones in australian cotton aphid aphis gossypii glover aphididae hemiptera
Pest Management Science, 2013Co-Authors: Yizhou Chen, Flavie Vanlerberghemasutti, Lewis J Wilson, I M Barchia, Martin O Mcloon, Tanya Smith, Grant A HerronAbstract:Background Aphis gossypii is an important pest of cotton that has developed resistance to many chemicals used for its control. Any lack of understanding of its genetic structure, resistance status and host plant specialisation hampers effective management. Rsults Eight microsatellite markers were genotyped for a collection of Australian A. gossypii field isolates from 55 plant species from major Australian cotton-producing regions. The aphid's Pirimicarb resistance status linked to the ACE1 (acetylcholinesterase) S431F mutation was determined by PCR-RFLP. Overall, the genetic diversity was low and there were only 13 multilocus genotype (MLG) groups found in a total of 936 aphids, suggesting asexual reproduction. Three MLGs (Aust-01, Aust-02 and Aust-04) represented 78% of all aphids tested. MLGs Aust-01 (41%) and Aust-02 (18%) were linked to the ACE1 S431F mutation and found on cotton and a range of hosts. Aust-04 (19%) hosted mainly on cotton (but also Asteraceae and Malvaceae) was predominantly susceptible to Pirimicarb. Given their abundance and widespread occurrence, these three clones were considered to be superclones. Conclusion The study demonstrated that any strategy to control A. gossypii and manage Pirimicarb resistance should target A. gossypii strains of all MLG types residing on any plant species and not just cotton.© 2012 Society of Chemical Industry
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insecticide resistance in aphis gossypii glover hemiptera aphididae a serious threat to australian cotton
Australian Journal of Entomology, 2001Co-Authors: Grant A Herron, Kevin Powis, Jeanette RophailAbstract:Populations of cotton aphid, Aphis gossypii Glover, were surveyed for insecticide resistance. Pirimicarb, organophosphate, endosulfan and pyrethroid resistance was identified. Aphis gossypii from New South Wales cotton-growing districts were organophosphate and Pirimicarb susceptible, whereas populations from similar districts in Western Australia, Queensland and Northern Territory displayed high to extreme resistance that was linked to control failure. New South Wales populations, however, were often endosulfan and pyrethroid resistant. Resistant A. gossypii have the potential to seriously impact on the Australian cotton industry and their resistance management is now incorporated into the resistance management strategy for Australian cotton.
Yoshiaki Kono - One of the best experts on this subject based on the ideXlab platform.
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an amino acid substitution on the second acetylcholinesterase in the Pirimicarb resistant strains of the peach potato aphid myzus persicae
Biochemical and Biophysical Research Communications, 2003Co-Authors: Takeshi Nabeshima, Toshinori Kozaki, Takashi Tomita, Yoshiaki KonoAbstract:cDNAs encoding two acetylcholinesterases (AChEs) were isolated from the peach potato aphid, Myzus persicae. MpAChE1 was orthologous and MpAChE2 was paralogous with the ace of Drosophila melanogaster. The deduced amino acid sequence of MpAChE1 cDNA was identical between the Pirimicarb susceptible and resistant strains. However, a single amino acid substitution of Ser431Phe on MpAchE2 was found in the Pirimicarb resistant strains. This substitution was located in the acyl pocket of the enzyme and was thought to alter the ligand specificity.
Guillermo Sebastian Natale - One of the best experts on this subject based on the ideXlab platform.
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lethal and sublethal effects of the Pirimicarb based formulation aficida on boana pulchella dumeril and bibron 1841 tadpoles anura hylidae
Ecotoxicology and Environmental Safety, 2018Co-Authors: Guillermo Sebastian Natale, Josefina Veracandioti, Ruiz C De Arcaute, Sonia Soloneski, Marcelo L LarramendyAbstract:Abstract Acute lethal and sublethal toxicity of the Pirimicarb-based commercial formulation Aficida ® were evaluated on Boana pulchella tadpoles. Whereas mortality was used as end point for lethality, frequency of micronuclei and other nuclear abnormalities as well as alterations in the frequency of erythroblasts in circulating blood as biomarkers for genotoxicity and cytotoxicity, respectively. Swimming, growth, developmental and morphological abnormalities were also employed as sublethal end points. Results show that the species is within the 13th percentile of the distribution of acute sensitivity of species to Pirimicarb for aquatic vertebrates. Results revealed values of 23.78 and 101.45 mg/L Pirimicarb as LC50 96 h for GS25 and GS36 tadpoles, respectively. The most evident effects were related with the swimming activity with NOEC and LOEC values within the 0.005–0.39 mg/L Pirimicarb concentration range. Aficida ® induced DNA damage at the chromosomal level by increasing micronuclei frequency and other nuclear abnormalities, i.e. , lobbed and notched nuclei and binucleated cells. Cellular cytotoxicity was found after Aficida ® treatment. The presence of abdominal oedemas in exposed organisms and thus flotation response of organisms could be proposed as a new sensitive exposure parameter. The multiple end point assessment approach used allowed a complete understanding the multi level of effects occurring by exposure to Pirimicarb, at least in B. pulchella .
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lethal and sublethal effects of the Pirimicarb based formulation aficida on boana pulchella dumeril and bibron 1841 tadpoles anura hylidae
Ecotoxicology and Environmental Safety, 2018Co-Authors: Guillermo Sebastian Natale, Josefina Veracandioti, Ruiz C De Arcaute, Sonia Soloneski, Marcelo L LarramendyAbstract:Abstract Acute lethal and sublethal toxicity of the Pirimicarb-based commercial formulation Aficida ® were evaluated on Boana pulchella tadpoles. Whereas mortality was used as end point for lethality, frequency of micronuclei and other nuclear abnormalities as well as alterations in the frequency of erythroblasts in circulating blood as biomarkers for genotoxicity and cytotoxicity, respectively. Swimming, growth, developmental and morphological abnormalities were also employed as sublethal end points. Results show that the species is within the 13th percentile of the distribution of acute sensitivity of species to Pirimicarb for aquatic vertebrates. Results revealed values of 23.78 and 101.45 mg/L Pirimicarb as LC50 96 h for GS25 and GS36 tadpoles, respectively. The most evident effects were related with the swimming activity with NOEC and LOEC values within the 0.005–0.39 mg/L Pirimicarb concentration range. Aficida ® induced DNA damage at the chromosomal level by increasing micronuclei frequency and other nuclear abnormalities, i.e. , lobbed and notched nuclei and binucleated cells. Cellular cytotoxicity was found after Aficida ® treatment. The presence of abdominal oedemas in exposed organisms and thus flotation response of organisms could be proposed as a new sensitive exposure parameter. The multiple end point assessment approach used allowed a complete understanding the multi level of effects occurring by exposure to Pirimicarb, at least in B. pulchella .