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Molecular mechanisms of Tetranychus urticae chemical adaptation in hop fields.

Piraneo TG, Bull J, Morales MA, Lavine LC, Walsh DB, Zhu F - Sci Rep (2015)

Bottom Line: Here, we investigated resistance ratios and distribution of multiple resistance-associated mutations in field collected T. urticae samples compared with a susceptible population.However, P450-mediated detoxification was observed and is a putative mechanism for abamectin resistance.Molecular mechanisms of T. urticae chemical adaptation in hopyards is imperative new information that will help growers develop effective and sustainable management strategies.

View Article: PubMed Central - PubMed

Affiliation: Irrigated Agriculture Research and Extension Center, Washington State University, Prosser, WA 99350, USA.

ABSTRACT
The two-spotted spider mite, Tetranychus urticae Koch is a major pest that feeds on >1,100 plant species. Many perennial crops including hop (Humulus lupulus) are routinely plagued by T. urticae infestations. Hop is a specialty crop in Pacific Northwest states, where 99% of all U.S. hops are produced. To suppress T. urticae, growers often apply various acaricides. Unfortunately T. urticae has been documented to quickly develop resistance to these acaricides which directly cause control failures. Here, we investigated resistance ratios and distribution of multiple resistance-associated mutations in field collected T. urticae samples compared with a susceptible population. Our research revealed that a mutation in the cytochrome b gene (G126S) in 35% tested T. urticae populations and a mutation in the voltage-gated sodium channel gene (F1538I) in 66.7% populations may contribute resistance to bifenazate and bifenthrin, respectively. No mutations were detected in Glutamate-gated chloride channel subunits tested, suggesting target site insensitivity may not be important in our hop T. urticae resistance to abamectin. However, P450-mediated detoxification was observed and is a putative mechanism for abamectin resistance. Molecular mechanisms of T. urticae chemical adaptation in hopyards is imperative new information that will help growers develop effective and sustainable management strategies.

No MeSH data available.


Related in: MedlinePlus

Pie charts showing proportions of resistance associated allele for G126S on cytb (A) and F1538I on VGSC (B).The colors green, blue, and orange stand for the susceptible allele, double alleles, and resistant allele, respectively.
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f4: Pie charts showing proportions of resistance associated allele for G126S on cytb (A) and F1538I on VGSC (B).The colors green, blue, and orange stand for the susceptible allele, double alleles, and resistant allele, respectively.

Mentions: Recent studies suggested that bifenazate resistance was closely correlated with mutation(s) in the mitochondrial cytb27. A combination of at least two cd1 helix mutations in the Qo pocket (G126S and I136T or G126S and S141F) and one mutation in the ef helix of Qo pocket (P262T) were linked with a high level of bifenazate resistance in T. urticae. We sequenced an 828 bp fragment of the T. urticae cytb gene, which included the G126, I136, S141, D161 and P262 sites (Fig. S2) that have been demonstrated to confer bifenazate resistance in T. urticae27. One amino acid substitution, G126S, was detected in T. urticae field populations. 35% of field samples field samples contained only the resistant allele, 20% contained both alleles (G/S) and 15% only the susceptible allele (G) (Table 4; Fig. 4A). Since the G126S mutation alone only causes low to moderate bifenazate resistance27, this result is consistent with the bifenazate resistance phenotype observed (Table 3).


Molecular mechanisms of Tetranychus urticae chemical adaptation in hop fields.

Piraneo TG, Bull J, Morales MA, Lavine LC, Walsh DB, Zhu F - Sci Rep (2015)

Pie charts showing proportions of resistance associated allele for G126S on cytb (A) and F1538I on VGSC (B).The colors green, blue, and orange stand for the susceptible allele, double alleles, and resistant allele, respectively.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4664861&req=5

f4: Pie charts showing proportions of resistance associated allele for G126S on cytb (A) and F1538I on VGSC (B).The colors green, blue, and orange stand for the susceptible allele, double alleles, and resistant allele, respectively.
Mentions: Recent studies suggested that bifenazate resistance was closely correlated with mutation(s) in the mitochondrial cytb27. A combination of at least two cd1 helix mutations in the Qo pocket (G126S and I136T or G126S and S141F) and one mutation in the ef helix of Qo pocket (P262T) were linked with a high level of bifenazate resistance in T. urticae. We sequenced an 828 bp fragment of the T. urticae cytb gene, which included the G126, I136, S141, D161 and P262 sites (Fig. S2) that have been demonstrated to confer bifenazate resistance in T. urticae27. One amino acid substitution, G126S, was detected in T. urticae field populations. 35% of field samples field samples contained only the resistant allele, 20% contained both alleles (G/S) and 15% only the susceptible allele (G) (Table 4; Fig. 4A). Since the G126S mutation alone only causes low to moderate bifenazate resistance27, this result is consistent with the bifenazate resistance phenotype observed (Table 3).

Bottom Line: Here, we investigated resistance ratios and distribution of multiple resistance-associated mutations in field collected T. urticae samples compared with a susceptible population.However, P450-mediated detoxification was observed and is a putative mechanism for abamectin resistance.Molecular mechanisms of T. urticae chemical adaptation in hopyards is imperative new information that will help growers develop effective and sustainable management strategies.

View Article: PubMed Central - PubMed

Affiliation: Irrigated Agriculture Research and Extension Center, Washington State University, Prosser, WA 99350, USA.

ABSTRACT
The two-spotted spider mite, Tetranychus urticae Koch is a major pest that feeds on >1,100 plant species. Many perennial crops including hop (Humulus lupulus) are routinely plagued by T. urticae infestations. Hop is a specialty crop in Pacific Northwest states, where 99% of all U.S. hops are produced. To suppress T. urticae, growers often apply various acaricides. Unfortunately T. urticae has been documented to quickly develop resistance to these acaricides which directly cause control failures. Here, we investigated resistance ratios and distribution of multiple resistance-associated mutations in field collected T. urticae samples compared with a susceptible population. Our research revealed that a mutation in the cytochrome b gene (G126S) in 35% tested T. urticae populations and a mutation in the voltage-gated sodium channel gene (F1538I) in 66.7% populations may contribute resistance to bifenazate and bifenthrin, respectively. No mutations were detected in Glutamate-gated chloride channel subunits tested, suggesting target site insensitivity may not be important in our hop T. urticae resistance to abamectin. However, P450-mediated detoxification was observed and is a putative mechanism for abamectin resistance. Molecular mechanisms of T. urticae chemical adaptation in hopyards is imperative new information that will help growers develop effective and sustainable management strategies.

No MeSH data available.


Related in: MedlinePlus