Biochemical and molecular diagnosis of insecticide resistance conferred by esterase, MACE, kdr and super-kdr based mechanisms in Italian strains of the peach potato aphid, Myzus persicae (Sulzer)

被引:34
作者
Criniti, A. [1 ,2 ]
Mazzoni, E.
Cassanelli, S. [1 ]
Cravedi, P. [2 ]
Tondelli, A. [3 ]
Bizzaro, D. [4 ]
Manicardi, G. C. [1 ]
机构
[1] Univ Modena, Dipartimento Sci Agrarie, I-42100 Reggio Emilia, Italy
[2] Univ Cattolica Sacro Cuore, Inst Entomol & Patol Vegetale, I-20123 Piacenza, Italy
[3] Ctr Ric Genom Postgenom Animale & Vegetale, Fiorenzula Darda, Italy
[4] Univ Politecn Marche, Inst Biol & Genet, Ancona, Italy
关键词
Myzus persicae; insecticide resistance; biochemical and molecular diagnosis; screening; RFLP-PCR; esterase; MACE; kdr; super-kdr; AChE;
D O I
10.1016/j.pestbp.2007.11.005
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
In this paper we analysed the basis of insecticide resistance in 59 Italian strains of the peach potato aphid Myzus persicae using both molecular and biochemical assays. Our data as a whole clearly indicate that most M. persicae strains (76.3%) have high or extremely high production of an esterase enzyme which sequester and detoxify insecticides with esteric group. Kdr genotypes conferring resistance towards pyrethoids are present in 57.7% of the analysed populations. Moreover, 26.5% of the kdr positive strains possess also the M918T mutation conferring super-kdr phenotype. Strains with modified AChE (MACE) are not so numerous (27.1%), although they can be found almost everywhere in Italy. Considering all the strains analysed, both MACE and kdr phenotypes are associated with high levels of esterase activity. In Central-Southern regions, kdr and MACE resistance mechanisms resulted in linkage disequilibrium. Bioassays performed in order to evaluate the efficacy of a pyrethroid insecticide against a strain possessing a F979S mutation within its paratype sodium channel gene suggests that this amino acid substitution could affect the sodium channel responsivity to pyrethroids. (c) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:168 / 174
页数:7
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