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Molecular characterisation of a sodium channel gene and identification of a Phe1538 to Ile mutation in citrus red mite, Panonychus citri
Author(s) -
Ding TianBo,
Zhong Rui,
Jiang XuanZhao,
Liao ChongYu,
Xia WenKai,
Liu Bin,
Dou Wei,
Wang JinJun
Publication year - 2015
Publication title -
pest management science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.296
H-Index - 125
eISSN - 1526-4998
pISSN - 1526-498X
DOI - 10.1002/ps.3802
Subject(s) - acaricide , biology , mite , knockdown resistance , point mutation , gene , genetics , pyrethroid , abamectin , mutant , sodium channel , botany , toxicology , pesticide , sodium , agronomy , chemistry , cyfluthrin , organic chemistry
BACKGROUND The citrus red mite, Panonychus citri ( McGregor ), is regarded as one of the most serious citrus pests in many countries and has developed high resistance to pyrethroids as a result of the intensive use of these acaricides. RESULTS The para sodium channel gene of P. citri (named PcNa v ), containing an entire coding region of 6729 bp, was cloned in this study. Three alternative splicing sites and 12 potential RNA editing sites were identified in PcNa v . Thus, exons alt 1 and alt 3‐v3 were found to be unique to PcNa v . Comparison of field fenpropathrin‐resistant ( WZ ) and susceptible ( LS ) strains identified the point mutation F1538I in IIIS6 of the sodium channel, which is known to confer strong resistance to pyrethroids in mites. Moreover, it was also found that the PcNa vmRNA was present during all life stages, and the transcript seems to be more abundant in larvae than in other developmental stages. CONCLUSION These results suggest that the F1538I mutation plays an important role in fenpropathrin resistance in citrus red mites. This is the first study of the sodium channel in P. citri and provides abundant information for further research on the mechanism of pyrethroid resistance. © 2014 Society of Chemical Industry