@article{reid_sun_becnel_clark_scott_2019, title={Overexpression of a glutathione S-transferase (Mdgst) and a galactosyltransferase-like gene (Mdgt1) is responsible for imidacloprid resistance in house flies}, volume={75}, ISSN={["1526-4998"]}, DOI={10.1002/ps.5125}, abstractNote={BACKGROUND
Neonicotinoids are the largest class of insecticides and are used for control of house fly populations at animal production facilities throughout the world. There have been several reports of neonicotinoid resistance in house fly populations, but identification of the factors involved in resistance has proven challenging. The KS8S3 population of house flies is highly resistant to the neonicotinoid insecticide imidacloprid due to two factors: one on chromosome 3 and one on chromosome 4.


RESULTS
A comparative transcriptomic approach was used, followed by validation using transgenic Drosophila melanogaster to investigate the genes responsible for resistance in the KS8S3 strain. Overexpression of a microsomal glutathione S-transferase (Mdgst) was identified as the factor likely responsible for resistance on chromosome 3. Resistance on chromosome 4 appears to be due to an unidentified trans-regulatory gene which causes overexpression of a galactosyltransferase-like gene (Mdgt1). No single nucleotide polymorphisms were found that could be associated with imidacloprid resistance.


CONCLUSION
Identification of the underlying processes that cause imidacloprid resistance is an important first step towards the development of novel and sensitive resistance monitoring techniques. It will be valuable to investigate if overexpression of Mdgst and Mdgt1 are found in other imidacloprid resistant populations. © 2018 Society of Chemical Industry.}, number={1}, journal={PEST MANAGEMENT SCIENCE}, author={Reid, William R. and Sun, Haina and Becnel, James J. and Clark, Andrew G. and Scott, Jeffrey G.}, year={2019}, month={Jan}, pages={37–44} }
 @article{reid_pilitt_alford_cervantes-medina_yu_aluvihare_harrell_david a. o'brochta_2018, title={An Anopheles stephensi Promoter-Trap: Augmenting Genome Annotation and Functional Genomics}, volume={8}, ISSN={["2160-1836"]}, DOI={10.1534/g3.118.200347}, abstractNote={The piggyBac transposon was modified to generate gene trap constructs, which were then incorporated into the genome of the Asian malaria vector, Anopheles stephensi and remobilized through genetic crosses using a piggyBac transposase expressing line. A total of 620 remobilization events were documented, and 73 were further characterized at the DNA level to identify patterns in insertion site preferences, remobilization frequencies, and remobilization patterns. Overall, the use of the tetameric AmCyan reporter as the fusion peptide displayed a preference for insertion into the 5′-end of transcripts. Notably 183 – 44882 bp upstream of the An. stephensi v1.0 ab initio gene models, which demonstrated that the promoter regions for the genes of An. stephensi are further upstream of the 5′-proximal regions of the genes in the ab inito models than may be otherwise predicted. RNA-Seq transcript coverage supported the insertion of the splice acceptor gene trap element into 5′-UTR introns for nearly half of all insertions identified. The use of a gene trap element that prefers insertion into the 5′-end of genes supports the use of this technology for the random generation of knock-out mutants, as well as the experimental confirmation of 5′-UTR introns in An. stephensi.}, number={10}, journal={G3-GENES GENOMES GENETICS}, author={Reid, William and Pilitt, Kristina and Alford, Robert and Cervantes-Medina, Adriana and Yu, Hao and Aluvihare, Channa and Harrell, Rob and David A. O'Brochta}, year={2018}, month={Oct}, pages={3119–3130} }
 @article{lu_wang_xu_shen_wei_li_reid_he_2017, title={Adaptation of acaricide stress facilitates Tetranychus urticae expanding against Tetranychus cinnabarinus in China}, volume={7}, number={4}, journal={Ecology and Evolution}, author={Lu, W. C. and Wang, M. Y. and Xu, Z. F. and Shen, G. M. and Wei, P. and Li, M. and Reid, W. and He, L.}, year={2017}, pages={1233–1249} }