@article{dworkin_kennerly_tack_hutchinson_brown_mahaffey_gibson_2009, title={Genomic Consequences of Background Effects on scalloped Mutant Expressivity in the Wing of Drosophila melanogaster}, volume={181}, ISSN={["1943-2631"]}, DOI={10.1534/genetics.108.096453}, abstractNote={Genetic background effects contribute to the phenotypic consequences of mutations and are pervasive across all domains of life that have been examined, yet little is known about how they modify genetic systems. In part this is due to the lack of tractable model systems that have been explicitly developed to study the genetic and evolutionary consequences of background effects. In this study we demonstrate that phenotypic expressivity of the scallopedE3 (sdE3) mutation of Drosophila melanogaster is background dependent and is the result of at least one major modifier segregating between two standard lab wild-type strains. We provide evidence that at least one of the modifiers is linked to the vestigial region and demonstrate that the background effects modify the spatial distribution of known sd target genes in a genotype-dependent manner. In addition, microarrays were used to examine the consequences of genetic background effects on the global transcriptome. Expression differences between wild-type strains were found to be as large as or larger than the effects of mutations with substantial phenotypic effects, and expression differences between wild type and mutant varied significantly between genetic backgrounds. Significantly, we demonstrate that the epistatic interaction between sdE3 and an optomotor blind mutation is background dependent. The results are discussed within the context of developing a complex but more realistic view of the consequences of genetic background effects with respect to mutational analysis and studies of epistasis and cryptic genetic variation segregating in natural populations.}, number={3}, journal={GENETICS}, author={Dworkin, Ian and Kennerly, Erin and Tack, David and Hutchinson, Jennifer and Brown, Julie and Mahaffey, James and Gibson, Greg}, year={2009}, month={Mar}, pages={1065–1076} }
 @article{kennerly_idaghdour_olby_munana_gibson_2009, title={Pharmacogenetic association study of 30 genes with phenobarbital drug response in epileptic dogs}, volume={19}, ISSN={1744-6872}, url={http://dx.doi.org/10.1097/fpc.0b013e3283307cba}, DOI={10.1097/FPC.0b013e3283307cba}, abstractNote={BackgroundEpilepsy, with a prevalence as high as 6%, is the most common neurological disorder in dogs. Although several antiepileptic drugs are in common use, in one-third of all epileptic dogs, adequate seizure control is not achieved with a single medication, and hence a combinatorial drug treatment must be adopted. Exploration of the genetic mechanisms involved in drug response may provide better treatment options for epileptic patients. Methods and resultsA custom Illumina BeadChip was designed for high throughput genotyping of 384 single nucleotide polymorphisms in 30 genes involved in drug metabolism, drug targeting, and drug transport. A case–control association study of 125 epileptic dogs identified five genes with suggestive association to phenobarbital drug response: KCNQ3, P=0.0003; SNC2A2, P=0.0008; EPOX HYD, P=0.0005; ABCC4, P=0.0091; and GABRA2, P=0.0130. These associations are not significant after adjustment for multiple comparisons, but on functional grounds may tag strong candidate genes. The study was powered to detect alleles with at least 3.5-fold additive increases in responsiveness. A combined area under the curve value of 0.74 from receiver operating curve analysis also provides suggestive support for their consideration as canine pharmacogenetic markers. ConclusionFurther replication and assessment of breed specificity is required before these markers can be considered as predictive of responsiveness to phenobarbital in dogs.}, number={12}, journal={Pharmacogenetics and Genomics}, publisher={Ovid Technologies (Wolters Kluwer Health)}, author={Kennerly, Erin M. and Idaghdour, Youssef and Olby, Natasha J. and Munana, Karen R. and Gibson, Greg}, year={2009}, month={Dec}, pages={911–922} }
 @article{thomson_kennerly_olby_mickelson_hoffmann_dickinson_gibson_breen_2005, title={Microarray analysis of differentially expressed genes of primary tumors in the canine central nervous system}, volume={42}, ISSN={["1544-2217"]}, DOI={10.1354/vp.42-5-550}, abstractNote={The pathophysiologic similarities of many human and canine cancers support the role of the domestic dog as a model for brain tumor research. Here we report the construction of a custom canine brain-specific cDNA microarray and the analysis of gene expression patterns of several different types of canine brain tumor The microarray contained 4000 clones from a canine brain specific cDNA library including 2161 clones that matched known genes or expressed sequence tags (ESTs) and 25 cancer-related genes. Our study included 16 brain tumors (seven meningiomas, five glial tumors, two ependymomas, and two choroid plexus papillomas) from a variety of different dog breeds. We identified several genes previously found to be differentially expressed in human brain tumors. This suggests that human and canine brain tumors share a common pathogenesis. In addition, we also found differentially expressed genes unique to either meningiomas or the glial tumors. This report represents the first global gene expression analysis of different types of canine brain tumors by cDNA microarrays and might aid in the identification of potential candidate genes involved in tumor formation and progression.}, number={5}, journal={VETERINARY PATHOLOGY}, author={Thomson, SAM and Kennerly, E and Olby, N and Mickelson, JR and Hoffmann, DE and Dickinson, PJ and Gibson, G and Breen, M}, year={2005}, month={Sep}, pages={550–558} }