@article{dworkin_anderson_idaghdour_parker_stone_gibson_2011, title={The Effects of Weak Genetic Perturbations on the Transcriptome of the Wing Imaginal Disc and Its Association With Wing Shape in Drosophila melanogaster}, volume={187}, ISSN={["1943-2631"]}, DOI={10.1534/genetics.110.125922}, abstractNote={Abstract
               A major objective of genomics is to elucidate the mapping between genotypic and phenotypic space as a step toward understanding how small changes in gene function can lead to elaborate phenotypic changes. One approach that has been utilized is to examine overall patterns of covariation between phenotypic variables of interest, such as morphology, physiology, and behavior, and underlying aspects of gene activity, in particular transcript abundance on a genome-wide scale. Numerous studies have demonstrated that such patterns of covariation occur, although these are often between samples with large numbers of unknown genetic differences (different strains or even species) or perturbations of large effect (sexual dimorphism or strong loss-of-function mutations) that may represent physiological changes outside of the normal experiences of the organism. We used weak mutational perturbations in genes affecting wing development in Drosophila melanogaster that influence wing shape relative to a co-isogenic wild type. We profiled transcription of 1150 genes expressed during wing development in 27 heterozygous mutants, as well as their co-isogenic wild type and one additional wild-type strain. Despite finding clear evidence of expression differences between mutants and wild type, transcriptional profiles did not covary strongly with shape, suggesting that information from transcriptional profiling may not generally be predictive of final phenotype. We discuss these results in the light of possible attractor states of gene expression and how this would affect interpretation of covariation between transcriptional profiles and other phenotypes.}, number={4}, journal={GENETICS}, author={Dworkin, Ian and Anderson, Julie A. and Idaghdour, Youssef and Parker, Erin Kennerly and Stone, Eric A. and Gibson, Greg}, year={2011}, month={Apr}, pages={1171–U314} }
 @article{idaghdour_czika_shianna_lee_visscher_martin_miclaus_jadallah_goldstein_wolfinger_et al._2010, title={Geographical genomics of human leukocyte gene expression variation in southern Morocco}, volume={42}, ISSN={["1546-1718"]}, DOI={10.1038/ng.495}, abstractNote={Greg Gibson and colleagues report an analysis of gene expression variation in relation to environmental geography and ethnicity in blood leukocyte samples from individuals in rural and urban southern Morocco. The study determined the contributions of geography and ethnicity to associations between genotypes and transcript abundance. Studies of the genetics of gene expression can identify expression SNPs (eSNPs) that explain variation in transcript abundance. Here we address the robustness of eSNP associations to environmental geography and population structure in a comparison of 194 Arab and Amazigh individuals from a city and two villages in southern Morocco. Gene expression differed between pairs of locations for up to a third of all transcripts, with notable enrichment of transcripts involved in ribosomal biosynthesis and oxidative phosphorylation. Robust associations were observed in the leukocyte samples: cis eSNPs (P < 10−08) were identified for 346 genes, and trans eSNPs (P < 10−11) for 10 genes. All of these associations were consistent both across the three sample locations and after controlling for ancestry and relatedness. No evidence of large-effect trans-acting mediators of the pervasive environmental influence was found; instead, genetic and environmental factors acted in a largely additive manner.}, number={1}, journal={NATURE GENETICS}, author={Idaghdour, Youssef and Czika, Wendy and Shianna, Kevin V. and Lee, Sang H. and Visscher, Peter M. and Martin, Hilary C. and Miclaus, Kelci and Jadallah, Sami J. and Goldstein, David B. and Wolfinger, Russell D. and et al.}, year={2010}, month={Jan}, pages={62–U79} }
 @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} }