@article{molo_white_cornish_gell_baars_singh_carbone_isakeit_wise_woloshuk_et al._2022, title={Asymmetrical lineage introgression and recombination in populations of Aspergillus flavus: Implications for biological control}, volume={17}, ISSN={["1932-6203"]}, url={https://doi.org/10.1371/journal.pone.0276556}, DOI={10.1371/journal.pone.0276556}, abstractNote={Aspergillus flavusis an agriculturally important fungus that causes ear rot of maize and produces aflatoxins, of which B1is the most carcinogenic naturally-produced compound. In the US, the management of aflatoxins includes the deployment of biological control agents that comprise two nonaflatoxigenicA.flavusstrains, either Afla-Guard (member of lineage IB) or AF36 (lineage IC). We used genotyping-by-sequencing to examine the influence of both biocontrol agents on native populations ofA.flavusin cornfields in Texas, North Carolina, Arkansas, and Indiana. This study examined up to 27,529 single-nucleotide polymorphisms (SNPs) in a total of 815A.flavusisolates, and 353 genome-wide haplotypes sampled before biocontrol application, three months after biocontrol application, and up to three years after initial application. Here, we report that the two distinctA.flavusevolutionary lineages IB and IC differ significantly in their frequency distributions across states. We provide evidence of increased unidirectional gene flow from lineage IB into IC, inferred to be due to the applied Afla-Guard biocontrol strain. Genetic exchange and recombination of biocontrol strains with native strains was detected in as little as three months after biocontrol application and up to one and three years later. There was limited inter-lineage migration in the untreated fields. These findings suggest that biocontrol products that include strains from lineage IB offer the greatest potential for sustained reductions in aflatoxin levels over several years. This knowledge has important implications for developing new biocontrol strategies.}, number={10}, journal={PLOS ONE}, author={Molo, Megan S. and White, James B. and Cornish, Vicki and Gell, Richard M. and Baars, Oliver and Singh, Rakhi and Carbone, Mary Anna and Isakeit, Thomas and Wise, Kiersten A. and Woloshuk, Charles P. and et al.}, editor={Nierman, William C.Editor}, year={2022}, month={Oct} } @article{baker_carbone_huang_anholt_mackay_2021, title={Genetic basis of variation in cocaine and methamphetamine consumption in outbred populations of Drosophila melanogaster}, volume={118}, ISSN={["0027-8424"]}, DOI={10.1073/pnas.2104131118}, abstractNote={Significance}, number={23}, journal={PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA}, author={Baker, Brandon M. and Carbone, Mary Anna and Huang, Wen and Anholt, Robert R. H. and Mackay, Trudy F. C.}, year={2021}, month={Jun} } @article{tallo_duncan_yamamoto_slaydon_arya_turlapati_mackay_carbone_2021, title={Heat shock proteins and small nucleolar RNAs are dysregulated in a Drosophila model for feline hypertrophic cardiomyopathy}, volume={11}, ISSN={["2160-1836"]}, DOI={10.1093/g3journal/jkaa014}, abstractNote={Abstract}, number={1}, journal={G3-GENES GENOMES GENETICS}, author={Tallo, Christian A. and Duncan, Laura H. and Yamamoto, Akihiko H. and Slaydon, Joshua D. and Arya, Gunjan H. and Turlapati, Lavanya and Mackay, Trudy F. C. and Carbone, Mary A.}, year={2021}, month={Jan} } @article{everett_huang_zhou_carbone_lyman_arya_geisz_ma_morgante_st armour_et al._2020, title={Gene expression networks in the Drosophila Genetic Reference Panel}, volume={30}, ISSN={["1549-5469"]}, DOI={10.1101/gr.257592.119}, abstractNote={A major challenge in modern biology is to understand how naturally occurring variation in DNA sequences affects complex organismal traits through networks of intermediate molecular phenotypes. This question is best addressed in a genetic mapping population in which all molecular polymorphisms are known and for which molecular endophenotypes and complex traits are assessed on the same genotypes. Here, we performed deep RNA sequencing of 200 Drosophila Genetic Reference Panel inbred lines with complete genome sequences and for which phenotypes of many quantitative traits have been evaluated. We mapped expression quantitative trait loci for annotated genes, novel transcribed regions, transposable elements, and microbial species. We identified host variants that affect expression of transposable elements, independent of their copy number, as well as microbiome composition. We constructed sex-specific expression quantitative trait locus regulatory networks. These networks are enriched for novel transcribed regions and target genes in heterochromatin and euchromatic regions of reduced recombination, as well as genes regulating transposable element expression. This study provides new insights regarding the role of natural genetic variation in regulating gene expression and generates testable hypotheses for future functional analyses.}, number={3}, journal={GENOME RESEARCH}, author={Everett, Logan J. and Huang, Wen and Zhou, Shanshan and Carbone, Mary Anna and Lyman, Richard F. and Arya, Gunjan H. and Geisz, Matthew S. and Ma, Junwu and Morgante, Fabio and St Armour, Genevieve and et al.}, year={2020}, month={Mar}, pages={485–496} } @article{huang_carbone_lyman_anholt_mackay_2020, title={Genotype by environment interaction for gene expression in Drosophila melanogaster}, volume={11}, ISSN={["2041-1723"]}, DOI={10.1038/s41467-020-19131-y}, abstractNote={Abstract}, number={1}, journal={NATURE COMMUNICATIONS}, author={Huang, Wen and Carbone, Mary Anna and Lyman, Richard F. and Anholt, Robert R. H. and Mackay, Trudy F. C.}, year={2020}, month={Oct} } @article{gabrawy_campbell_carbone_morozova_arya_turlapati_walston_starz-gaiano_everett_mackay_et al._2019, title={Lisinopril Preserves Physical Resilience and Extends Life Span in a Genotype-Specific Manner in Drosophila melanogaster}, volume={74}, ISSN={["1758-535X"]}, DOI={10.1093/gerona/glz152}, abstractNote={Abstract}, number={12}, journal={JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES}, author={Gabrawy, Mariann M. and Campbell, Sarah and Carbone, Mary Anna and Morozova, Tatiana V and Arya, Gunjan H. and Turlapati, Lavanya B. and Walston, Jeremy D. and Starz-Gaiano, Michelle and Everett, Logan and Mackay, Trudy F. C. and et al.}, year={2019}, month={Dec}, pages={1844–1852} } @article{garcia_carbone_mackay_anholt_2017, title={Regulation of Drosophila Lifespan by bellwether Promoter Alleles}, volume={7}, ISSN={2045-2322}, url={http://dx.doi.org/10.1038/S41598-017-04530-X}, DOI={10.1038/S41598-017-04530-X}, abstractNote={Abstract}, number={1}, journal={Scientific Reports}, publisher={Springer Nature}, author={Garcia, Júlia Frankenberg and Carbone, Mary Anna and Mackay, Trudy F. C. and Anholt, Robert R. H.}, year={2017}, month={Jun} } @article{carbone_yamamoto_huang_lyman_meadors_yamamoto_anholt_mackay_2016, title={Genetic architecture of natural variation in visual senescence in Drosophila}, volume={113}, ISSN={0027-8424 1091-6490}, url={http://dx.doi.org/10.1073/PNAS.1613833113}, DOI={10.1073/PNAS.1613833113}, abstractNote={Significance}, number={43}, journal={Proceedings of the National Academy of Sciences}, publisher={Proceedings of the National Academy of Sciences}, author={Carbone, Mary Anna and Yamamoto, Akihiko and Huang, Wen and Lyman, Rachel A. and Meadors, Tess Brune and Yamamoto, Ryoan and Anholt, Robert R. H. and Mackay, Trudy F. C.}, year={2016}, month={Oct}, pages={E6620–E6629} } @article{shorter_couch_huang_carbone_peiffer_anholt_mackay_2015, title={Genetic architecture of natural variation in Drosophila melanogaster aggressive behavior}, volume={112}, ISSN={0027-8424 1091-6490}, url={http://dx.doi.org/10.1073/PNAS.1510104112}, DOI={10.1073/PNAS.1510104112}, abstractNote={Significance}, number={27}, journal={Proceedings of the National Academy of Sciences}, publisher={Proceedings of the National Academy of Sciences}, author={Shorter, John and Couch, Charlene and Huang, Wen and Carbone, Mary Anna and Peiffer, Jason and Anholt, Robert R. H. and Mackay, Trudy F. C.}, year={2015}, month={Jun}, pages={E3555–E3563} } @article{dembeck_huang_carbone_mackay_2015, title={Genetic basis of natural variation in body pigmentation in Drosophila melanogaster}, volume={9}, ISSN={1933-6934 1933-6942}, url={http://dx.doi.org/10.1080/19336934.2015.1102807}, DOI={10.1080/19336934.2015.1102807}, abstractNote={Body pigmentation in insects and other organisms is typically variable within and between species and is often associated with fitness. Regulatory variants with large effects at bab1, t and e affect variation in abdominal pigmentation in several populations of Drosophila melanogaster. Recently, we performed a genome wide association (GWA) analysis of variation in abdominal pigmentation using the inbred, sequenced lines of the Drosophila Genetic Reference Panel (DGRP). We confirmed the large effects of regulatory variants in bab1, t and e; identified 81 additional candidate genes; and validated 17 candidate genes (out of 28 tested) using RNAi knockdown of gene expression and mutant alleles. However, these analyses are imperfect proxies for the effects of segregating variants. Here, we describe the results of an extreme quantitative trait locus (xQTL) GWA analysis of female body pigmentation in an outbred population derived from light and dark DGRP lines. We replicated the effects on pigmentation of 28 genes implicated by the DGRP GWA study, including bab1, t and e and 7 genes previously validated by RNAi and/or mutant analyses. We also identified many additional loci. The genetic architecture of Drosophila pigmentation is complex, with a few major genes and many other loci with smaller effects.}, number={2}, journal={Fly}, publisher={Informa UK Limited}, author={Dembeck, Lauren M and Huang, Wen and Carbone, Mary Anna and Mackay, Trudy F C}, year={2015}, month={Apr}, pages={75–81} } @article{huang_carbone_magwire_peiffer_lyman_stone_anholt_mackay_2015, title={Genetic basis of transcriptome diversity in Drosophila melanogaster}, volume={112}, ISSN={0027-8424 1091-6490}, url={http://dx.doi.org/10.1073/PNAS.1519159112}, DOI={10.1073/PNAS.1519159112}, abstractNote={Significance}, number={44}, journal={Proceedings of the National Academy of Sciences}, publisher={Proceedings of the National Academy of Sciences}, author={Huang, Wen and Carbone, Mary Anna and Magwire, Michael M. and Peiffer, Jason A. and Lyman, Richard F. and Stone, Eric A. and Anholt, Robert R. H. and Mackay, Trudy F. C.}, year={2015}, month={Oct}, pages={E6010–E6019} } @article{huang_massouras_inoue_peiffer_ramia_tarone_turlapati_zichner_zhu_lyman_et al._2014, title={Natural variation in genome architecture among 205 Drosophila melanogaster Genetic Reference Panel lines}, volume={24}, number={7}, journal={Genome Research}, author={Huang, W. and Massouras, A. and Inoue, Y. and Peiffer, J. and Ramia, M. and Tarone, A. M. and Turlapati, L. and Zichner, T. and Zhu, D. H. and Lyman, R. F. and et al.}, year={2014}, pages={1193–1208} } @misc{anholt_carbone_2013, title={A molecular mechanism for glaucoma: endoplasmic reticulum stress and the unfolded protein response}, volume={19}, ISSN={["1471-499X"]}, DOI={10.1016/j.molmed.2013.06.005}, abstractNote={Primary open angle glaucoma (POAG) is a common late-onset neurodegenerative disease. Ocular hypertension represents a major risk factor, but POAG etiology remains poorly understood. Some cases of early-onset congenital glaucoma and adult POAG are linked to mutations in myocilin, a secreted protein of poorly defined function. Transgenic overexpression of myocilin in Drosophila and experiments in mice and human populations implicate the unfolded protein response (UPR) in the pathogenesis of glaucoma. We postulate that compromised ability of the UPR to eliminate misfolded mutant or damaged proteins, including myocilin, causes endoplasmic reticulum stress, resulting in functional impairment of trabecular meshwork cells that regulate intraocular pressure. This mechanism of POAG is reminiscent of other age-dependent neurodegenerative diseases that involve accumulation of protein aggregates.}, number={10}, journal={TRENDS IN MOLECULAR MEDICINE}, author={Anholt, Robert R. H. and Carbone, Mary Anna}, year={2013}, month={Oct}, pages={586–593} } @article{huang_richards_carbone_zhu_anholt_ayroles_duncan_jordan_lawrence_magwire_et al._2012, title={Epistasis dominates the genetic architecture of Drosophila quantitative traits}, volume={109}, ISSN={0027-8424 1091-6490}, url={http://dx.doi.org/10.1073/pnas.1213423109}, DOI={10.1073/pnas.1213423109}, abstractNote={ Epistasis—nonlinear genetic interactions between polymorphic loci—is the genetic basis of canalization and speciation, and epistatic interactions can be used to infer genetic networks affecting quantitative traits. However, the role that epistasis plays in the genetic architecture of quantitative traits is controversial. Here, we compared the genetic architecture of three Drosophila life history traits in the sequenced inbred lines of the Drosophila melanogaster Genetic Reference Panel (DGRP) and a large outbred, advanced intercross population derived from 40 DGRP lines (Flyland). We assessed allele frequency changes between pools of individuals at the extremes of the distribution for each trait in the Flyland population by deep DNA sequencing. The genetic architecture of all traits was highly polygenic in both analyses. Surprisingly, none of the SNPs associated with the traits in Flyland replicated in the DGRP and vice versa. However, the majority of these SNPs participated in at least one epistatic interaction in the DGRP. Despite apparent additive effects at largely distinct loci in the two populations, the epistatic interactions perturbed common, biologically plausible, and highly connected genetic networks. Our analysis underscores the importance of epistasis as a principal factor that determines variation for quantitative traits and provides a means to uncover genetic networks affecting these traits. Knowledge of epistatic networks will contribute to our understanding of the genetic basis of evolutionarily and clinically important traits and enhance predictive ability at an individualized level in medicine and agriculture. }, number={39}, journal={Proceedings of the National Academy of Sciences}, publisher={Proceedings of the National Academy of Sciences}, author={Huang, W. and Richards, S. and Carbone, M. A. and Zhu, D. and Anholt, R. R. H. and Ayroles, J. F. and Duncan, L. and Jordan, K. W. and Lawrence, F. and Magwire, M. M. and et al.}, year={2012}, month={Sep}, pages={15553–15559} } @article{mackay_richards_stone_barbadilla_ayroles_zhu_casillas_han_magwire_cridland_et al._2012, title={The Drosophila melanogaster Genetic Reference Panel}, volume={482}, ISSN={0028-0836 1476-4687}, url={http://dx.doi.org/10.1038/nature10811}, DOI={10.1038/nature10811}, abstractNote={A major challenge of biology is understanding the relationship between molecular genetic variation and variation in quantitative traits, including fitness. This relationship determines our ability to predict phenotypes from genotypes and to understand how evolutionary forces shape variation within and between species. Previous efforts to dissect the genotype–phenotype map were based on incomplete genotypic information. Here, we describe the Drosophila melanogaster Genetic Reference Panel (DGRP), a community resource for analysis of population genomics and quantitative traits. The DGRP consists of fully sequenced inbred lines derived from a natural population. Population genomic analyses reveal reduced polymorphism in centromeric autosomal regions and the X chromosome, evidence for positive and negative selection, and rapid evolution of the X chromosome. Many variants in novel genes, most at low frequency, are associated with quantitative traits and explain a large fraction of the phenotypic variance. The DGRP facilitates genotype–phenotype mapping using the power of Drosophila genetics. A new resource for the analysis of population genomics and quantitative traits, the Drosophila melanogaster Genetic Reference Panel is presented. The Drosophila melanogaster Genetic Reference Panel (DGRP) is a community resource charting the molecular and phenotypic variation in 168 fully sequenced fruitfly strains derived from a single outbred natural population. The first set of analyses of DGRP data provides insights into the genomic landscape of genetic variation, positive and negative selection, and rapid evolution of the X chromosome. The results also reveal many low frequency variants in novel loci that are associated with quantitative traits, and explain a large fraction of the phenotypic variance.}, number={7384}, journal={Nature}, publisher={Springer Science and Business Media LLC}, author={Mackay, Trudy F. C. and Richards, Stephen and Stone, Eric A. and Barbadilla, Antonio and Ayroles, Julien F. and Zhu, Dianhui and Casillas, Sònia and Han, Yi and Magwire, Michael M. and Cridland, Julie M. and et al.}, year={2012}, month={Feb}, pages={173–178} } @article{zwarts_magwire_carbone_versteven_herteleer_anholt_callaerts_mackay_2011, title={Complex genetic architecture of Drosophila aggressive behavior}, volume={108}, ISSN={0027-8424 1091-6490}, url={http://dx.doi.org/10.1073/pnas.1113877108}, DOI={10.1073/pnas.1113877108}, abstractNote={ Epistasis and pleiotropy feature prominently in the genetic architecture of quantitative traits but are difficult to assess in outbred populations. We performed a diallel cross among coisogenic Drosophila P -element mutations associated with hyperaggressive behavior and showed extensive epistatic and pleiotropic effects on aggression, brain morphology, and genome-wide transcript abundance in head tissues. Epistatic interactions were often of greater magnitude than homozygous effects, and the topology of epistatic networks varied among these phenotypes. The transcriptional signatures of homozygous and double heterozygous genotypes derived from the six mutations imply a large mutational target for aggressive behavior and point to evolutionarily conserved genetic mechanisms and neural signaling pathways affecting this universal fitness trait. }, number={41}, journal={Proceedings of the National Academy of Sciences}, publisher={Proceedings of the National Academy of Sciences}, author={Zwarts, L. and Magwire, M. M. and Carbone, M. A. and Versteven, M. and Herteleer, L. and Anholt, R. R. H. and Callaerts, P. and Mackay, T. F. C.}, year={2011}, month={Sep}, pages={17070–17075} } @article{carbone_chen_hughes_weinreb_zabriskie_zhang_anholt_2011, title={Genes of the Unfolded Protein Response Pathway Harbor Risk Alleles for Primary Open Angle Glaucoma}, volume={6}, ISSN={["1932-6203"]}, DOI={10.1371/journal.pone.0020649}, abstractNote={The statistical power of genome-wide association (GWA) studies to detect risk alleles for human diseases is limited by the unfavorable ratio of SNPs to study subjects. This multiple testing problem can be surmounted with very large population sizes when common alleles of large effects give rise to disease status. However, GWA approaches fall short when many rare alleles may give rise to a common disease, or when the number of subjects that can be recruited is limited. Here, we demonstrate that this multiple testing problem can be overcome by a comparative genomics approach in which an initial genome-wide screen in a genetically amenable model organism is used to identify human orthologues that may harbor risk alleles for adult-onset primary open angle glaucoma (POAG). Glaucoma is a major cause of blindness, which affects over 60 million people worldwide. Several genes have been associated with juvenile onset glaucoma, but genetic factors that predispose to adult onset primary open angle glaucoma (POAG) remain largely unknown. Previous genome-wide analysis in a Drosophila ocular hypertension model identified transcripts with altered regulation and showed induction of the unfolded protein response (UPR) upon overexpression of transgenic human glaucoma-associated myocilin (MYOC). We selected 16 orthologous genes with 62 polymorphic markers and identified in two independent human populations two genes of the UPR that harbor POAG risk alleles, BIRC6 and PDIA5. Thus, effectiveness of the UPR in response to accumulation of misfolded or aggregated proteins may contribute to the pathogenesis of POAG and provide targets for early therapeutic intervention.}, number={5}, journal={PLOS ONE}, author={Carbone, Mary Anna and Chen, Yuhong and Hughes, Guy A. and Weinreb, Robert N. and Zabriskie, Norman A. and Zhang, Kang and Anholt, Robert R. H.}, year={2011}, month={May} } @article{morozova_ayroles_jordan_duncan_carbone_lyman_stone_govindaraju_ellison_mackay_et al._2009, title={Alcohol Sensitivity in Drosophila: Translational Potential of Systems Genetics}, volume={183}, ISSN={["1943-2631"]}, DOI={10.1534/genetics.109.107490}, abstractNote={Abstract}, number={2}, journal={GENETICS}, author={Morozova, Tatiana V. and Ayroles, Julien F. and Jordan, Katherine W. and Duncan, Laura H. and Carbone, Mary Anna and Lyman, Richard E. and Stone, Eric A. and Govindaraju, Diddahally R. and Ellison, R. Curtis and Mackay, Trudy F. C. and et al.}, year={2009}, month={Oct}, pages={733–745} } @article{harbison_carbone_ayroles_stone_lyman_mackay_2009, title={Co-regulated transcriptional networks contribute to natural genetic variation in Drosophila sleep}, volume={41}, ISSN={["1546-1718"]}, DOI={10.1038/ng.330}, abstractNote={Sleep disorders are common in humans, and sleep loss increases the risk of obesity and diabetes. Studies in Drosophila have revealed molecular pathways and neural tissues regulating sleep; however, genes that maintain genetic variation for sleep in natural populations are unknown. Here, we characterized sleep in 40 wild-derived Drosophila lines and observed abundant genetic variation in sleep architecture. We associated sleep with genome-wide variation in gene expression to identify candidate genes. We independently confirmed that molecular polymorphisms in Catsup (Catecholamines up) are associated with variation in sleep and that P-element mutations in four candidate genes affect sleep and gene expression. Transcripts associated with sleep grouped into biologically plausible genetically correlated transcriptional modules. We confirmed co-regulated gene expression using P-element mutants. Quantitative genetic analysis of natural phenotypic variation is an efficient method for revealing candidate genes and pathways.}, number={3}, journal={NATURE GENETICS}, author={Harbison, Susan T. and Carbone, Mary Anna and Ayroles, Julien F. and Stone, Eric A. and Lyman, Richard F. and Mackay, Trudy F. C.}, year={2009}, month={Mar}, pages={371–375} } @article{ayroles_carbone_stone_jordan_lyman_magwire_rollmann_duncan_lawrence_anholt_et al._2009, title={Systems genetics of complex traits in Drosophila melanogaster}, volume={41}, ISSN={["1546-1718"]}, DOI={10.1038/ng.332}, abstractNote={Determining the genetic architecture of complex traits is challenging because phenotypic variation arises from interactions between multiple, environmentally sensitive alleles. We quantified genome-wide transcript abundance and phenotypes for six ecologically relevant traits in D. melanogaster wild-derived inbred lines. We observed 10,096 genetically variable transcripts and high heritabilities for all organismal phenotypes. The transcriptome is highly genetically intercorrelated, forming 241 transcriptional modules. Modules are enriched for transcripts in common pathways, gene ontology categories, tissue-specific expression and transcription factor binding sites. The high degree of transcriptional connectivity allows us to infer genetic networks and the function of predicted genes from annotations of other genes in the network. Regressions of organismal phenotypes on transcript abundance implicate several hundred candidate genes that form modules of biologically meaningful correlated transcripts affecting each phenotype. Overlapping transcripts in modules associated with different traits provide insight into the molecular basis of pleiotropy between complex traits.}, number={3}, journal={NATURE GENETICS}, author={Ayroles, Julien F. and Carbone, Mary Anna and Stone, Eric A. and Jordan, Katherine W. and Lyman, Richard F. and Magwire, Michael M. and Rollmann, Stephanie M. and Duncan, Laura H. and Lawrence, Faye and Anholt, Robert R. H. and et al.}, year={2009}, month={Mar}, pages={299–307} } @misc{propper_moore_mills-koonce_halpern_hill-soderlund_calkins_carbone_cox_2008, title={Gene-environment contributions to the development of infant vagal reactivity: The interaction of dopamine and maternal sensitivity}, volume={79}, ISSN={["1467-8624"]}, DOI={10.1111/j.1467-8624.2008.01194.x}, abstractNote={This study investigated dopamine receptor genes (DRD2 and DRD4) and maternal sensitivity as predictors of infant respiratory sinus arrhythmia (RSA) and RSA reactivity, purported indices of vagal tone and vagal regulation, in a challenge task at 3, 6, and 12 months in 173 infant–mother dyads. Hierarchical linear modeling (HLM) revealed that at 3 and 6 months, RSA withdrawal in response to maternal separation was greater (suggesting expected physiological regulation) in infants without the DRD2 risk allele than those with the risk allele. At 12 months, infants with the risk allele who were also exposed to maternal sensitivity showed levels of RSA withdrawal comparable to infants who were not at genetic risk. Findings demonstrate the importance of developmental analysis of gene–environment interaction.}, number={5}, journal={CHILD DEVELOPMENT}, author={Propper, Cathi and Moore, Ginger A. and Mills-Koonce, W. Roger and Halpern, Carolyn Tucker and Hill-Soderlund, Ashley L. and Calkins, Susan D. and Carbone, Mary Anna and Cox, Martha}, year={2008}, pages={1377–1394} } @article{sambandan_carbone_anholt_mackay_2008, title={Phenotypic plasticity and genotype by environment interaction for olfactory behavior in Drosophila melanogaster}, volume={179}, ISSN={["0016-6731"]}, DOI={10.1534/genetics.108.086769}, abstractNote={Abstract}, number={2}, journal={GENETICS}, author={Sambandan, Deepa and Carbone, Mary Anna and Anholt, Robert R. H. and Mackay, Trudy E. C.}, year={2008}, month={Jun}, pages={1079–1088} } @article{propper_willoughby_halpern_carbone_cox_2007, title={Parenting quality, DRD4, and the prediction of externalizing and internalizing behaviors in early childhood}, volume={49}, ISSN={0012-1630 1098-2302}, url={http://dx.doi.org/10.1002/dev.20249}, DOI={10.1002/dev.20249}, abstractNote={Abstract}, number={6}, journal={Developmental Psychobiology}, publisher={Wiley}, author={Propper, C. and Willoughby, M. and Halpern, C.T. and Carbone, M.A. and Cox, M.}, year={2007}, pages={619–632} } @article{carbone_jordan_lyman_harbison_leips_morgan_deluca_awadalla_mackay_2006, title={Phenotypic variation and natural selection at Catsup, a pleiotropic quantitative trait gene in Drosphila}, volume={16}, ISSN={["1879-0445"]}, DOI={10.1016/j.cub.2006.03.051}, abstractNote={Quantitative traits are shaped by networks of pleiotropic genes . To understand the mechanisms that maintain genetic variation for quantitative traits in natural populations and to predict responses to artificial and natural selection, we must evaluate pleiotropic effects of underlying quantitative trait genes and define functional allelic variation at the level of quantitative trait nucleotides (QTNs). Catecholamines up (Catsup), which encodes a negative regulator of tyrosine hydroxylase , the rate-limiting step in the synthesis of the neurotransmitter dopamine, is a pleiotropic quantitative trait gene in Drosophila melanogaster. We used association mapping to determine whether the same or different QTNs at Catsup are associated with naturally occurring variation in multiple quantitative traits. We sequenced 169 Catsup alleles from a single population and detected 33 polymorphisms with little linkage disequilibrium (LD). Different molecular polymorphisms in Catsup are independently associated with variation in longevity, locomotor behavior, and sensory bristle number. Most of these polymorphisms are potentially functional variants in protein coding regions, have large effects, and are not common. Thus, Catsup is a pleiotropic quantitative trait gene, but individual QTNs do not have pleiotropic effects. Molecular population genetic analyses of Catsup sequences are consistent with balancing selection maintaining multiple functional polymorphisms.}, number={9}, journal={CURRENT BIOLOGY}, author={Carbone, Mary Anna and Jordan, Katherine W. and Lyman, Richard F. and Harbison, Susan T. and Leips, Jeff and Morgan, Theodore J. and DeLuca, Maria and Awadalla, Philip and Mackay, Trudy F. C.}, year={2006}, month={May}, pages={912–919} } @article{carbone_llopart_deangelis_coyne_mackay_2005, title={Quantitative trait loci affecting the difference in pigmentation between Drosophila yakuba and D. santomea}, volume={171}, ISSN={["1943-2631"]}, DOI={10.1534/genetics.105.044412}, abstractNote={Abstract}, number={1}, journal={GENETICS}, author={Carbone, MA and Llopart, A and DeAngelis, M and Coyne, JA and Mackay, TFC}, year={2005}, month={Sep}, pages={211–225} } @article{zwarts_magwire_carbone_versteven_herteleer_anholt_callaerts_mackay, title={Complex genetic architecture of Drosophila aggressive behavior}, volume={108}, number={41}, journal={Proceedings of the National Academy of Sciences of the United States of America}, author={Zwarts, L. and Magwire, M. M. and Carbone, M. A. and Versteven, M. and Herteleer, L. and Anholt, R. R. H. and Callaerts, P. and Mackay, T. F. C.}, pages={17070–17075} } @article{huang_richards_carbone_zhu_anholt_ayroles_duncan_jordan_lawrence_magwire_et al., title={Epistasis dominates the genetic architecture of Drosophila quantitative traits}, volume={109}, number={39}, journal={Proceedings of the National Academy of Sciences of the United States of America}, author={Huang, W. and Richards, S. and Carbone, M. A. and Zhu, D. H. and Anholt, R. R. H. and Ayroles, J. F. and Duncan, L. and Jordan, K. W. and Lawrence, F. and Magwire, M. M. and et al.}, pages={15553–15559} } @article{carbone_yamamoto_huang_lyman_meadors_yamamoto_anholt_mackay, title={Genetic architecture of natural variation in visual senescence in Drosophila}, volume={113}, number={43}, journal={Proceedings of the National Academy of Sciences of the United States of America}, author={Carbone, M. A. and Yamamoto, A. and Huang, W. and Lyman, R. A. and Meadors, T. B. and Yamamoto, R. and Anholt, R. R. H. and Mackay, T. F. 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