@article{cevik_skaar_jima_liu_ostbye_whitson_jirtle_hoyo_planchart_2024, title={DNA methylation of imprint control regions associated with Alzheimer's disease in non-Hispanic Blacks and non-Hispanic Whites}, volume={16}, ISSN={["1868-7083"]}, DOI={10.1186/s13148-024-01672-4}, abstractNote={Alzheimer's disease (AD) prevalence is twice as high in non-Hispanic Blacks (NHBs) as in non-Hispanic Whites (NHWs). The objective of this study was to determine whether aberrant methylation at imprint control regions (ICRs) is associated with AD. Differentially methylated regions (DMRs) were bioinformatically identified from whole-genome bisulfite sequenced DNA derived from brain tissue of 9 AD (5 NHBs and 4 NHWs) and 8 controls (4 NHBs and 4 NHWs). We identified DMRs located within 120 regions defined as candidate ICRs in the human imprintome ( https://genome.ucsc.edu/s/imprintome/hg38.AD.Brain_track ). Eighty-one ICRs were differentially methylated in NHB-AD, and 27 ICRs were differentially methylated in NHW-AD, with two regions common to both populations that are proximal to the inflammasome gene, NLRP1, and a known imprinted gene, MEST/MESTIT1. These findings indicate that early developmental alterations in DNA methylation of regions regulating genomic imprinting may contribute to AD risk and that this epigenetic risk differs between NHBs and NHWs.}, number={1}, journal={CLINICAL EPIGENETICS}, author={Cevik, Sebnem E. and Skaar, David A. and Jima, Dereje D. and Liu, Andy J. and Ostbye, Truls and Whitson, Heather E. and Jirtle, Randy L. and Hoyo, Cathrine and Planchart, Antonio}, year={2024}, month={Apr} } @article{grzymkowski_chiu_jima_wyatt_jayachandran_stutts_nascone-yoder_2024, title={Developmental regulation of cellular metabolism is required for intestinal elongation and rotation}, volume={151}, ISSN={["1477-9129"]}, url={https://doi.org/10.1242/dev.202020}, DOI={10.1242/dev.202020}, abstractNote={ABSTRACT}, number={1}, journal={DEVELOPMENT}, author={Grzymkowski, Julia K. and Chiu, Yu-Chun and Jima, Dereje D. and Wyatt, Brent H. and Jayachandran, Sudhish and Stutts, Whitney L. and Nascone-Yoder, Nanette M.}, year={2024}, month={Jan} } @article{vidal_chandramouli_marchesoni_brown_liu_murphy_maguire_wang_abdelmalek_mavis_et al._2023, title={AHRR Hypomethylation mediates the association between maternal smoking and metabolic profiles in children}, volume={7}, ISSN={["2471-254X"]}, DOI={10.1097/HC9.0000000000000243}, abstractNote={ Background: Tobacco smoking during pregnancy is associated with metabolic dysfunction in children, but mechanistic insights remain limited. Hypomethylation of cg05575921 in the aryl hydrocarbon receptor repressor (AHRR) gene is associated with in utero tobacco smoke exposure. In this study, we evaluated whether AHRR hypomethylation mediates the association between maternal smoking and metabolic dysfunction in children. }, number={10}, journal={HEPATOLOGY COMMUNICATIONS}, author={Vidal, Adriana C. and Chandramouli, Shivram A. and Marchesoni, Joddy and Brown, Nia and Liu, Yukun and Murphy, Susan K. and Maguire, Rachel and Wang, Yaxu and Abdelmalek, Manal F. and Mavis, Alisha M. and et al.}, year={2023}, month={Oct} } @article{harris_friedman_starling_dabelea_johnson_fuemmeler_jima_murphy_hoyo_jansen_et al._2023, title={An epigenome-wide association study of child appetitive traits and DNA methylation}, volume={191}, ISSN={["1095-8304"]}, DOI={10.1016/j.appet.2023.107086}, abstractNote={The etiology of childhood appetitive traits is poorly understood. Early-life epigenetic processes may be involved in the developmental programming of appetite regulation in childhood. One such process is DNA methylation (DNAm), whereby a methyl group is added to a specific part of DNA, where a cytosine base is next to a guanine base, a CpG site. We meta-analyzed epigenome-wide association studies (EWASs) of cord blood DNAm and early-childhood appetitive traits. Data were from two independent cohorts: the Generation R Study (n = 1,086, Rotterdam, the Netherlands) and the Healthy Start study (n = 236, Colorado, USA). DNAm at autosomal methylation sites in cord blood was measured using the Illumina Infinium HumanMethylation450 BeadChip. Parents reported on their child's food responsiveness, emotional undereating, satiety responsiveness and food fussiness using the Children's Eating Behaviour Questionnaire at age 4-5 years. Multiple regression models were used to examine the association of DNAm (predictor) at the individual site- and regional-level (using DMRff) with each appetitive trait (outcome), adjusting for covariates. Bonferroni-correction was applied to adjust for multiple testing. There were no associations of DNAm and any appetitive trait when examining individual CpG-sites. However, when examining multiple CpGs jointly in so-called differentially methylated regions, we identified 45 associations of DNAm with food responsiveness, 7 associations of DNAm with emotional undereating, 13 associations of DNAm with satiety responsiveness, and 9 associations of DNAm with food fussiness. This study shows that DNAm in the newborn may partially explain variation in appetitive traits expressed in early childhood and provides preliminary support for early programming of child appetitive traits through DNAm. Investigating differential DNAm associated with appetitive traits could be an important first step in identifying biological pathways underlying the development of these behaviors.}, journal={APPETITE}, author={Harris, Holly A. and Friedman, Chloe and Starling, Anne P. and Dabelea, Dana and Johnson, Susan L. and Fuemmeler, Bernard F. and Jima, Dereje and Murphy, Susan K. and Hoyo, Cathrine and Jansen, Pauline W. and et al.}, year={2023}, month={Dec} } @article{kadalayil_alam_white_ghantous_walton_gruzieva_merid_kumar_roy_solomon_et al._2023, title={Analysis of DNA methylation at birth and in childhood reveals changes associated with season of birth and latitude}, volume={15}, ISSN={["1868-7083"]}, DOI={10.1186/s13148-023-01542-5}, abstractNote={Abstract}, number={1}, journal={CLINICAL EPIGENETICS}, author={Kadalayil, Latha and Alam, Md. Zahangir and White, Cory Haley and Ghantous, Akram and Walton, Esther and Gruzieva, Olena and Merid, Simon Kebede and Kumar, Ashish and Roy, Ritu P. and Solomon, Olivia and et al.}, year={2023}, month={Sep} } @article{house_gray_owen_jima_smart_hall_2023, title={C/EBP beta deficiency enhances the keratinocyte innate immune response to direct activators of cytosolic pattern recognition receptors}, volume={29}, ISSN={["1753-4267"]}, DOI={10.1177/17534259231162192}, abstractNote={ The skin is the first line of defense to cutaneous microbes and viruses, and epidermal keratinocytes play a critical role in preventing infection by viruses and pathogens through activation of the type I interferon (IFN) response. Using RNAseq analysis, here we report that the conditional deletion of C/EBPβ transcription factor in mouse epidermis (CKOβ mice) resulted in the upregulation of IFNβ and numerous keratinocyte interferon-stimulated genes (ISGs). The expression of cytosolic pattern recognition receptors (cPRRs), that recognize viral RNA and DNA, were significantly increased, and enriched in the RNAseq data set. cPRRs stimulate a type I IFN response that can trigger cell death to eliminate infected cells. To determine if the observed increases in cPRRs had functional consequences, we transfected CKOβ primary keratinocytes with the pathogen and viral mimics poly(I:C) (dsRNA) or poly(dA:dT) (synthetic B-DNA) that directly activate PRRs. Transfected CKOβ primary keratinocytes displayed an amplified type I IFN response which was accompanied by increased activation of IRF3, enhanced ISG expression, enhanced activation of caspase-8, caspase-3 and increased apoptosis. Our results identify C/EBPβ as a critical repressor of the keratinocyte type I IFN response, and demonstrates that the loss of C/EBPβ primes keratinocytes to the activation of cytosolic PRRs by pathogen RNA and DNA to induce cell death mediated by caspase-8 and caspase-3. }, number={1-2}, journal={INNATE IMMUNITY}, author={House, John S. and Gray, Sophia and Owen, Jennifer R. and Jima, Dereje D. and Smart, Robert C. and Hall, Jonathan R.}, year={2023}, month={Jan}, pages={14–24} } @article{simmers_jima_tsuji_cowley_2023, title={LncRNA Tuna is activated in cadmium-induced placental insufficiency and drives the NRF2-mediated oxidative stress response}, volume={11}, ISSN={["2296-634X"]}, DOI={10.3389/fcell.2023.1151108}, abstractNote={Cadmium (Cd) is a toxic heavy metal found throughout the environment and one of the top ten toxicants of major public health concern identified by the World Health Organization. In utero Cd exposure causes fetal growth restriction, malformation, and spontaneous abortion; however, the mechanisms by which Cd impacts these outcomes are poorly understood. Cd accumulates in the placenta, suggesting that these negative outcomes may be a consequence of disrupted placental function and placental insufficiency. To understand the impact of Cd on gene expression within the placenta, we developed a mouse model of Cd-induced fetal growth restriction through maternal consumption of CdCl2 and performed RNA-seq on control and CdCl2 exposed placentae. The top differentially expressed transcript was the Tcl1 Upstream Neuron-Associated (Tuna) long non-coding RNA, which was upregulated over 25-fold in CdCl2 exposed placentae. Tuna has been shown to be critical for neural stem cell differentiation. However, within the placenta, there is no evidence that Tuna is normally expressed or functional at any developmental stage. To determine the spatial expression of Cd-activated Tuna within the placenta, we used in situ hybridization as well as placental layer-specific RNA isolation and analysis. Both methods confirmed the absence of Tuna expression in control samples and determined that Cd-induced Tuna expression is specific to the junctional zone. Since many lncRNAs regulate gene expression, we hypothesized that Tuna forms part of the mechanism of Cd-induced transcriptomic changes. To test this, we over-expressed Tuna in cultured choriocarcinoma cells and compared gene expression profiles to those of control and CdCl2 exposed cells. We demonstrate significant overlap between genes activated by Tuna overexpression and genes activated by CdCl2 exposure, with enrichment in the NRF2-mediated oxidative stress response. Herein we analyze the NRF2 pathway and show that Tuna increases NRF2/NRF2 both at the transcript and protein levels. Tuna drives increased NRF2 target gene expression, a result that is abrogated with the use of an NRF2 inhibitor, confirming that Tuna activates oxidative stress response genes through this pathway. This work identifies the lncRNA Tuna as a potential novel player in Cd-induced placental insufficiency.}, journal={FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY}, author={Simmers, Mark D. and Jima, Dereje D. and Tsuji, Yoshiaki and Cowley, Michael}, year={2023}, month={Jun} } @article{newell_jima_reading_patisaul_2023, title={Machine learning reveals common transcriptomic signatures across rat brain and placenta following developmental organophosphate ester exposure}, volume={7}, ISSN={["1096-0929"]}, DOI={10.1093/toxsci/kfad062}, abstractNote={Abstract}, journal={TOXICOLOGICAL SCIENCES}, author={Newell, Andrew J. and Jima, Dereje and Reading, Benjamin and Patisaul, Heather B.}, year={2023}, month={Jul} } @article{choudhary_monasso_karhunen_ronkainen_mancano_howe_niu_zeng_guan_dou_et al._2023, title={Maternal educational attainment in pregnancy and epigenome-wide DNA methylation changes in the offspring from birth until adolescence}, volume={12}, ISSN={["1476-5578"]}, DOI={10.1038/s41380-023-02331-5}, abstractNote={Abstract}, journal={MOLECULAR PSYCHIATRY}, author={Choudhary, Priyanka and Monasso, Giulietta S. and Karhunen, Ville and Ronkainen, Justiina and Mancano, Giulia and Howe, Caitlin G. and Niu, Zhongzheng and Zeng, Xuehuo and Guan, Weihua and Dou, John and et al.}, year={2023}, month={Dec} } @article{orr_collins_jima_buchwalter_2023, title={Salinity-induced ionoregulatory changes in the gill proteome of the mayfly, Neocloeon triangulifer}, volume={316}, ISSN={["1873-6424"]}, url={https://doi.org/10.1016/j.envpol.2022.120609}, DOI={10.1016/j.envpol.2022.120609}, abstractNote={Ecologists have observed declines in the biodiversity of sensitive freshwater organisms in response to increasing concentrations of major ions (salinization). Yet, how changing salinities physiologically challenge aquatic organisms, such as mayflies, remains remarkably understudied. Moreover, it is not well understood the degree to which species respond and acclimate to salinity changes. Our lab is developing the Baetid mayfly, N. triangulifer, as a model organism for physiological research. We have previously described acclimatory changes in both ion flux rates and altered mRNA transcript levels in response to chronic exposures to elevated major ion concentrations at the whole animal level. In the present study, we use shotgun proteomics to identify the specific proteins associated with apical ion transport and how their abundance changes in response to chronic salinity exposures in gills. Gills were isolated from the penultimate nymphal stage of N. triangulifer reared under control culture conditions, elevated NaCl (157 mg L-1 Na), elevated CaCl2 (121 mg L-1 Ca), elevated Ca/MgSO4 (735 mg L-1 SO4). These conditions mirrored those from previously published physiological work. We also acutely exposed nymphs to dilute (50% dilution of culture water with deionized water) to explore proteomic changes in the gills in response to dilute conditions. We report 710 unique peptide sequences among treatment groups, including important apical ion transporters such as Ca-ATPase, Na/K ATPase, and V-ATPase. Treatment with elevated NaCl and Ca/MgSO4 appeared to cause more significant differential protein expression (452 and 345, respectively) compared to CaCl2 and dilute groups (134 and 17, respectively). Finally, we demonstrated the breadth of physiological functions in gills by exploring non-transport related pathways found in our dataset, including ATP synthesis, calcium signaling, and oxidative stress response. We discuss our results in the context of freshwater salinization and the challenges of working with non-model species without fully sequenced and annotated genomes.}, journal={ENVIRONMENTAL POLLUTION}, author={Orr, Sarah E. and Collins, Leonard B. and Jima, Dereje D. and Buchwalter, David B.}, year={2023}, month={Jan} } @article{zhou_gallins_etheridge_jima_scholl_wright_innocenti_2022, title={A resource for integrated genomic analysis of the human liver}, volume={12}, ISSN={["2045-2322"]}, url={https://doi.org/10.1038/s41598-022-18506-z}, DOI={10.1038/s41598-022-18506-z}, abstractNote={Abstract}, number={1}, journal={SCIENTIFIC REPORTS}, author={Zhou, Yi-Hui and Gallins, Paul J. and Etheridge, Amy S. and Jima, Dereje and Scholl, Elizabeth and Wright, Fred A. and Innocenti, Federico}, year={2022}, month={Sep} } @article{moylan_mavis_jima_maguire_bashir_hyun_cabezas_parish_niedzwiecki_diehl_et al._2022, title={Alterations in DNA methylation associate with fatty liver and metabolic abnormalities in a multi-ethnic cohort of pre-teenage children}, ISSN={["1559-2308"]}, DOI={10.1080/15592294.2022.2039850}, abstractNote={ABSTRACT Non-Alcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease in children. Epigenetic alterations, such as through DNA methylation (DNAm), may link adverse childhood exposures and fatty liver and provide non-invasive methods for identifying children at high risk for NAFLD and associated metabolic dysfunction. We investigated the association between differential DNAm and liver fat content (LFC) and liver injury in pre-adolescent children. Leveraging data from the Newborn Epigenetics Study (NEST), we enrolled 90 mother-child dyads and used linear regression to identify CpG sites and differentially methylated regions (DMRs) in peripheral blood associated with LFC and alanine aminotransferase (ALT) levels in 7–12yo children. DNAm was measured using Infinium HumanMethylationEPIC BeadChips (Illumina). LFC and fibrosis were quantified by magnetic resonance imaging proton density fat fraction and elastography. Median LFC was 1.4% (range, 0.3–13.4%) and MRE was 2.5 kPa (range, 1.5–3.6kPa). Three children had LFC ≥ 5%, while six (7.6%) met our definition of NAFLD (LFC ≥ 3.7%). All children with NAFLD were obese and five were Black. LFC was associated with 88 DMRs and 106 CpGs (FDR<5%). The top two CpGs, cg25474373 and cg07264203, mapped to or near RFTN2 and PRICKLE2 genes. These two CpG sites were also significantly associated with a NAFLD diagnosis. As higher LFC associates with an adverse cardiometabolic profile already in childhood, altered DNAm may identify these children early in disease course for targeted intervention. Larger, longitudinal studies are needed to validate these findings and determine mechanistic relevance.}, journal={EPIGENETICS}, author={Moylan, Cynthia A. and Mavis, Alisha M. and Jima, Dereje and Maguire, Rachel and Bashir, Mustafa and Hyun, Jeongeun and Cabezas, Melanie N. and Parish, Alice and Niedzwiecki, Donna and Diehl, Anna Mae and et al.}, year={2022}, month={Feb} } @article{ligaba-osena_salehin_numan_wang_choi_jima_bobay_guo_2022, title={Genome-wide transcriptome analysis of the orphan crop tef (Eragrostis tef (Zucc.) Trotter) under long-term low calcium stress}, volume={12}, ISSN={2045-2322}, url={http://dx.doi.org/10.1038/s41598-022-23844-z}, DOI={10.1038/s41598-022-23844-z}, abstractNote={Abstract}, number={1}, journal={Scientific Reports}, publisher={Springer Science and Business Media LLC}, author={Ligaba-Osena, Ayalew and Salehin, Mohammad and Numan, Muhammad and Wang, Xuegeng and Choi, Sang-Chul and Jima, Dereje and Bobay, Louis-Marie and Guo, Wanli}, year={2022}, month={Nov} } @article{jima_skaar_planchart_motsinger-reif_cevik_park_cowley_wright_house_liu_et al._2022, title={Genomic map of candidate human imprint control regions: the imprintome}, volume={6}, ISSN={["1559-2308"]}, url={https://doi.org/10.1080/15592294.2022.2091815}, DOI={10.1080/15592294.2022.2091815}, abstractNote={ABSTRACT Imprinted genes – critical for growth, metabolism, and neuronal function – are expressed from one parental allele. Parent-of-origin-dependent CpG methylation regulates this expression at imprint control regions (ICRs). Since ICRs are established before tissue specification, these methylation marks are similar across cell types. Thus, they are attractive for investigating the developmental origins of adult diseases using accessible tissues, but remain unknown. We determined genome-wide candidate ICRs in humans by performing whole-genome bisulphite sequencing (WGBS) of DNA derived from the three germ layers and from gametes. We identified 1,488 hemi-methylated candidate ICRs, including 19 of 25 previously characterized ICRs (https://humanicr.org/). Gamete methylation approached 0% or 100% in 332 ICRs (178 paternally and 154 maternally methylated), supporting parent-of-origin-specific methylation, and 65% were in well-described CTCF-binding or DNaseI hypersensitive regions. This draft of the human imprintome will allow for the systematic determination of the role of early-acquired imprinting dysregulation in the pathogenesis of human diseases and developmental and behavioural disorders.}, journal={EPIGENETICS}, author={Jima, Dereje D. and Skaar, David A. and Planchart, Antonio and Motsinger-Reif, Alison and Cevik, Sebnem E. and Park, Sarah S. and Cowley, Michael and Wright, Fred and House, John and Liu, Andy and et al.}, year={2022}, month={Jun} } @article{harlow_gandawijaya_bamford_martin_wood_most_tanaka_leonard_etheridge_innocenti_et al._2022, title={Identification and single-base gene-editing functional validation of a cis-EPO variant as a genetic predictor for EPO-increasing therapies}, volume={109}, ISSN={["1537-6605"]}, DOI={10.1016/j.ajhg.2022.08.004}, abstractNote={Hypoxia-inducible factor prolyl hydroxylase inhibitors (HIF-PHIs) are currently under clinical development for treating anemia in chronic kidney disease (CKD), but it is important to monitor their cardiovascular safety. Genetic variants can be used as predictors to help inform the potential risk of adverse effects associated with drug treatments. We therefore aimed to use human genetics to help assess the risk of adverse cardiovascular events associated with therapeutically altered EPO levels to help inform clinical trials studying the safety of HIF-PHIs. By performing a genome-wide association meta-analysis of EPO (n = 6,127), we identified a cis-EPO variant (rs1617640) lying in the EPO promoter region. We validated this variant as most likely causal in controlling EPO levels by using genetic and functional approaches, including single-base gene editing. Using this variant as a partial predictor for therapeutic modulation of EPO and large genome-wide association data in Mendelian randomization tests, we found no evidence (at p < 0.05) that genetically predicted long-term rises in endogenous EPO, equivalent to a 2.2-unit increase, increased risk of coronary artery disease (CAD, OR [95% CI] = 1.01 [0.93, 1.07]), myocardial infarction (MI, OR [95% CI] = 0.99 [0.87, 1.15]), or stroke (OR [95% CI] = 0.97 [0.87, 1.07]). We could exclude increased odds of 1.15 for cardiovascular disease for a 2.2-unit EPO increase. A combination of genetic and functional studies provides a powerful approach to investigate the potential therapeutic profile of EPO-increasing therapies for treating anemia in CKD.}, number={9}, journal={AMERICAN JOURNAL OF HUMAN GENETICS}, author={Harlow, Charli E. and Gandawijaya, Josan and Bamford, Rosemary A. and Martin, Emily-Rose and Wood, Andrew R. and Most, Peter J. and Tanaka, Toshiko and Leonard, Hampton L. and Etheridge, Amy S. and Innocenti, Federico and et al.}, year={2022}, month={Sep}, pages={1638–1652} } @misc{solomon_huen_yousefi_kupers_gonzalez_suderman_reese_page_gruzieva_rzehak_et al._2022, title={Meta-analysis of epigenome-wide association studies in newborns and children show widespread sex differences in blood DNA methylation}, volume={789}, ISSN={["1388-2139"]}, DOI={10.1016/j.mrrev.2022.108415}, abstractNote={Among children, sex-specific differences in disease prevalence, age of onset, and susceptibility have been observed in health conditions including asthma, immune response, metabolic health, some pediatric and adult cancers, and psychiatric disorders. Epigenetic modifications such as DNA methylation may play a role in the sexual differences observed in diseases and other physiological traits. We performed a meta-analysis of the association of sex and cord blood DNA methylation at over 450,000 CpG sites in 8438 newborns from 17 cohorts participating in the Pregnancy And Childhood Epigenetics (PACE) Consortium. We also examined associations of child sex with DNA methylation in older children ages 5.5–10 years from 8 cohorts (n = 4268). In newborn blood, sex was associated at Bonferroni level significance with differences in DNA methylation at 46,979 autosomal CpG sites (p < 1.3 × 10−7) after adjusting for white blood cell proportions and batch. Most of those sites had lower methylation levels in males than in females. Of the differentially methylated CpG sites identified in newborn blood, 68% (31,727) met look-up level significance (p < 1.1 × 10−6) in older children and had methylation differences in the same direction. This is a large-scale meta-analysis examining sex differences in DNA methylation in newborns and older children. Expanding upon previous studies, we replicated previous findings and identified additional autosomal sites with sex-specific differences in DNA methylation. Differentially methylated sites were enriched in genes involved in cancer, psychiatric disorders, and cardiovascular phenotypes.}, journal={MUTATION RESEARCH-REVIEWS IN MUTATION RESEARCH}, author={Solomon, Olivia and Huen, Karen and Yousefi, Paul and Kupers, Leanne K. and Gonzalez, Juan R. and Suderman, Matthew and Reese, Sarah E. and Page, Christian M. and Gruzieva, Olena and Rzehak, Peter and et al.}, year={2022} } @article{watson_carmona baez_jima_reif_ding_roberts_kullman_2022, title={TCDD alters essential transcriptional regulators of osteogenic differentiation in multipotent mesenchymal stem cells}, volume={11}, ISSN={["1096-0929"]}, url={https://doi.org/10.1093/toxsci/kfac120}, DOI={10.1093/toxsci/kfac120}, abstractNote={Abstract}, journal={TOXICOLOGICAL SCIENCES}, author={Watson, AtLee T. D. and Carmona Baez, Aldo and Jima, Dereje and Reif, David and Ding, Jun and Roberts, Reade and Kullman, Seth W.}, year={2022}, month={Nov} } @article{riegl_starnes_jima_baptissart_diehl_belcher_cowley_2022, title={The imprinted gene Zac1 regulates steatosis in developmental cadmium-induced nonalcoholic fatty liver disease}, volume={10}, ISSN={["1096-0929"]}, url={https://doi.org/10.1093/toxsci/kfac106}, DOI={10.1093/toxsci/kfac106}, abstractNote={Abstract}, journal={TOXICOLOGICAL SCIENCES}, author={Riegl, Sierra D. and Starnes, Cassie and Jima, Dereje D. and Baptissart, Marine and Diehl, Anna Mae and Belcher, Scott M. and Cowley, Michael}, year={2022}, month={Oct} } @article{baptissart_bradish_jones_walsh_tehrani_marrero-colon_mehta_jima_oh_diehl_et al._2022, title={Zac1 and the Imprinted Gene Network program juvenile NAFLD in response to maternal metabolic syndrome}, volume={2}, ISSN={["1527-3350"]}, url={https://doi.org/10.1002/hep.32363}, DOI={10.1002/hep.32363}, abstractNote={Abstract}, journal={HEPATOLOGY}, author={Baptissart, Marine and Bradish, Christine M. and Jones, Brie S. and Walsh, Evan and Tehrani, Jesse and Marrero-Colon, Vicmarie and Mehta, Sanya and Jima, Dereje D. and Oh, Seh Hoon and Diehl, Anna Mae and et al.}, year={2022}, month={Feb} } @article{bosire_vidal_smith_jima_huang_skaar_valea_bentley_gradison_yarnall_et al._2021, title={Association between PEG3 DNA methylation and high-grade cervical intraepithelial neoplasia}, volume={16}, ISSN={["1750-9378"]}, DOI={10.1186/s13027-021-00382-3}, abstractNote={Abstract}, number={1}, journal={INFECTIOUS AGENTS AND CANCER}, author={Bosire, Claire and Vidal, Adriana C. and Smith, Jennifer S. and Jima, Dereje and Huang, Zhiqing and Skaar, David and Valea, Fidel and Bentley, Rex and Gradison, Margaret and Yarnall, Kimberly S. H. and et al.}, year={2021}, month={Jun} } @article{hudson_shiver_yu_mehta_jima_kane_patisaul_cowley_2021, title={Transcriptomic, proteomic, and metabolomic analyses identify candidate pathways linking maternal cadmium exposure to altered neurodevelopment and behavior}, volume={11}, ISSN={["2045-2322"]}, url={https://europepmc.org/articles/PMC8357970}, DOI={10.1038/s41598-021-95630-2}, abstractNote={Abstract}, number={1}, journal={SCIENTIFIC REPORTS}, author={Hudson, Kathleen M. and Shiver, Emily and Yu, Jianshi and Mehta, Sanya and Jima, Dereje D. and Kane, Maureen A. and Patisaul, Heather B. and Cowley, Michael}, year={2021}, month={Aug} } @article{etheridge_gallins_jima_broadaway_ratain_schuetz_schadt_schroder_molony_zhou_et al._2020, title={A New Liver Expression Quantitative Trait Locus Map From 1,183 Individuals Provides Evidence for Novel Expression Quantitative Trait Loci of Drug Response, Metabolic, and Sex-Biased Phenotypes}, volume={107}, ISSN={["1532-6535"]}, DOI={10.1002/cpt.1751}, abstractNote={Expression quantitative trait locus (eQTL) studies in human liver are crucial for elucidating how genetic variation influences variability in disease risk and therapeutic outcomes and may help guide strategies to obtain maximal efficacy and safety of clinical interventions. Associations between expression microarray and genome‐wide genotype data from four human liver eQTL studies (n = 1,183) were analyzed. More than 2.3 million cis‐eQTLs for 15,668 genes were identified. When eQTLs were filtered against a list of 1,496 drug response genes, 187,829 cis‐eQTLs for 1,191 genes were identified. Additionally, 1,683 sex‐biased cis‐eQTLs were identified, as well as 49 and 73 cis‐eQTLs that colocalized with genome‐wide association study signals for blood metabolite or lipid levels, respectively. Translational relevance of these results is evidenced by linking DPYD eQTLs to differences in safety of chemotherapy, linking the sex‐biased regulation of PCSK9 expression to anti‐lipid therapy, and identifying the G‐protein coupled receptor GPR180 as a novel drug target for hypertriglyceridemia.}, number={6}, journal={CLINICAL PHARMACOLOGY & THERAPEUTICS}, author={Etheridge, Amy S. and Gallins, Paul J. and Jima, Dereje and Broadaway, K. Alaine and Ratain, Mark J. and Schuetz, Erin and Schadt, Eric and Schroder, Adrian and Molony, Cliona and Zhou, Yihui and et al.}, year={2020}, month={Jun}, pages={1383–1393} } @article{neumann_walton_alemany_cecil_gonzalez_jima_lahti_tuominen_barker_binder_et al._2020, title={Association between DNA methylation and ADHD symptoms from birth to school age: a prospective meta-analysis}, volume={10}, ISSN={["2158-3188"]}, DOI={10.1038/s41398-020-01058-z}, abstractNote={Abstract}, number={1}, journal={TRANSLATIONAL PSYCHIATRY}, author={Neumann, Alexander and Walton, Esther and Alemany, Silvia and Cecil, Charlotte and Gonzalez, Juan Ramon and Jima, Dereje D. and Lahti, Jari and Tuominen, Samuli T. and Barker, Edward D. and Binder, Elisabeth and et al.}, year={2020}, month={Nov} } @article{vehmeijer_kuepers_sharp_salas_lent_jima_tindula_reese_qi_gruzieva_et al._2020, title={DNA methylation and body mass index from birth to adolescence: meta-analyses of epigenome-wide association studies}, volume={12}, ISSN={["1756-994X"]}, DOI={10.1186/s13073-020-00810-w}, abstractNote={Abstract}, number={1}, journal={GENOME MEDICINE}, author={Vehmeijer, Florianne O. L. and Kuepers, Leanne K. and Sharp, Gemma C. and Salas, Lucas A. and Lent, Samantha and Jima, Dereje D. and Tindula, Gwen and Reese, Sarah and Qi, Cancan and Gruzieva, Olena and et al.}, year={2020}, month={Dec} } @article{rock_st armour_horman_phillips_ruis_stewart_jima_muddiman_stapleton_patisaul_2020, title={Effects of Prenatal Exposure to a Mixture of Organophosphhate Flame Ritardants on Placental Gene Expression and Serotonergic Innervaion in the Fetal Rat Brain}, volume={176}, ISSN={["1096-0929"]}, DOI={10.1093/toxsci/kfaa046}, abstractNote={Abstract}, number={1}, journal={TOXICOLOGICAL SCIENCES}, author={Rock, Kylie D. and St Armour, Genevieve and Horman, Brian and Phillips, Allison and Ruis, Matthew and Stewart, Allison K. and Jima, Dereje and Muddiman, David C. and Stapleton, Heather M. and Patisaul, Heather B.}, year={2020}, month={Jul}, pages={203–223} } @article{shafiee-kermani_carney_jima_utin_farrar_oputa_hines_kinyamu_trotter_archer_et al._2020, title={Expression of UDP Glucuronosyltransferases2B15and2B17is associated with methylation status in prostate cancer cells}, ISBN={1559-2308}, DOI={10.1080/15592294.2020.1795601}, abstractNote={ABSTRACT Studies have suggested that abrogated expression of detoxification enzymes, UGT2B15 and UGT2B17, are associated with prostate tumour risk and progression. We investigated the role of EGF on the expression of these enzymes since it interacts with signalling pathways to also affect prostate tumour progression and is additionally associated with decreased DNA methylation. The expression of UGT2B15, UGT2B17, de novo methyltransferases, DNMT3A and DNMT3B was assessed in prostate cancer cells (LNCaP) treated with EGF, an EGFR inhibitor PD16893, and the methyltransferase inhibitor, 5-azacytidine, respectively. The results showed that EGF treatment decreased levels of expression of all four genes and that their expression was reversed by PD16893. Treatment with 5-azacytidine, markedly decreased expression of UGT2B15 and UGT2B17 over 85% as well as significantly decreased expression of DNMT3B, but not the expression of DNMT3A. DNMT3B siRNA treated LNCaP cells had decreased expression of UGT2B15 and UGT2B17, while DNMT3A siRNA treated cells had only moderately decreased UGT2B15 expression. Treatment with DNMT methyltransferase inhibitor, RG108, significantly decreased UGT2B17 expression. Additionally, methylation differences between prostate cancer samples and benign prostate samples from an Illumina 450K Methylation Array study were assessed. The results taken together suggest that hypomethylation of the UGT2B15 and UGT2B17 genes contributes to increased risk of prostate cancer and may provide a putative biomarker or epigenetic target for chemotherapeutics. Mechanistic studies are warranted to determine the role of the methylation marks in prostate cancer.}, journal={EPIGENETICS}, author={Shafiee-Kermani, Farideh and Carney, Skyla T. and Jima, Dereje and Utin, Utibe C. and Farrar, LaNeisha B. and Oputa, Melvin O. and Hines, Marcono R., Jr. and Kinyamu, H. Karimi and Trotter, Kevin W. and Archer, Trevor K. and et al.}, year={2020} } @article{chou_jima_funk_jackson_sweeney_buchwalter_2020, title={Transcriptomic and life history responses of the mayfly Neocloeon triangulifer to chronic diel thermal challenge}, volume={10}, ISSN={["2045-2322"]}, DOI={10.1038/s41598-020-75064-y}, abstractNote={Abstract}, number={1}, journal={SCIENTIFIC REPORTS}, author={Chou, Hsuan and Jima, Dereje D. and Funk, David H. and Jackson, John K. and Sweeney, Bernard W. and Buchwalter, David B.}, year={2020}, month={Nov} } @article{knuth_mahapatra_jima_wan_hammock_law_kullman_2020, title={Vitamin D deficiency serves as a precursor to stunted growth and central adiposity in zebrafish}, volume={10}, ISSN={["2045-2322"]}, DOI={10.1038/s41598-020-72622-2}, abstractNote={Abstract}, number={1}, journal={SCIENTIFIC REPORTS}, author={Knuth, Megan M. and Mahapatra, Debabrata and Jima, Dereje and Wan, Debin and Hammock, Bruce D. and Law, Mac and Kullman, Seth W.}, year={2020}, month={Sep} } @article{tam_hall_messenger_jima_house_linder_smart_2019, title={C/EBP beta suppresses keratinocyte autonomous type 1 IFN response and p53 to increase cell survival and susceptibility to UVB-induced skin cancer}, volume={40}, ISSN={["1460-2180"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-85083447649&partnerID=MN8TOARS}, DOI={10.1093/carcin/bgz012}, abstractNote={Abstract}, number={9}, journal={CARCINOGENESIS}, author={Tam, Hann W. and Hall, Jonathan R. and Messenger, Zachary J. and Jima, Dereje D. and House, John S. and Linder, Keith and Smart, Robert C.}, year={2019}, month={Sep}, pages={1099–1109} } @article{reese_xu_dekker_lee_sikdar_ruiz-arenas_merid_rezwan_page_ullemar_et al._2019, title={Epigenome-wide meta-analysis of DNA methylation and childhood asthma}, volume={143}, ISSN={["1097-6825"]}, DOI={10.1016/j.jaci.2018.11.043}, abstractNote={Epigenetic mechanisms, including methylation, can contribute to childhood asthma. Identifying DNA methylation profiles in asthmatic patients can inform disease pathogenesis.We sought to identify differential DNA methylation in newborns and children related to childhood asthma.Within the Pregnancy And Childhood Epigenetics consortium, we performed epigenome-wide meta-analyses of school-age asthma in relation to CpG methylation (Illumina450K) in blood measured either in newborns, in prospective analyses, or cross-sectionally in school-aged children. We also identified differentially methylated regions.In newborns (8 cohorts, 668 cases), 9 CpGs (and 35 regions) were differentially methylated (epigenome-wide significance, false discovery rate < 0.05) in relation to asthma development. In a cross-sectional meta-analysis of asthma and methylation in children (9 cohorts, 631 cases), we identified 179 CpGs (false discovery rate < 0.05) and 36 differentially methylated regions. In replication studies of methylation in other tissues, most of the 179 CpGs discovered in blood replicated, despite smaller sample sizes, in studies of nasal respiratory epithelium or eosinophils. Pathway analyses highlighted enrichment for asthma-relevant immune processes and overlap in pathways enriched both in newborns and children. Gene expression correlated with methylation at most loci. Functional annotation supports a regulatory effect on gene expression at many asthma-associated CpGs. Several implicated genes are targets for approved or experimental drugs, including IL5RA and KCNH2.Novel loci differentially methylated in newborns represent potential biomarkers of risk of asthma by school age. Cross-sectional associations in children can reflect both risk for and effects of disease. Asthma-related differential methylation in blood in children was substantially replicated in eosinophils and respiratory epithelium.}, number={6}, journal={JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY}, author={Reese, Sarah E. and Xu, Cheng-Jian and Dekker, Herman T. and Lee, Mi Kyeong and Sikdar, Sinjini and Ruiz-Arenas, Carlos and Merid, Simon K. and Rezwan, Faisal I and Page, Christian M. and Ullemar, Vilhelmina and et al.}, year={2019}, month={Jun}, pages={2062–2074} } @article{martin_jima_sharp_mccullough_park_gowdy_skaar_cowley_maguire_fuemmeler_et al._2019, title={Maternal pre-pregnancy obesity, offspring cord blood DNA methylation, and offspring cardiometabolic health in early childhood: an epigenome-wide association study}, volume={14}, ISSN={["1559-2308"]}, url={https://doi.org/10.1080/15592294.2019.1581594}, DOI={10.1080/15592294.2019.1581594}, abstractNote={ABSTRACT Pre-pregnancy obesity is an established risk factor for adverse sex-specific cardiometabolic health in offspring. Epigenetic alterations, such as in DNA methylation (DNAm), are a hypothesized link; however, sex-specific epigenomic targets remain unclear. Leveraging data from the Newborn Epigenetics Study (NEST) cohort, linear regression models were used to identify CpG sites in cord blood leukocytes associated with pre-pregnancy obesity in 187 mother-female and 173 mother-male offsprings. DNAm in cord blood was measured using the Illumina HumanMethylation450k BeadChip. Replication analysis was conducted among the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort. Associations between pre-pregnancy obesity-associated CpG sites and offspring BMI z-score (BMIz) and blood pressure (BP) percentiles at 4–5-years of age were also examined. Maternal pre-pregnacy obesity was associated with 876 CpGs in female and 293 CpGs in male offspring (false discovery rate <5%). Among female offspring, 57 CpG sites, including the top 18, mapped to the TAPBP gene (range of effect estimates: −0.83% decrease to 4.02% increase in methylation). CpG methylation differences in the TAPBP gene were also observed among males (range of effect estimates: −0.30% decrease to 2.59% increase in methylation). While technically validated, none of the TAPBP CpG sites were replicated in ALSPAC. In NEST, methylation differences at CpG sites of the TAPBP gene were associated with BMI z-score (cg23922433 and cg17621507) and systolic BP percentile (cg06230948) in female and systolic (cg06230948) and diastolic (cg03780271) BP percentile in male offspring. Together, these findings suggest sex-specific effects, which, if causal, may explain observed sex-specific effects of maternal obesity.}, number={4}, journal={EPIGENETICS}, author={Martin, Chantel L. and Jima, Dereje and Sharp, Gemma C. and McCullough, Lauren E. and Park, Sarah S. and Gowdy, Kymberly M. and Skaar, David and Cowley, Michael and Maguire, Rachel L. and Fuemmeler, Bernard and et al.}, year={2019}, month={Apr}, pages={325–340} } @article{frayling_beaumont_jones_yaghootkar_tuke_ruth_casanova_west_locke_sharp_et al._2018, title={A common allele in FGF21 associated with sugar intake is associated with body shape, lower total body-fat percentage, and higher blood pressure}, volume={23}, number={2}, journal={Cell reports}, author={Frayling, T. M. and Beaumont, R. N. and Jones, S. E. and Yaghootkar, H. and Tuke, M. A. and Ruth, K. S. and Casanova, F. and West, B. and Locke, J. and Sharp, S. and et al.}, year={2018}, pages={327–336} } @article{messenger_hall_jima_house_tam_tokarz_smart_2018, title={C/EBPβ deletion in oncogenic Ras skin tumors is a synthetic lethal event}, volume={9}, ISSN={2041-4889}, url={http://dx.doi.org/10.1038/S41419-018-1103-Y}, DOI={10.1038/s41419-018-1103-y}, abstractNote={Abstract}, number={11}, journal={Cell Death & Disease}, publisher={Springer Science and Business Media LLC}, author={Messenger, Zachary J. and Hall, Jonathan R. and Jima, Dereje D. and House, John S. and Tam, Hann W. and Tokarz, Debra A. and Smart, Robert C.}, year={2018}, month={Oct} } @article{felix_joubert_baccarelli_sharp_almqvist_annesi-maesano_arshad_baiz_bakermans-kranenburg_bakulski_et al._2018, title={Cohort profile: Pregnancy and childhood epigenetics (PACE) consortium}, volume={47}, number={1}, journal={International Journal of Epidemiology}, author={Felix, J. F. and Joubert, B. R. and Baccarelli, A. A. and Sharp, G. C. and Almqvist, C. and Annesi-Maesano, I. and Arshad, H. and Baiz, N. and Bakermans-Kranenburg, M. J. and Bakulski, K. M. and et al.}, year={2018}, pages={22-} } @article{rock_horman_phillips_mcritchie_watson_deese-spruill_jima_sumner_stapleton_patisaul_et al._2018, title={EDC IMPACT: Molecular effects of developmental FM 550 exposure in Wistar rat placenta and fetal forebrain}, volume={7}, ISSN={["2049-3614"]}, DOI={10.1530/ec-17-0373}, abstractNote={Firemaster 550 (FM 550) is a flame retardant (FR) mixture that has become one of the most commonly used FRs in foam-based furniture and baby products. Human exposure to this commercial mixture, composed of brominated and organophosphate components, is widespread. We have repeatedly shown that developmental exposure can lead to sex-specific behavioral effects in rats. Accruing evidence of endocrine disruption and potential neurotoxicity has raised concerns regarding the neurodevelopmental effects of FM 550 exposure, but the specific mechanisms of action remains unclear. Additionally, we observed significant, and in some cases sex-specific, accumulation of FM 550 in placental tissue following gestational exposure. Because the placenta is an important source of hormones and neurotransmitters for the developing brain, it may be a critical target of toxicity to consider in the context of developmental neurotoxicity. Using a mixture of targeted and exploratory approaches, the goal of the present study was to identify possible mechanisms of action in the developing forebrain and placenta. Wistar rat dams were orally exposed to FM 550 (0, 300 or 1000 µg/day) for 10 days during gestation and placenta and fetal forebrain tissue collected for analysis. In placenta, evidence of endocrine, inflammatory and neurotransmitter signaling pathway disruption was identified. Notably, 5-HT turnover was reduced in placental tissue and fetal forebrains indicating that 5-HT signaling between the placenta and the embryonic brain may be disrupted. These findings demonstrate that environmental contaminants, like FM 550, have the potential to impact the developing brain by disrupting normal placental functions.}, number={2}, journal={ENDOCRINE CONNECTIONS}, author={Rock, K. D. and Horman, B. and Phillips, A. L. and McRitchie, S. L. and Watson, S. and Deese-Spruill, J. and Jima, D. and Sumner, S. and Stapleton, H. M. and Patisaul, Heather and et al.}, year={2018}, month={Feb}, pages={305–324} } @article{cowley_skaar_jima_maguire_hudson_park_sorrow_hoyo_2018, title={Effects of cadmium exposure on DNA methylation at imprinting control regions and genome-wide in mothers and newborn children}, volume={126}, number={3}, journal={Environmental Health Perspectives}, author={Cowley, M. and Skaar, D. A. and Jima, D. D. and Maguire, R. L. and Hudson, K. M. and Park, S. S. and Sorrow, P. and Hoyo, C.}, year={2018} } @article{li_jima_wright_nobel_2018, title={HT-eQTL: integrative expression quantitative trait loci analysis in a large number of human tissues}, volume={19}, journal={BMC Bioinformatics}, author={Li, G. and Jima, D. and Wright, F. A. and Nobel, A. B.}, year={2018} } @article{arambula_jima_patisaul_2018, title={Prenatal bisphenol A (BPA) exposure alters the transcriptome of the neonate rat amygdala in a sex-specific manner: a CLARITY-BPA consortium study}, volume={65}, ISSN={["1872-9711"]}, DOI={10.1016/j.neuro.2017.10.005}, abstractNote={Bisphenol A (BPA) is a widely recognized endocrine disruptor prevalent in many household items. Because experimental and epidemiological data suggest links between prenatal BPA exposure and altered affective behaviors in children, even at levels below the current US FDA No Observed Adverse Effect Level (NOAEL) of 5mg/kg body weight (bw)/day, there is concern that early life exposure may alter neurodevelopment. The current study was conducted as part of the CLARITY-BPA (Consortium Linking Academic and Regulatory Insights on BPA Toxicity) program and examined the full amygdalar transcriptome on postnatal day (PND) 1, with the hypothesis that prenatal BPA exposure would alter the expression of genes and pathways fundamental to sex-specific affective behaviors. NCTR Sprague-Dawley dams were gavaged from gestational day 6 until parturition with BPA (2.5, 25, 250, 2500, or 25000μg/kg bw/day), a reference estrogen (0.05 or 0.5μg ethinyl estradiol (EE2)/kg bw/day), or vehicle. PND 1 amygdalae were microdissected and gene expression was assessed with qRT-PCR (all exposure groups) and RNAseq (vehicle, 25 and 250μg BPA, and 0.5μg EE2 groups only). Our results demonstrate that that prenatal BPA exposure can disrupt the transcriptome of the neonate amygdala, at doses below the FDA NOAEL, in a sex-specific manner and indicate that the female amygdala may be more sensitive to BPA exposure during fetal development. We also provide additional evidence that developmental BPA exposure can interfere with estrogen, oxytocin, and vasopressin signaling pathways in the developing brain and alter signaling pathways critical for synaptic organization and transmission.}, journal={NEUROTOXICOLOGY}, author={Arambula, Sheryl E. and Jima, Dereje and Patisaul, Heather B.}, year={2018}, month={Mar}, pages={207–220} } @article{chou_pathmasiri_deese-spruill_sumner_jima_funk_jackson_sweeney_buchwalter_2018, title={The Good, the Bad, and the Lethal: Gene Expression and Metabolomics Reveal Physiological Mechanisms Underlying Chronic Thermal Effects in Mayfly Larvae (Neocloeon triangulifer)}, volume={6}, ISSN={["2296-701X"]}, DOI={10.3389/fevo.2018.00027}, abstractNote={Temperature dictates the performance of aquatic ectotherms. However, the physiological and biochemical processes that drive thermally-mediated life history patterns (and limits) remain poorly understood because they are rarely studied simultaneously. In our previous work, we have established life history outcomes (e.g. survivorship, development time, growth rates and fitness) in mayflies (Neocloeon triangulifer) reared at static temperatures ranging from 14°C - 30°C at 2°C intervals. In this study, we conducted biochemical measurements (RT-qPCR of select genes and targeted, quantitative metabolomic profiling) on N. triangulifer mature larvae reared at temperatures associated with excellent survival and fitness (22-24°C), compromised survival and fitness (28°C), and chronic lethality (30°C -larvae survived for a few weeks but failed to emerge to adulthood). Patterns of gene expression were similar to those observed in acute ramping experiments reported previously: larvae reared at 30°C resulted in significant upregulation in the thermally responsive gene HEAT SHOCK PROTEIN 90 (HSP90) but no significant changes in hypoxia responsive genes (EGG LAYING DEFECTIVE 9 (EGL-9) and LACTATE DEHYDROGENASE (LDH)). Additionally, primers for genes associated with energy: INSULIN RECEPTOR (IR), mechanistic TARGET OF RAPAMYCIN (mTOR) and TREHALOSE 6 PHOSPHATE SYNTHASE (T6PS) were developed for this study. IR and mTOR were significantly upregulated while T6PS showed trend of downregulation in larvae reared at 30°C. Metabolomic profiles revealed general depletion of lipids and acylcarnitines in larvae exposed to chronic thermal stress, suggesting that larvae were energetically challenged despite continuous access to food. For example, concentrations of lysoPhosphatidylcholine (lysoPC) a C20:3 decreased as fitness decreased with increasing temperature (2.3 fold and 2.4 fold at 28 and 30°C relative to controls). Tissue concentrations of the biogenic amine histamine increased 2.1 and 3.1 fold with increasing temperature, and were strongly and negatively correlated with performance. Thus, both histamine and lysoPC a C20:3 are potential biomarkers of thermal stress. Taken together, our results primarily associate energetic challenge with thermally mediated fitness reduction in N. triangulifer.}, journal={FRONTIERS IN ECOLOGY AND EVOLUTION}, author={Chou, Hsuan and Pathmasiri, Wimal and Deese-spruill, Jocelin and Sumner, Susan J. and Jima, Dereje D. and Funk, David H. and Jackson, John K. and Sweeney, Bernard W. and Buchwalter, David B.}, year={2018}, month={Mar} } @article{house_grimm_jima_zhou_rusyn_wright_2017, title={A Pipeline for high-throughput concentration response modeling of gene expression for toxicogenomics}, volume={8}, journal={Frontiers in Genetics}, author={House, J. S. and Grimm, F. A. and Jima, D. D. and Zhou, Y. H. and Rusyn, I. and Wright, F. A.}, year={2017} } @article{tokarz_heffelfinger_jima_gerlach_shah_rodriguez-nunez_kortum_fletcher_nordone_law_et al._2017, title={Disruption of Trim9 function abrogates macrophage motility in vivo}, volume={102}, ISSN={0741-5400 1938-3673}, url={http://dx.doi.org/10.1189/jlb.1A0816-371R}, DOI={10.1189/jlb.1a0816-371r}, abstractNote={Abstract}, number={6}, journal={Journal of Leukocyte Biology}, publisher={Wiley}, author={Tokarz, Debra A. and Heffelfinger, Amy K. and Jima, Dereje D. and Gerlach, Jamie and Shah, Radhika N. and Rodriguez-Nunez, Ivan and Kortum, Amanda N. and Fletcher, Ashley A. and Nordone, Shila K. and Law, J. McHugh and et al.}, year={2017}, month={Oct}, pages={1371–1380} } @article{reaves_hoadley_fagan-solis_jima_bereman_thorpe_hicks_mcdonald_troester_perou_et al._2017, title={Nuclear Localized LSR: A Novel Regulator of Breast Cancer Behavior and Tumorigenesis}, volume={15}, ISSN={["1557-3125"]}, DOI={10.1158/1541-7786.mcr-16-0085-t}, abstractNote={Abstract}, number={2}, journal={MOLECULAR CANCER RESEARCH}, author={Reaves, Denise K. and Hoadley, Katherine A. and Fagan-Solis, Katerina D. and Jima, Dereje D. and Bereman, Michael and Thorpe, Lynnelle and Hicks, Jyla and McDonald, David and Troester, Melissa A. and Perou, Charles M. and et al.}, year={2017}, month={Feb}, pages={165–178} } @article{lee_ward_jima_parsons_kathariou_2017, title={The Arsenic Resistance-Associated Listeria Genomic Island LGI2 Exhibits Sequence and Integration Site Diversity and a Propensity for Three Listeria monocytogenes Clones with Enhanced Virulence}, volume={83}, ISSN={["1098-5336"]}, DOI={10.1128/aem.01189-17}, abstractNote={ABSTRACT}, number={21}, journal={APPLIED AND ENVIRONMENTAL MICROBIOLOGY}, author={Lee, Sangmi and Ward, Todd J. and Jima, Dereje D. and Parsons, Cameron and Kathariou, Sophia}, year={2017}, month={Nov} } @article{jima_shah_orcutt_joshi_law_litman_trede_yoder_2009, title={Enhanced transcription of complement and coagulation genes in the absence of adaptive immunity}, volume={46}, ISSN={0161-5890}, url={http://dx.doi.org/10.1016/j.molimm.2008.12.021}, DOI={10.1016/j.molimm.2008.12.021}, abstractNote={A recessive nonsense mutation in the zebrafish recombination activating gene 1 (rag1) gene results in defective V(D)J recombination; however, animals homozygous for this mutation (rag1(-/-)) are reportedly viable and fertile in standard, nonsterile aquarium conditions but display increased mortality after intraperitoneal injection with mycobacteria. Based on their survival in nonsterile environments, we hypothesized that the rag1(-/-) zebrafish may possess an "enhanced" innate immune response to compensate for the lack of an adaptive immune system. To test this hypothesis, microarray analyses were used to compare the expression profiles of the intestines and hematopoietic kidneys of rag1 deficient zebrafish to the expression profiles of control (heterozygous) siblings. The expression levels of 12 genes were significantly altered in the rag1(-/-) kidney including the up regulation of a putative interferon stimulated gene, and the down regulation of genes encoding fatty acid binding protein 10, keratin 5 and multiple heat shock proteins. The expression levels of 87 genes were shown to be significantly altered in the rag1(-/-) intestine; the majority of these differences reflect increased expression of innate immune genes, including those of the coagulation and complement pathways. Subsequent analyses of orthologous coagulation and complement genes in Rag1(-/-) mice indicate increased transcription of the complement C4 gene in the Rag1(-/-) intestine.}, number={7}, journal={Molecular Immunology}, publisher={Elsevier BV}, author={Jima, Dereje D. and Shah, Radhika N. and Orcutt, Timothy M. and Joshi, Deepa and Law, J. McHugh and Litman, Gary W. and Trede, Nikolaus S. and Yoder, Jeffrey A.}, year={2009}, month={Apr}, pages={1505–1516} }