Igseo Choi
Michigan State University
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Featured researches published by Igseo Choi.
Frontiers in Genetics | 2011
Igseo Choi; Juan P. Steibel; R. O. Bates; Nancy E. Raney; Janice M. Rumph; C. W. Ernst
A three-generation resource population was constructed by crossing pigs from the Duroc and Pietrain breeds. In this study, 954 F2 animals were used to identify quantitative trait loci (QTL) affecting carcass and meat quality traits. Based on results of the first scan analyzed with a line-cross (LC) model using 124 microsatellite markers and 510 F2 animals, 9 chromosomes were selected for genotyping of additional markers. Twenty additional markers were genotyped for 954 F2 animals and 20 markers used in the first scan were genotyped for 444 additional F2 animals. Three different Mendelian models using least-squares for QTL analysis were applied for the second scan: a LC model, a half-sib (HS) model, and a combined LC and HS model. Significance thresholds were determined by false discovery rate (FDR). In total, 50 QTL using the LC model, 38 QTL using the HS model, and 3 additional QTL using the combined LC and HS model were identified (q < 0.05). The LC and HS models revealed strong evidence for QTL regions on SSC6 for carcass traits (e.g., 10th-rib backfat; q < 0.0001) and on SSC15 for meat quality traits (e.g., tenderness, color, pH; q < 0.01), respectively. QTL for pH (SSC3), dressing percent (SSC7), marbling score and moisture percent (SSC12), CIE a* (SSC16), and carcass length and spareribs weight (SSC18) were also significant (q < 0.01). Additional marker and animal genotypes increased the statistical power for QTL detection, and applying different analysis models allowed confirmation of QTL and detection of new QTL.
Frontiers in Genetics | 2013
Maria E. Arceo; C. W. Ernst; Joan K. Lunney; Igseo Choi; Nancy E. Raney; Tinghua Huang; Christopher K. Tuggle; Raymond R. R. Rowland; Juan P. Steibel
We evaluated differences in gene expression in pigs from the Porcine Reproductive and Respiratory Syndrome (PRRS) Host Genetics Consortium initiative showing a range of responses to PRRS virus infection. Pigs were allocated into four phenotypic groups according to their serum viral level and weight gain. RNA obtained from blood at 0, 4, 7, 11, 14, 28, and 42 days post-infection (DPI) was hybridized to the 70-mer 20K Pigoligoarray. We used a blocked reference design for the microarray experiment. This allowed us to account for individual biological variation in gene expression, and to assess baseline effects before infection (0 DPI). Additionally, this design has the flexibility of incorporating future data for differential expression analysis. We focused on evaluating transcripts showing significant interaction of weight gain and serum viral level. We identified 491 significant comparisons [false discovery rate (FDR) = 10%] across all DPI and phenotypic groups. We corroborated the overall trend in direction and level of expression (measured as fold change) at 4 DPI using qPCR (r = 0.91, p ≤ 0.0007). At 4 and 7 DPI, network and functional analyses were performed to assess if immune related gene sets were enriched for genes differentially expressed (DE) across four phenotypic groups. We identified cell death function as being significantly associated (FDR ≤ 5%) with several networks enriched for DE transcripts. We found the genes interferon-alpha 1(IFNA1), major histocompatibility complex, class II, DQ alpha 1 (SLA-DQA1), and major histocompatibility complex, class II, DR alpha (SLA-DRA) to be DE (p ≤ 0.05) between phenotypic groups. Finally, we performed a power analysis to estimate sample size and sampling time-points for future experiments. We concluded the best scenario for investigation of early response to PRRSV infection consists of sampling at 0, 4, and 7 DPI using about 30 pigs per phenotypic group.
BMC Genetics | 2010
Igseo Choi; Juan P. Steibel; R. O. Bates; Nancy E. Raney; Janice M. Rumph; C. W. Ernst
BackgroundA variety of analysis approaches have been applied to detect quantitative trait loci (QTL) in experimental populations. The initial genome scan of our Duroc x Pietrain F2 resource population included 510 F2 animals genotyped with 124 microsatellite markers and analyzed using a line-cross model. For the second scan, 20 additional markers on 9 chromosomes were genotyped for 954 F2 animals and 20 markers used in the first scan were genotyped for 444 additional F2 animals. Three least-squares Mendelian models for QTL analysis were applied for the second scan: a line-cross model, a half-sib model, and a combined line-cross and half-sib model.ResultsIn total, 26 QTL using the line-cross model, 12 QTL using the half-sib model and 3 additional QTL using the combined line-cross and half-sib model were detected for growth traits with a 5% false discovery rate (FDR) significance level. In the line-cross analysis, highly significant QTL for fat deposition at 10-, 13-, 16-, 19-, and 22-wk of age were detected on SSC6. In the half-sib analysis, a QTL for loin muscle area at 19-wk of age was detected on SSC7 and QTL for 10th-rib backfat at 19- and 22-wk of age were detected on SSC15.ConclusionsAdditional markers and animals contributed to reduce the confidence intervals and increase the test statistics for QTL detection. Different models allowed detection of new QTL which indicated differing frequencies for alternative alleles in parental breeds.
Meat Science | 2012
Igseo Choi; R. O. Bates; Nancy E. Raney; Juan P. Steibel; C. W. Ernst
Putative quantitative trait loci (QTL) regions on 5 chromosomes (SSC3, 6, 12, 15, and 18) were selected from our previous genome scans of a Duroc×Pietrain F(2) resource population for further evaluation in a US commercial Duroc population (n=331). A total of 81 gene-specific single nucleotide polymorphism (SNP) markers were genotyped and 33 markers were segregating. The MDH1 SNP on SSC3 was associated with 45-min and ultimate pH (pHu), and pH decline. PRKAG3 on SSC15 was associated with pHu. The HSPG2 SNP on SSC6 was associated with marbling score and days to 113kg. Markers for NUP88 and FKBP10 on SSC12 were associated with 45-min pH and L*, respectively. The SSC15 marker SF3B1 was associated with L* and LMA, and the SSC18 marker ARF5 was associated with pHu and color score. These results in a commercial Duroc population showed a general consistency with our previous genome scan.
Scientific Reports | 2017
Arun Kommadath; Hua Bao; Igseo Choi; James M. Reecy; James E. Koltes; Elyn Fritz-Waters; Chris Eisley; Jason R. Grant; Robert R. R. Rowland; Christopher K. Tuggle; Jack C. M. Dekkers; Joan K. Lunney; Le Luo Guan; Paul Stothard; Graham Plastow
It has been shown that inter-individual variation in host response to porcine reproductive and respiratory syndrome (PRRS) has a heritable component, yet little is known about the underlying genetic architecture of gene expression in response to PRRS virus (PRRSV) infection. Here, we integrated genome-wide genotype, gene expression, viremia level, and weight gain data to identify genetic polymorphisms that are associated with variation in inter-individual gene expression and response to PRRSV infection in pigs. RNA-seq analysis of peripheral blood samples collected just prior to experimental challenge (day 0) and at 4, 7, 11 and 14 days post infection from 44 pigs revealed 6,430 differentially expressed genes at one or more time points post infection compared to the day 0 baseline. We mapped genetic polymorphisms that were associated with inter-individual differences in expression at each day and found evidence of cis-acting expression quantitative trait loci (cis-eQTL) for 869 expressed genes (qval < 0.05). Associations between cis-eQTL markers and host response phenotypes using 383 pigs suggest that host genotype-dependent differences in expression of GBP5, GBP6, CCHCR1 and CMPK2 affect viremia levels or weight gain in response to PRRSV infection.
Journal of Genomics | 2017
El Hamidi A. Hay; Igseo Choi; Lingyang Xu; Yang Zhou; Robert R. R. Rowland; Joan K Lunney; George E. Liu
Porcine reproductive and respiratory syndrome (PRRS) is a devastating disease with a significant impact on the swine industry causing major economic losses. The objective of this study is to examine copy number variations (CNVs) associated with the group-specific host responses to PRRS virus infection. We performed a genome-wide CNV analysis using 660 animals genotyped with on the porcine SNP60 BeadChip and discovered 7097 CNVs and 271 CNV regions (CNVRs). For this study, we used two established traits related to host response to the virus, i.e. viral load (VL, area under the curve of log-transformed serum viremia from 0 to 21 days post infection) and weight gain (WG42 from 0 to 42 days post infection). To investigate the effects of CNVs on differential host responses to PRRS, we compared groups of animals with extreme high and low estimated breeding values (EBVs) for both traits using a case-control study design. For VL, we identified 163 CNVRs (84 Mb) from the high group and 159 CNVRs (76 Mb) from the low group. For WG42, we detected 126 (68 Mb) and 156 (79 Mb) CNVRs for high and low groups, respectively. Based on gene annotation within group-specific CNVRs, we performed network analyses and observed some potential candidate genes. Our results revealed these group-specific genes are involved in regulating innate and acquired immune response pathways. Specifically, molecules like interferons and interleukins are closely related to host responses to PRRS virus infection.
Canadian Journal of Animal Science | 2017
Igseo Choi; R. O. Bates; Nancy E. Raney; C. W. Ernst
Abstract A single-nucleotide polymorphism within the corticotropin-releasing hormone receptor 2 (CRHR2) gene was identified and evaluated in two pig populations. The CRHR2 genotype was significantly associated with nine carcass and meat quality traits in the F2 resource population and exhibited a suggestive association with the stress response trait blotching in the halothane challenge population.
BMC Genomics | 2015
James E. Koltes; Eric R. Fritz-Waters; Christopher J. Eisley; Igseo Choi; Hua Bao; Arun Kommadath; Nick V. L. Serão; Nicholas James Boddicker; Samuel M Abrams; Martine Schroyen; Hyelee Loyd; Christopher K. Tuggle; Graham Plastow; Le Luo Guan; Paul Stothard; Joan K. Lunney; Peng Liu; Susan Carpenter; Raymond R. R. Rowland; Jack C. M. Dekkers; James M. Reecy
BMC Genomics | 2015
Martine Schroyen; Juan P. Steibel; James E. Koltes; Igseo Choi; Nancy E. Raney; Christopher J. Eisley; Eric R. Fritz-Waters; James M. Reecy; Jack C. M. Dekkers; Robert R. R. Rowland; Joan K. Lunney; C. W. Ernst; Christopher K. Tuggle
BMC Genomics | 2016
Martine Schroyen; Christopher J. Eisley; James E. Koltes; Eric R. Fritz-Waters; Igseo Choi; Graham Plastow; Le Luo Guan; Paul Stothard; Hua Bao; Arun Kommadath; James M. Reecy; Joan K. Lunney; Robert R. R. Rowland; Jack C. M. Dekkers; Christopher K. Tuggle