Identification of a putative quantitative trait nucleotide in guanylate binding protein 5 for host response to PRRS virus infection
Background Previously, we identified a major quantitative trait locus (QTL) for host response to Porcine Respiratory and Reproductive Syndrome virus (PRRSV) infection in high linkage disequilibrium (LD) with SNP rs80800372 on Sus scrofa chromosome 4 (SSC4). Results Within this QTL, guanylate binding...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Koltes, James E. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2015 |
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| Schlagwörter: |
Quantitative Trait Locus Region |
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| Anmerkung: |
© Koltes et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
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| Übergeordnetes Werk: |
Enthalten in: BMC genomics - London : BioMed Central, 2000, 16(2015), 1 vom: 28. Mai |
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| Übergeordnetes Werk: |
volume:16 ; year:2015 ; number:1 ; day:28 ; month:05 |
| Links: |
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| DOI / URN: |
10.1186/s12864-015-1635-9 |
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| Katalog-ID: |
SPR027107310 |
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| 100 | 1 | |a Koltes, James E. |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Identification of a putative quantitative trait nucleotide in guanylate binding protein 5 for host response to PRRS virus infection |
| 264 | 1 | |c 2015 | |
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| 500 | |a © Koltes et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( | ||
| 520 | |a Background Previously, we identified a major quantitative trait locus (QTL) for host response to Porcine Respiratory and Reproductive Syndrome virus (PRRSV) infection in high linkage disequilibrium (LD) with SNP rs80800372 on Sus scrofa chromosome 4 (SSC4). Results Within this QTL, guanylate binding protein 5 (GBP5) was differentially expressed (DE) (p < 0.05) in blood from AA versus AB rs80800372 genotyped pigs at 7,11, and 14 days post PRRSV infection. All variants within the GBP5 transcript in LD with rs80800372 exhibited allele specific expression (ASE) in AB individuals (p < 0.0001). A transcript re-assembly revealed three alternatively spliced transcripts for GBP5. An intronic SNP in GBP5, rs340943904, introduces a splice acceptor site that inserts five nucleotides into the transcript. Individuals homozygous for the unfavorable AA genotype predominantly produced this transcript, with a shifted reading frame and early stop codon that truncates the 88 C-terminal amino acids of the protein. RNA-seq analysis confirmed this SNP was associated with differential splicing by QTL genotype (p < 0.0001) and this was validated by quantitative capillary electrophoresis (p < 0.0001). The wild-type transcript was expressed at a higher level in AB versus AA individuals, whereas the five-nucleotide insertion transcript was the dominant form in AA individuals. Splicing and ASE results are consistent with the observed dominant nature of the favorable QTL allele. The rs340943904 SNP was also 100 % concordant with rs80800372 in a validation population that possessed an alternate form of the favorable B QTL haplotype. Conclusions GBP5 is known to play a role in inflammasome assembly during immune response. However, the role of GBP5 host genetic variation in viral immunity is novel. These findings demonstrate that rs340943904 is a strong candidate causal mutation for the SSC4 QTL that controls variation in host response to PRRSV. | ||
| 650 | 4 | |a Quantitative Trait Locus |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Differentially Express |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Quantitative Trait Locus Region |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Quantitative Trait Locus Allele |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Allele Specific Expression |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Fritz-Waters, Eric |4 aut | |
| 700 | 1 | |a Eisley, Chris J. |4 aut | |
| 700 | 1 | |a Choi, Igseo |4 aut | |
| 700 | 1 | |a Bao, Hua |4 aut | |
| 700 | 1 | |a Kommadath, Arun |4 aut | |
| 700 | 1 | |a Serão, Nick V. L. |4 aut | |
| 700 | 1 | |a Boddicker, Nicholas J. |4 aut | |
| 700 | 1 | |a Abrams, Sam M. |4 aut | |
| 700 | 1 | |a Schroyen, Martine |4 aut | |
| 700 | 1 | |a Loyd, Hyelee |4 aut | |
| 700 | 1 | |a Tuggle, Chris K. |4 aut | |
| 700 | 1 | |a Plastow, Graham S. |4 aut | |
| 700 | 1 | |a Guan, Leluo |4 aut | |
| 700 | 1 | |a Stothard, Paul |4 aut | |
| 700 | 1 | |a Lunney, Joan K. |4 aut | |
| 700 | 1 | |a Liu, Peng |4 aut | |
| 700 | 1 | |a Carpenter, Susan |4 aut | |
| 700 | 1 | |a Rowland, Robert R. R. |4 aut | |
| 700 | 1 | |a Dekkers, Jack C. M. |4 aut | |
| 700 | 1 | |a Reecy, James M. |4 aut | |
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10.1186/s12864-015-1635-9 doi (DE-627)SPR027107310 (SPR)s12864-015-1635-9-e DE-627 ger DE-627 rakwb eng Koltes, James E. verfasserin aut Identification of a putative quantitative trait nucleotide in guanylate binding protein 5 for host response to PRRS virus infection 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Koltes et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Previously, we identified a major quantitative trait locus (QTL) for host response to Porcine Respiratory and Reproductive Syndrome virus (PRRSV) infection in high linkage disequilibrium (LD) with SNP rs80800372 on Sus scrofa chromosome 4 (SSC4). Results Within this QTL, guanylate binding protein 5 (GBP5) was differentially expressed (DE) (p < 0.05) in blood from AA versus AB rs80800372 genotyped pigs at 7,11, and 14 days post PRRSV infection. All variants within the GBP5 transcript in LD with rs80800372 exhibited allele specific expression (ASE) in AB individuals (p < 0.0001). A transcript re-assembly revealed three alternatively spliced transcripts for GBP5. An intronic SNP in GBP5, rs340943904, introduces a splice acceptor site that inserts five nucleotides into the transcript. Individuals homozygous for the unfavorable AA genotype predominantly produced this transcript, with a shifted reading frame and early stop codon that truncates the 88 C-terminal amino acids of the protein. RNA-seq analysis confirmed this SNP was associated with differential splicing by QTL genotype (p < 0.0001) and this was validated by quantitative capillary electrophoresis (p < 0.0001). The wild-type transcript was expressed at a higher level in AB versus AA individuals, whereas the five-nucleotide insertion transcript was the dominant form in AA individuals. Splicing and ASE results are consistent with the observed dominant nature of the favorable QTL allele. The rs340943904 SNP was also 100 % concordant with rs80800372 in a validation population that possessed an alternate form of the favorable B QTL haplotype. Conclusions GBP5 is known to play a role in inflammasome assembly during immune response. However, the role of GBP5 host genetic variation in viral immunity is novel. These findings demonstrate that rs340943904 is a strong candidate causal mutation for the SSC4 QTL that controls variation in host response to PRRSV. Quantitative Trait Locus (dpeaa)DE-He213 Differentially Express (dpeaa)DE-He213 Quantitative Trait Locus Region (dpeaa)DE-He213 Quantitative Trait Locus Allele (dpeaa)DE-He213 Allele Specific Expression (dpeaa)DE-He213 Fritz-Waters, Eric aut Eisley, Chris J. aut Choi, Igseo aut Bao, Hua aut Kommadath, Arun aut Serão, Nick V. L. aut Boddicker, Nicholas J. aut Abrams, Sam M. aut Schroyen, Martine aut Loyd, Hyelee aut Tuggle, Chris K. aut Plastow, Graham S. aut Guan, Leluo aut Stothard, Paul aut Lunney, Joan K. aut Liu, Peng aut Carpenter, Susan aut Rowland, Robert R. R. aut Dekkers, Jack C. M. aut Reecy, James M. aut Enthalten in BMC genomics London : BioMed Central, 2000 16(2015), 1 vom: 28. Mai (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:16 year:2015 number:1 day:28 month:05 https://dx.doi.org/10.1186/s12864-015-1635-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2015 1 28 05 |
| spelling |
10.1186/s12864-015-1635-9 doi (DE-627)SPR027107310 (SPR)s12864-015-1635-9-e DE-627 ger DE-627 rakwb eng Koltes, James E. verfasserin aut Identification of a putative quantitative trait nucleotide in guanylate binding protein 5 for host response to PRRS virus infection 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Koltes et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Previously, we identified a major quantitative trait locus (QTL) for host response to Porcine Respiratory and Reproductive Syndrome virus (PRRSV) infection in high linkage disequilibrium (LD) with SNP rs80800372 on Sus scrofa chromosome 4 (SSC4). Results Within this QTL, guanylate binding protein 5 (GBP5) was differentially expressed (DE) (p < 0.05) in blood from AA versus AB rs80800372 genotyped pigs at 7,11, and 14 days post PRRSV infection. All variants within the GBP5 transcript in LD with rs80800372 exhibited allele specific expression (ASE) in AB individuals (p < 0.0001). A transcript re-assembly revealed three alternatively spliced transcripts for GBP5. An intronic SNP in GBP5, rs340943904, introduces a splice acceptor site that inserts five nucleotides into the transcript. Individuals homozygous for the unfavorable AA genotype predominantly produced this transcript, with a shifted reading frame and early stop codon that truncates the 88 C-terminal amino acids of the protein. RNA-seq analysis confirmed this SNP was associated with differential splicing by QTL genotype (p < 0.0001) and this was validated by quantitative capillary electrophoresis (p < 0.0001). The wild-type transcript was expressed at a higher level in AB versus AA individuals, whereas the five-nucleotide insertion transcript was the dominant form in AA individuals. Splicing and ASE results are consistent with the observed dominant nature of the favorable QTL allele. The rs340943904 SNP was also 100 % concordant with rs80800372 in a validation population that possessed an alternate form of the favorable B QTL haplotype. Conclusions GBP5 is known to play a role in inflammasome assembly during immune response. However, the role of GBP5 host genetic variation in viral immunity is novel. These findings demonstrate that rs340943904 is a strong candidate causal mutation for the SSC4 QTL that controls variation in host response to PRRSV. Quantitative Trait Locus (dpeaa)DE-He213 Differentially Express (dpeaa)DE-He213 Quantitative Trait Locus Region (dpeaa)DE-He213 Quantitative Trait Locus Allele (dpeaa)DE-He213 Allele Specific Expression (dpeaa)DE-He213 Fritz-Waters, Eric aut Eisley, Chris J. aut Choi, Igseo aut Bao, Hua aut Kommadath, Arun aut Serão, Nick V. L. aut Boddicker, Nicholas J. aut Abrams, Sam M. aut Schroyen, Martine aut Loyd, Hyelee aut Tuggle, Chris K. aut Plastow, Graham S. aut Guan, Leluo aut Stothard, Paul aut Lunney, Joan K. aut Liu, Peng aut Carpenter, Susan aut Rowland, Robert R. R. aut Dekkers, Jack C. M. aut Reecy, James M. aut Enthalten in BMC genomics London : BioMed Central, 2000 16(2015), 1 vom: 28. Mai (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:16 year:2015 number:1 day:28 month:05 https://dx.doi.org/10.1186/s12864-015-1635-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2015 1 28 05 |
| allfields_unstemmed |
10.1186/s12864-015-1635-9 doi (DE-627)SPR027107310 (SPR)s12864-015-1635-9-e DE-627 ger DE-627 rakwb eng Koltes, James E. verfasserin aut Identification of a putative quantitative trait nucleotide in guanylate binding protein 5 for host response to PRRS virus infection 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Koltes et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Previously, we identified a major quantitative trait locus (QTL) for host response to Porcine Respiratory and Reproductive Syndrome virus (PRRSV) infection in high linkage disequilibrium (LD) with SNP rs80800372 on Sus scrofa chromosome 4 (SSC4). Results Within this QTL, guanylate binding protein 5 (GBP5) was differentially expressed (DE) (p < 0.05) in blood from AA versus AB rs80800372 genotyped pigs at 7,11, and 14 days post PRRSV infection. All variants within the GBP5 transcript in LD with rs80800372 exhibited allele specific expression (ASE) in AB individuals (p < 0.0001). A transcript re-assembly revealed three alternatively spliced transcripts for GBP5. An intronic SNP in GBP5, rs340943904, introduces a splice acceptor site that inserts five nucleotides into the transcript. Individuals homozygous for the unfavorable AA genotype predominantly produced this transcript, with a shifted reading frame and early stop codon that truncates the 88 C-terminal amino acids of the protein. RNA-seq analysis confirmed this SNP was associated with differential splicing by QTL genotype (p < 0.0001) and this was validated by quantitative capillary electrophoresis (p < 0.0001). The wild-type transcript was expressed at a higher level in AB versus AA individuals, whereas the five-nucleotide insertion transcript was the dominant form in AA individuals. Splicing and ASE results are consistent with the observed dominant nature of the favorable QTL allele. The rs340943904 SNP was also 100 % concordant with rs80800372 in a validation population that possessed an alternate form of the favorable B QTL haplotype. Conclusions GBP5 is known to play a role in inflammasome assembly during immune response. However, the role of GBP5 host genetic variation in viral immunity is novel. These findings demonstrate that rs340943904 is a strong candidate causal mutation for the SSC4 QTL that controls variation in host response to PRRSV. Quantitative Trait Locus (dpeaa)DE-He213 Differentially Express (dpeaa)DE-He213 Quantitative Trait Locus Region (dpeaa)DE-He213 Quantitative Trait Locus Allele (dpeaa)DE-He213 Allele Specific Expression (dpeaa)DE-He213 Fritz-Waters, Eric aut Eisley, Chris J. aut Choi, Igseo aut Bao, Hua aut Kommadath, Arun aut Serão, Nick V. L. aut Boddicker, Nicholas J. aut Abrams, Sam M. aut Schroyen, Martine aut Loyd, Hyelee aut Tuggle, Chris K. aut Plastow, Graham S. aut Guan, Leluo aut Stothard, Paul aut Lunney, Joan K. aut Liu, Peng aut Carpenter, Susan aut Rowland, Robert R. R. aut Dekkers, Jack C. M. aut Reecy, James M. aut Enthalten in BMC genomics London : BioMed Central, 2000 16(2015), 1 vom: 28. Mai (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:16 year:2015 number:1 day:28 month:05 https://dx.doi.org/10.1186/s12864-015-1635-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2015 1 28 05 |
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10.1186/s12864-015-1635-9 doi (DE-627)SPR027107310 (SPR)s12864-015-1635-9-e DE-627 ger DE-627 rakwb eng Koltes, James E. verfasserin aut Identification of a putative quantitative trait nucleotide in guanylate binding protein 5 for host response to PRRS virus infection 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Koltes et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Previously, we identified a major quantitative trait locus (QTL) for host response to Porcine Respiratory and Reproductive Syndrome virus (PRRSV) infection in high linkage disequilibrium (LD) with SNP rs80800372 on Sus scrofa chromosome 4 (SSC4). Results Within this QTL, guanylate binding protein 5 (GBP5) was differentially expressed (DE) (p < 0.05) in blood from AA versus AB rs80800372 genotyped pigs at 7,11, and 14 days post PRRSV infection. All variants within the GBP5 transcript in LD with rs80800372 exhibited allele specific expression (ASE) in AB individuals (p < 0.0001). A transcript re-assembly revealed three alternatively spliced transcripts for GBP5. An intronic SNP in GBP5, rs340943904, introduces a splice acceptor site that inserts five nucleotides into the transcript. Individuals homozygous for the unfavorable AA genotype predominantly produced this transcript, with a shifted reading frame and early stop codon that truncates the 88 C-terminal amino acids of the protein. RNA-seq analysis confirmed this SNP was associated with differential splicing by QTL genotype (p < 0.0001) and this was validated by quantitative capillary electrophoresis (p < 0.0001). The wild-type transcript was expressed at a higher level in AB versus AA individuals, whereas the five-nucleotide insertion transcript was the dominant form in AA individuals. Splicing and ASE results are consistent with the observed dominant nature of the favorable QTL allele. The rs340943904 SNP was also 100 % concordant with rs80800372 in a validation population that possessed an alternate form of the favorable B QTL haplotype. Conclusions GBP5 is known to play a role in inflammasome assembly during immune response. However, the role of GBP5 host genetic variation in viral immunity is novel. These findings demonstrate that rs340943904 is a strong candidate causal mutation for the SSC4 QTL that controls variation in host response to PRRSV. Quantitative Trait Locus (dpeaa)DE-He213 Differentially Express (dpeaa)DE-He213 Quantitative Trait Locus Region (dpeaa)DE-He213 Quantitative Trait Locus Allele (dpeaa)DE-He213 Allele Specific Expression (dpeaa)DE-He213 Fritz-Waters, Eric aut Eisley, Chris J. aut Choi, Igseo aut Bao, Hua aut Kommadath, Arun aut Serão, Nick V. L. aut Boddicker, Nicholas J. aut Abrams, Sam M. aut Schroyen, Martine aut Loyd, Hyelee aut Tuggle, Chris K. aut Plastow, Graham S. aut Guan, Leluo aut Stothard, Paul aut Lunney, Joan K. aut Liu, Peng aut Carpenter, Susan aut Rowland, Robert R. R. aut Dekkers, Jack C. M. aut Reecy, James M. aut Enthalten in BMC genomics London : BioMed Central, 2000 16(2015), 1 vom: 28. Mai (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:16 year:2015 number:1 day:28 month:05 https://dx.doi.org/10.1186/s12864-015-1635-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2015 1 28 05 |
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10.1186/s12864-015-1635-9 doi (DE-627)SPR027107310 (SPR)s12864-015-1635-9-e DE-627 ger DE-627 rakwb eng Koltes, James E. verfasserin aut Identification of a putative quantitative trait nucleotide in guanylate binding protein 5 for host response to PRRS virus infection 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Koltes et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Previously, we identified a major quantitative trait locus (QTL) for host response to Porcine Respiratory and Reproductive Syndrome virus (PRRSV) infection in high linkage disequilibrium (LD) with SNP rs80800372 on Sus scrofa chromosome 4 (SSC4). Results Within this QTL, guanylate binding protein 5 (GBP5) was differentially expressed (DE) (p < 0.05) in blood from AA versus AB rs80800372 genotyped pigs at 7,11, and 14 days post PRRSV infection. All variants within the GBP5 transcript in LD with rs80800372 exhibited allele specific expression (ASE) in AB individuals (p < 0.0001). A transcript re-assembly revealed three alternatively spliced transcripts for GBP5. An intronic SNP in GBP5, rs340943904, introduces a splice acceptor site that inserts five nucleotides into the transcript. Individuals homozygous for the unfavorable AA genotype predominantly produced this transcript, with a shifted reading frame and early stop codon that truncates the 88 C-terminal amino acids of the protein. RNA-seq analysis confirmed this SNP was associated with differential splicing by QTL genotype (p < 0.0001) and this was validated by quantitative capillary electrophoresis (p < 0.0001). The wild-type transcript was expressed at a higher level in AB versus AA individuals, whereas the five-nucleotide insertion transcript was the dominant form in AA individuals. Splicing and ASE results are consistent with the observed dominant nature of the favorable QTL allele. The rs340943904 SNP was also 100 % concordant with rs80800372 in a validation population that possessed an alternate form of the favorable B QTL haplotype. Conclusions GBP5 is known to play a role in inflammasome assembly during immune response. However, the role of GBP5 host genetic variation in viral immunity is novel. These findings demonstrate that rs340943904 is a strong candidate causal mutation for the SSC4 QTL that controls variation in host response to PRRSV. Quantitative Trait Locus (dpeaa)DE-He213 Differentially Express (dpeaa)DE-He213 Quantitative Trait Locus Region (dpeaa)DE-He213 Quantitative Trait Locus Allele (dpeaa)DE-He213 Allele Specific Expression (dpeaa)DE-He213 Fritz-Waters, Eric aut Eisley, Chris J. aut Choi, Igseo aut Bao, Hua aut Kommadath, Arun aut Serão, Nick V. L. aut Boddicker, Nicholas J. aut Abrams, Sam M. aut Schroyen, Martine aut Loyd, Hyelee aut Tuggle, Chris K. aut Plastow, Graham S. aut Guan, Leluo aut Stothard, Paul aut Lunney, Joan K. aut Liu, Peng aut Carpenter, Susan aut Rowland, Robert R. R. aut Dekkers, Jack C. M. aut Reecy, James M. aut Enthalten in BMC genomics London : BioMed Central, 2000 16(2015), 1 vom: 28. Mai (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:16 year:2015 number:1 day:28 month:05 https://dx.doi.org/10.1186/s12864-015-1635-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2015 1 28 05 |
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Koltes, James E. @@aut@@ Fritz-Waters, Eric @@aut@@ Eisley, Chris J. @@aut@@ Choi, Igseo @@aut@@ Bao, Hua @@aut@@ Kommadath, Arun @@aut@@ Serão, Nick V. L. @@aut@@ Boddicker, Nicholas J. @@aut@@ Abrams, Sam M. @@aut@@ Schroyen, Martine @@aut@@ Loyd, Hyelee @@aut@@ Tuggle, Chris K. @@aut@@ Plastow, Graham S. @@aut@@ Guan, Leluo @@aut@@ Stothard, Paul @@aut@@ Lunney, Joan K. @@aut@@ Liu, Peng @@aut@@ Carpenter, Susan @@aut@@ Rowland, Robert R. R. @@aut@@ Dekkers, Jack C. M. @@aut@@ Reecy, James M. @@aut@@ |
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Koltes, James E. misc Quantitative Trait Locus misc Differentially Express misc Quantitative Trait Locus Region misc Quantitative Trait Locus Allele misc Allele Specific Expression Identification of a putative quantitative trait nucleotide in guanylate binding protein 5 for host response to PRRS virus infection |
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Identification of a putative quantitative trait nucleotide in guanylate binding protein 5 for host response to PRRS virus infection Quantitative Trait Locus (dpeaa)DE-He213 Differentially Express (dpeaa)DE-He213 Quantitative Trait Locus Region (dpeaa)DE-He213 Quantitative Trait Locus Allele (dpeaa)DE-He213 Allele Specific Expression (dpeaa)DE-He213 |
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Koltes, James E. Fritz-Waters, Eric Eisley, Chris J. Choi, Igseo Bao, Hua Kommadath, Arun Serão, Nick V. L. Boddicker, Nicholas J. Abrams, Sam M. Schroyen, Martine Loyd, Hyelee Tuggle, Chris K. Plastow, Graham S. Guan, Leluo Stothard, Paul Lunney, Joan K. Liu, Peng Carpenter, Susan Rowland, Robert R. R. Dekkers, Jack C. M. Reecy, James M. |
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identification of a putative quantitative trait nucleotide in guanylate binding protein 5 for host response to prrs virus infection |
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Identification of a putative quantitative trait nucleotide in guanylate binding protein 5 for host response to PRRS virus infection |
| abstract |
Background Previously, we identified a major quantitative trait locus (QTL) for host response to Porcine Respiratory and Reproductive Syndrome virus (PRRSV) infection in high linkage disequilibrium (LD) with SNP rs80800372 on Sus scrofa chromosome 4 (SSC4). Results Within this QTL, guanylate binding protein 5 (GBP5) was differentially expressed (DE) (p < 0.05) in blood from AA versus AB rs80800372 genotyped pigs at 7,11, and 14 days post PRRSV infection. All variants within the GBP5 transcript in LD with rs80800372 exhibited allele specific expression (ASE) in AB individuals (p < 0.0001). A transcript re-assembly revealed three alternatively spliced transcripts for GBP5. An intronic SNP in GBP5, rs340943904, introduces a splice acceptor site that inserts five nucleotides into the transcript. Individuals homozygous for the unfavorable AA genotype predominantly produced this transcript, with a shifted reading frame and early stop codon that truncates the 88 C-terminal amino acids of the protein. RNA-seq analysis confirmed this SNP was associated with differential splicing by QTL genotype (p < 0.0001) and this was validated by quantitative capillary electrophoresis (p < 0.0001). The wild-type transcript was expressed at a higher level in AB versus AA individuals, whereas the five-nucleotide insertion transcript was the dominant form in AA individuals. Splicing and ASE results are consistent with the observed dominant nature of the favorable QTL allele. The rs340943904 SNP was also 100 % concordant with rs80800372 in a validation population that possessed an alternate form of the favorable B QTL haplotype. Conclusions GBP5 is known to play a role in inflammasome assembly during immune response. However, the role of GBP5 host genetic variation in viral immunity is novel. These findings demonstrate that rs340943904 is a strong candidate causal mutation for the SSC4 QTL that controls variation in host response to PRRSV. © Koltes et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
| abstractGer |
Background Previously, we identified a major quantitative trait locus (QTL) for host response to Porcine Respiratory and Reproductive Syndrome virus (PRRSV) infection in high linkage disequilibrium (LD) with SNP rs80800372 on Sus scrofa chromosome 4 (SSC4). Results Within this QTL, guanylate binding protein 5 (GBP5) was differentially expressed (DE) (p < 0.05) in blood from AA versus AB rs80800372 genotyped pigs at 7,11, and 14 days post PRRSV infection. All variants within the GBP5 transcript in LD with rs80800372 exhibited allele specific expression (ASE) in AB individuals (p < 0.0001). A transcript re-assembly revealed three alternatively spliced transcripts for GBP5. An intronic SNP in GBP5, rs340943904, introduces a splice acceptor site that inserts five nucleotides into the transcript. Individuals homozygous for the unfavorable AA genotype predominantly produced this transcript, with a shifted reading frame and early stop codon that truncates the 88 C-terminal amino acids of the protein. RNA-seq analysis confirmed this SNP was associated with differential splicing by QTL genotype (p < 0.0001) and this was validated by quantitative capillary electrophoresis (p < 0.0001). The wild-type transcript was expressed at a higher level in AB versus AA individuals, whereas the five-nucleotide insertion transcript was the dominant form in AA individuals. Splicing and ASE results are consistent with the observed dominant nature of the favorable QTL allele. The rs340943904 SNP was also 100 % concordant with rs80800372 in a validation population that possessed an alternate form of the favorable B QTL haplotype. Conclusions GBP5 is known to play a role in inflammasome assembly during immune response. However, the role of GBP5 host genetic variation in viral immunity is novel. These findings demonstrate that rs340943904 is a strong candidate causal mutation for the SSC4 QTL that controls variation in host response to PRRSV. © Koltes et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
| abstract_unstemmed |
Background Previously, we identified a major quantitative trait locus (QTL) for host response to Porcine Respiratory and Reproductive Syndrome virus (PRRSV) infection in high linkage disequilibrium (LD) with SNP rs80800372 on Sus scrofa chromosome 4 (SSC4). Results Within this QTL, guanylate binding protein 5 (GBP5) was differentially expressed (DE) (p < 0.05) in blood from AA versus AB rs80800372 genotyped pigs at 7,11, and 14 days post PRRSV infection. All variants within the GBP5 transcript in LD with rs80800372 exhibited allele specific expression (ASE) in AB individuals (p < 0.0001). A transcript re-assembly revealed three alternatively spliced transcripts for GBP5. An intronic SNP in GBP5, rs340943904, introduces a splice acceptor site that inserts five nucleotides into the transcript. Individuals homozygous for the unfavorable AA genotype predominantly produced this transcript, with a shifted reading frame and early stop codon that truncates the 88 C-terminal amino acids of the protein. RNA-seq analysis confirmed this SNP was associated with differential splicing by QTL genotype (p < 0.0001) and this was validated by quantitative capillary electrophoresis (p < 0.0001). The wild-type transcript was expressed at a higher level in AB versus AA individuals, whereas the five-nucleotide insertion transcript was the dominant form in AA individuals. Splicing and ASE results are consistent with the observed dominant nature of the favorable QTL allele. The rs340943904 SNP was also 100 % concordant with rs80800372 in a validation population that possessed an alternate form of the favorable B QTL haplotype. Conclusions GBP5 is known to play a role in inflammasome assembly during immune response. However, the role of GBP5 host genetic variation in viral immunity is novel. These findings demonstrate that rs340943904 is a strong candidate causal mutation for the SSC4 QTL that controls variation in host response to PRRSV. © Koltes et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
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This is an Open Access article distributed under the terms of the Creative Commons Attribution License (</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Previously, we identified a major quantitative trait locus (QTL) for host response to Porcine Respiratory and Reproductive Syndrome virus (PRRSV) infection in high linkage disequilibrium (LD) with SNP rs80800372 on Sus scrofa chromosome 4 (SSC4). Results Within this QTL, guanylate binding protein 5 (GBP5) was differentially expressed (DE) (p < 0.05) in blood from AA versus AB rs80800372 genotyped pigs at 7,11, and 14 days post PRRSV infection. All variants within the GBP5 transcript in LD with rs80800372 exhibited allele specific expression (ASE) in AB individuals (p < 0.0001). A transcript re-assembly revealed three alternatively spliced transcripts for GBP5. An intronic SNP in GBP5, rs340943904, introduces a splice acceptor site that inserts five nucleotides into the transcript. Individuals homozygous for the unfavorable AA genotype predominantly produced this transcript, with a shifted reading frame and early stop codon that truncates the 88 C-terminal amino acids of the protein. RNA-seq analysis confirmed this SNP was associated with differential splicing by QTL genotype (p < 0.0001) and this was validated by quantitative capillary electrophoresis (p < 0.0001). The wild-type transcript was expressed at a higher level in AB versus AA individuals, whereas the five-nucleotide insertion transcript was the dominant form in AA individuals. Splicing and ASE results are consistent with the observed dominant nature of the favorable QTL allele. The rs340943904 SNP was also 100 % concordant with rs80800372 in a validation population that possessed an alternate form of the favorable B QTL haplotype. Conclusions GBP5 is known to play a role in inflammasome assembly during immune response. However, the role of GBP5 host genetic variation in viral immunity is novel. These findings demonstrate that rs340943904 is a strong candidate causal mutation for the SSC4 QTL that controls variation in host response to PRRSV.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Quantitative Trait Locus</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Differentially Express</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Quantitative Trait Locus Region</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Quantitative Trait Locus Allele</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Allele Specific Expression</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Fritz-Waters, Eric</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Eisley, Chris J.</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Choi, Igseo</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Bao, Hua</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kommadath, Arun</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Serão, Nick V. 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