FGF4 retrogene on CFA12 is responsible for chondrodystrophy and intervertebral disc disease in dogs
Chondrodystrophy in dogs is defined by dysplastic, shortened long bones and premature degeneration and calcification of intervertebral discs. Independent genome-wide association analyses for skeletal dysplasia (short limbs) within a single breed ([P.sub.Bonferroni] = 0.01) and intervertebral disc di...
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| Autor*in: |
Brown, Emily A [verfasserIn] |
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| Format: |
Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2017 |
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| Rechteinformationen: |
Nutzungsrecht: © COPYRIGHT 2017 National Academy of Sciences |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Proceedings of the National Academy of Sciences of the United States of America - Washington, DC : NAS, 1877, 114(2017), 43, Seite 11476 |
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| Übergeordnetes Werk: |
volume:114 ; year:2017 ; number:43 ; pages:11476 |
| Links: |
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| DOI / URN: |
10.1073/pnas.1709082114 |
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| 245 | 1 | 0 | |a FGF4 retrogene on CFA12 is responsible for chondrodystrophy and intervertebral disc disease in dogs |
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| 520 | |a Chondrodystrophy in dogs is defined by dysplastic, shortened long bones and premature degeneration and calcification of intervertebral discs. Independent genome-wide association analyses for skeletal dysplasia (short limbs) within a single breed ([P.sub.Bonferroni] = 0.01) and intervertebral disc disease (IVDD) across breeds ([P.sub.Bonferroni] = 4.0 x [10.sup.-10]) both identified a significant association to the same region on CFA12. Whole genome sequencing identified a highly expressed FGF4 retrogene within this shared region. The FGF4 retrogene segregated with limb length and had an odds ratio of 51.23 (95% CI = 46.69, 56.20) for IVDD. Long bone length in dogs is a unique example of multiple disease-causing retrocopies of the same parental gene in a mammalian species. FGF signaling abnormalities have been associated with skeletal dysplasia in humans, and our findings present opportunities for both selective elimination of a medically and financially devastating disease in dogs and further understanding of the ever-growing complexity of retrogene biology. | ||
| 540 | |a Nutzungsrecht: © COPYRIGHT 2017 National Academy of Sciences | ||
| 650 | 4 | |a Fibroblast growth factors | |
| 650 | 4 | |a Intervertebral disk | |
| 650 | 4 | |a Intervertebral disk displacement | |
| 650 | 4 | |a Health aspects | |
| 650 | 4 | |a Hernia | |
| 650 | 4 | |a Dogs | |
| 650 | 4 | |a Diseases | |
| 650 | 4 | |a Genetic aspects | |
| 700 | 1 | |a Dickinson, Peter J |4 oth | |
| 700 | 1 | |a Mansour, Tamer |4 oth | |
| 700 | 1 | |a Sturges, Beverly K |4 oth | |
| 700 | 1 | |a Aguilar, Miriam |4 oth | |
| 700 | 1 | |a Young, Amy E |4 oth | |
| 700 | 1 | |a Korff, Courtney |4 oth | |
| 700 | 1 | |a Lind, Jenna |4 oth | |
| 700 | 1 | |a Ettinger, Cassandra L |4 oth | |
| 700 | 1 | |a Varon, Samuel |4 oth | |
| 700 | 1 | |a Pollard, Rachel |4 oth | |
| 700 | 1 | |a Brown, C. Titus |4 oth | |
| 700 | 1 | |a Raudsepp, Terje |4 oth | |
| 700 | 1 | |a Bannasch, Danika L |4 oth | |
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10.1073/pnas.1709082114 doi PQ20171228 (DE-627)OLC1999834895 (DE-599)GBVOLC1999834895 (PRQ)g599-c828563fbc1cb29fc6cfbaf114d414f59575e5a671550e056075bfe5502e89840 (KEY)0583363920170000114004311476fgf4retrogeneoncfa12isresponsibleforchondrodystrop DE-627 ger DE-627 rakwb eng 500 DE-101 570 AVZ LING fid BIODIV fid Brown, Emily A verfasserin aut FGF4 retrogene on CFA12 is responsible for chondrodystrophy and intervertebral disc disease in dogs 2017 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Chondrodystrophy in dogs is defined by dysplastic, shortened long bones and premature degeneration and calcification of intervertebral discs. Independent genome-wide association analyses for skeletal dysplasia (short limbs) within a single breed ([P.sub.Bonferroni] = 0.01) and intervertebral disc disease (IVDD) across breeds ([P.sub.Bonferroni] = 4.0 x [10.sup.-10]) both identified a significant association to the same region on CFA12. Whole genome sequencing identified a highly expressed FGF4 retrogene within this shared region. The FGF4 retrogene segregated with limb length and had an odds ratio of 51.23 (95% CI = 46.69, 56.20) for IVDD. Long bone length in dogs is a unique example of multiple disease-causing retrocopies of the same parental gene in a mammalian species. FGF signaling abnormalities have been associated with skeletal dysplasia in humans, and our findings present opportunities for both selective elimination of a medically and financially devastating disease in dogs and further understanding of the ever-growing complexity of retrogene biology. Nutzungsrecht: © COPYRIGHT 2017 National Academy of Sciences Fibroblast growth factors Intervertebral disk Intervertebral disk displacement Health aspects Hernia Dogs Diseases Genetic aspects Dickinson, Peter J oth Mansour, Tamer oth Sturges, Beverly K oth Aguilar, Miriam oth Young, Amy E oth Korff, Courtney oth Lind, Jenna oth Ettinger, Cassandra L oth Varon, Samuel oth Pollard, Rachel oth Brown, C. Titus oth Raudsepp, Terje oth Bannasch, Danika L oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 114(2017), 43, Seite 11476 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:114 year:2017 number:43 pages:11476 http://dx.doi.org/10.1073/pnas.1709082114 Volltext GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 114 2017 43 11476 |
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10.1073/pnas.1709082114 doi PQ20171228 (DE-627)OLC1999834895 (DE-599)GBVOLC1999834895 (PRQ)g599-c828563fbc1cb29fc6cfbaf114d414f59575e5a671550e056075bfe5502e89840 (KEY)0583363920170000114004311476fgf4retrogeneoncfa12isresponsibleforchondrodystrop DE-627 ger DE-627 rakwb eng 500 DE-101 570 AVZ LING fid BIODIV fid Brown, Emily A verfasserin aut FGF4 retrogene on CFA12 is responsible for chondrodystrophy and intervertebral disc disease in dogs 2017 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Chondrodystrophy in dogs is defined by dysplastic, shortened long bones and premature degeneration and calcification of intervertebral discs. Independent genome-wide association analyses for skeletal dysplasia (short limbs) within a single breed ([P.sub.Bonferroni] = 0.01) and intervertebral disc disease (IVDD) across breeds ([P.sub.Bonferroni] = 4.0 x [10.sup.-10]) both identified a significant association to the same region on CFA12. Whole genome sequencing identified a highly expressed FGF4 retrogene within this shared region. The FGF4 retrogene segregated with limb length and had an odds ratio of 51.23 (95% CI = 46.69, 56.20) for IVDD. Long bone length in dogs is a unique example of multiple disease-causing retrocopies of the same parental gene in a mammalian species. FGF signaling abnormalities have been associated with skeletal dysplasia in humans, and our findings present opportunities for both selective elimination of a medically and financially devastating disease in dogs and further understanding of the ever-growing complexity of retrogene biology. Nutzungsrecht: © COPYRIGHT 2017 National Academy of Sciences Fibroblast growth factors Intervertebral disk Intervertebral disk displacement Health aspects Hernia Dogs Diseases Genetic aspects Dickinson, Peter J oth Mansour, Tamer oth Sturges, Beverly K oth Aguilar, Miriam oth Young, Amy E oth Korff, Courtney oth Lind, Jenna oth Ettinger, Cassandra L oth Varon, Samuel oth Pollard, Rachel oth Brown, C. Titus oth Raudsepp, Terje oth Bannasch, Danika L oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 114(2017), 43, Seite 11476 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:114 year:2017 number:43 pages:11476 http://dx.doi.org/10.1073/pnas.1709082114 Volltext GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 114 2017 43 11476 |
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10.1073/pnas.1709082114 doi PQ20171228 (DE-627)OLC1999834895 (DE-599)GBVOLC1999834895 (PRQ)g599-c828563fbc1cb29fc6cfbaf114d414f59575e5a671550e056075bfe5502e89840 (KEY)0583363920170000114004311476fgf4retrogeneoncfa12isresponsibleforchondrodystrop DE-627 ger DE-627 rakwb eng 500 DE-101 570 AVZ LING fid BIODIV fid Brown, Emily A verfasserin aut FGF4 retrogene on CFA12 is responsible for chondrodystrophy and intervertebral disc disease in dogs 2017 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Chondrodystrophy in dogs is defined by dysplastic, shortened long bones and premature degeneration and calcification of intervertebral discs. Independent genome-wide association analyses for skeletal dysplasia (short limbs) within a single breed ([P.sub.Bonferroni] = 0.01) and intervertebral disc disease (IVDD) across breeds ([P.sub.Bonferroni] = 4.0 x [10.sup.-10]) both identified a significant association to the same region on CFA12. Whole genome sequencing identified a highly expressed FGF4 retrogene within this shared region. The FGF4 retrogene segregated with limb length and had an odds ratio of 51.23 (95% CI = 46.69, 56.20) for IVDD. Long bone length in dogs is a unique example of multiple disease-causing retrocopies of the same parental gene in a mammalian species. FGF signaling abnormalities have been associated with skeletal dysplasia in humans, and our findings present opportunities for both selective elimination of a medically and financially devastating disease in dogs and further understanding of the ever-growing complexity of retrogene biology. Nutzungsrecht: © COPYRIGHT 2017 National Academy of Sciences Fibroblast growth factors Intervertebral disk Intervertebral disk displacement Health aspects Hernia Dogs Diseases Genetic aspects Dickinson, Peter J oth Mansour, Tamer oth Sturges, Beverly K oth Aguilar, Miriam oth Young, Amy E oth Korff, Courtney oth Lind, Jenna oth Ettinger, Cassandra L oth Varon, Samuel oth Pollard, Rachel oth Brown, C. Titus oth Raudsepp, Terje oth Bannasch, Danika L oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 114(2017), 43, Seite 11476 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:114 year:2017 number:43 pages:11476 http://dx.doi.org/10.1073/pnas.1709082114 Volltext GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 114 2017 43 11476 |
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10.1073/pnas.1709082114 doi PQ20171228 (DE-627)OLC1999834895 (DE-599)GBVOLC1999834895 (PRQ)g599-c828563fbc1cb29fc6cfbaf114d414f59575e5a671550e056075bfe5502e89840 (KEY)0583363920170000114004311476fgf4retrogeneoncfa12isresponsibleforchondrodystrop DE-627 ger DE-627 rakwb eng 500 DE-101 570 AVZ LING fid BIODIV fid Brown, Emily A verfasserin aut FGF4 retrogene on CFA12 is responsible for chondrodystrophy and intervertebral disc disease in dogs 2017 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Chondrodystrophy in dogs is defined by dysplastic, shortened long bones and premature degeneration and calcification of intervertebral discs. Independent genome-wide association analyses for skeletal dysplasia (short limbs) within a single breed ([P.sub.Bonferroni] = 0.01) and intervertebral disc disease (IVDD) across breeds ([P.sub.Bonferroni] = 4.0 x [10.sup.-10]) both identified a significant association to the same region on CFA12. Whole genome sequencing identified a highly expressed FGF4 retrogene within this shared region. The FGF4 retrogene segregated with limb length and had an odds ratio of 51.23 (95% CI = 46.69, 56.20) for IVDD. Long bone length in dogs is a unique example of multiple disease-causing retrocopies of the same parental gene in a mammalian species. FGF signaling abnormalities have been associated with skeletal dysplasia in humans, and our findings present opportunities for both selective elimination of a medically and financially devastating disease in dogs and further understanding of the ever-growing complexity of retrogene biology. Nutzungsrecht: © COPYRIGHT 2017 National Academy of Sciences Fibroblast growth factors Intervertebral disk Intervertebral disk displacement Health aspects Hernia Dogs Diseases Genetic aspects Dickinson, Peter J oth Mansour, Tamer oth Sturges, Beverly K oth Aguilar, Miriam oth Young, Amy E oth Korff, Courtney oth Lind, Jenna oth Ettinger, Cassandra L oth Varon, Samuel oth Pollard, Rachel oth Brown, C. Titus oth Raudsepp, Terje oth Bannasch, Danika L oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 114(2017), 43, Seite 11476 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:114 year:2017 number:43 pages:11476 http://dx.doi.org/10.1073/pnas.1709082114 Volltext GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 114 2017 43 11476 |
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Brown, Emily A @@aut@@ Dickinson, Peter J @@oth@@ Mansour, Tamer @@oth@@ Sturges, Beverly K @@oth@@ Aguilar, Miriam @@oth@@ Young, Amy E @@oth@@ Korff, Courtney @@oth@@ Lind, Jenna @@oth@@ Ettinger, Cassandra L @@oth@@ Varon, Samuel @@oth@@ Pollard, Rachel @@oth@@ Brown, C. Titus @@oth@@ Raudsepp, Terje @@oth@@ Bannasch, Danika L @@oth@@ |
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FGF4 retrogene on CFA12 is responsible for chondrodystrophy and intervertebral disc disease in dogs |
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FGF4 retrogene on CFA12 is responsible for chondrodystrophy and intervertebral disc disease in dogs |
| abstract |
Chondrodystrophy in dogs is defined by dysplastic, shortened long bones and premature degeneration and calcification of intervertebral discs. Independent genome-wide association analyses for skeletal dysplasia (short limbs) within a single breed ([P.sub.Bonferroni] = 0.01) and intervertebral disc disease (IVDD) across breeds ([P.sub.Bonferroni] = 4.0 x [10.sup.-10]) both identified a significant association to the same region on CFA12. Whole genome sequencing identified a highly expressed FGF4 retrogene within this shared region. The FGF4 retrogene segregated with limb length and had an odds ratio of 51.23 (95% CI = 46.69, 56.20) for IVDD. Long bone length in dogs is a unique example of multiple disease-causing retrocopies of the same parental gene in a mammalian species. FGF signaling abnormalities have been associated with skeletal dysplasia in humans, and our findings present opportunities for both selective elimination of a medically and financially devastating disease in dogs and further understanding of the ever-growing complexity of retrogene biology. |
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Chondrodystrophy in dogs is defined by dysplastic, shortened long bones and premature degeneration and calcification of intervertebral discs. Independent genome-wide association analyses for skeletal dysplasia (short limbs) within a single breed ([P.sub.Bonferroni] = 0.01) and intervertebral disc disease (IVDD) across breeds ([P.sub.Bonferroni] = 4.0 x [10.sup.-10]) both identified a significant association to the same region on CFA12. Whole genome sequencing identified a highly expressed FGF4 retrogene within this shared region. The FGF4 retrogene segregated with limb length and had an odds ratio of 51.23 (95% CI = 46.69, 56.20) for IVDD. Long bone length in dogs is a unique example of multiple disease-causing retrocopies of the same parental gene in a mammalian species. FGF signaling abnormalities have been associated with skeletal dysplasia in humans, and our findings present opportunities for both selective elimination of a medically and financially devastating disease in dogs and further understanding of the ever-growing complexity of retrogene biology. |
| abstract_unstemmed |
Chondrodystrophy in dogs is defined by dysplastic, shortened long bones and premature degeneration and calcification of intervertebral discs. Independent genome-wide association analyses for skeletal dysplasia (short limbs) within a single breed ([P.sub.Bonferroni] = 0.01) and intervertebral disc disease (IVDD) across breeds ([P.sub.Bonferroni] = 4.0 x [10.sup.-10]) both identified a significant association to the same region on CFA12. Whole genome sequencing identified a highly expressed FGF4 retrogene within this shared region. The FGF4 retrogene segregated with limb length and had an odds ratio of 51.23 (95% CI = 46.69, 56.20) for IVDD. Long bone length in dogs is a unique example of multiple disease-causing retrocopies of the same parental gene in a mammalian species. FGF signaling abnormalities have been associated with skeletal dysplasia in humans, and our findings present opportunities for both selective elimination of a medically and financially devastating disease in dogs and further understanding of the ever-growing complexity of retrogene biology. |
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FGF4 retrogene on CFA12 is responsible for chondrodystrophy and intervertebral disc disease in dogs |
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Dickinson, Peter J Mansour, Tamer Sturges, Beverly K Aguilar, Miriam Young, Amy E Korff, Courtney Lind, Jenna Ettinger, Cassandra L Varon, Samuel Pollard, Rachel Brown, C. Titus Raudsepp, Terje Bannasch, Danika L |
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Independent genome-wide association analyses for skeletal dysplasia (short limbs) within a single breed ([P.sub.Bonferroni] = 0.01) and intervertebral disc disease (IVDD) across breeds ([P.sub.Bonferroni] = 4.0 x [10.sup.-10]) both identified a significant association to the same region on CFA12. Whole genome sequencing identified a highly expressed FGF4 retrogene within this shared region. The FGF4 retrogene segregated with limb length and had an odds ratio of 51.23 (95% CI = 46.69, 56.20) for IVDD. Long bone length in dogs is a unique example of multiple disease-causing retrocopies of the same parental gene in a mammalian species. 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Titus</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Raudsepp, Terje</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Bannasch, Danika L</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Proceedings of the National Academy of Sciences of the United States of America</subfield><subfield code="d">Washington, DC : NAS, 1877</subfield><subfield code="g">114(2017), 43, Seite 11476</subfield><subfield code="w">(DE-627)129505269</subfield><subfield code="w">(DE-600)209104-5</subfield><subfield code="w">(DE-576)014909189</subfield><subfield code="x">0027-8424</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:114</subfield><subfield code="g">year:2017</subfield><subfield code="g">number:43</subfield><subfield code="g">pages:11476</subfield></datafield><datafield tag="856" ind1="4" ind2="1"><subfield code="u">http://dx.doi.org/10.1073/pnas.1709082114</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_OLC</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">FID-LING</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">FID-BIODIV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHY</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-CHE</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-MAT</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-FOR</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-DE-84</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-MAT</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-FOR</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_59</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">114</subfield><subfield code="j">2017</subfield><subfield code="e">43</subfield><subfield code="h">11476</subfield></datafield></record></collection>
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