DA rats from two colonies differ genetically and in their arthritis susceptibility
Identifieur interne : 000292 ( Pmc/Curation ); précédent : 000291; suivant : 000293DA rats from two colonies differ genetically and in their arthritis susceptibility
Auteurs : Carola Rintisch [Suède] ; Rikard Holmdahl [Suède]Source :
- Mammalian Genome [ 0938-8990 ] ; 2008.
Abstract
The arthritis-susceptible DA rat is one of the most commonly used rat strains for genetic linkage analysis and is instrumental for the identification of many genetic loci. Even though DA rats were kept as inbred lines at different institutes and suppliers, it became obvious that the various breeding stocks differed genetically. To be able to compare the results from different linkage studies it is very import to verify the genetic background of the substrains used in those studies. We performed a genetic and phenotypic analysis of two DA substrains, DA/ZtmRhd and DA/OlaHsd, and found several genetic differences. One of the allelic differences between the DA/ZtmRhd and the DA/OlaHsd strain was located at rat chromosome 3, a 17-Mb large fragment, including the peak marker of a previously identified quantitative trait locus (QTL) for collagen-induced arthritis,
The online version of this article (doi:10.1007/s00335-008-9125-x) contains supplementary material, which is available to authorized users.
Url:
DOI: 10.1007/s00335-008-9125-x
PubMed: 18668290
PubMed Central: 7088020
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when="2008">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The arthritis-susceptible DA rat is one of the most commonly used rat strains for genetic linkage analysis and is instrumental for the identification of many genetic loci. Even though DA rats were kept as inbred lines at different institutes and suppliers, it became obvious that the various breeding stocks differed genetically. To be able to compare the results from different linkage studies it is very import to verify the genetic background of the substrains used in those studies. We performed a genetic and phenotypic analysis of two DA substrains, DA/ZtmRhd and DA/OlaHsd, and found several genetic differences. One of the allelic differences between the DA/ZtmRhd and the DA/OlaHsd strain was located at rat chromosome 3, a 17-Mb large fragment, including the peak marker of a previously identified quantitative trait locus (QTL) for collagen-induced arthritis, <italic>Cia11</italic>. In addition, the substrains exhibited a significant difference in the susceptibility to pristane-induced arthritis (PIA) and disease severity of collagen-induced arthritis and PIA. However, by generating and testing a congenic line, we could demonstrate that phenotypic differences were not due to the contaminating fragment on chromosome 3. Nevertheless, we conclude that DA substrains show distinct genetic differences and caution should be taken when comparing arthritis data from different DA substrains.</p><sec><title>Electronic supplementary material</title><p>The online version of this article (doi:10.1007/s00335-008-9125-x) contains supplementary material, which is available to authorized users.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Alamanos, Y" uniqKey="Alamanos Y">Y Alamanos</name></author><author><name sortKey="Drosos, Aa" uniqKey="Drosos A">AA Drosos</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Brenner, M" uniqKey="Brenner M">M Brenner</name></author><author><name sortKey="Meng, Hc" uniqKey="Meng H">HC Meng</name></author><author><name sortKey="Yarlett, Nc" uniqKey="Yarlett N">NC Yarlett</name></author><author><name sortKey="Joe, B" uniqKey="Joe B">B Joe</name></author><author><name sortKey="Griffiths, 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Mamm Genome</journal-id><journal-id journal-id-type="iso-abbrev">Mamm. Genome</journal-id><journal-title-group><journal-title>Mammalian Genome</journal-title></journal-title-group><issn pub-type="ppub">0938-8990</issn><issn pub-type="epub">1432-1777</issn><publisher><publisher-name>Springer-Verlag</publisher-name><publisher-loc>New York</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">18668290</article-id><article-id pub-id-type="pmc">7088020</article-id><article-id pub-id-type="publisher-id">9125</article-id><article-id pub-id-type="doi">10.1007/s00335-008-9125-x</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>DA rats from two colonies differ genetically and in their arthritis susceptibility</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Rintisch</surname><given-names>Carola</given-names></name><xref ref-type="aff" rid="Aff1">1</xref><xref ref-type="aff" rid="Aff2">2</xref></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Holmdahl</surname><given-names>Rikard</given-names></name><address><email>Rikard.Holmdahl@ki.se</email></address><xref ref-type="aff" rid="Aff1">1</xref><xref ref-type="aff" rid="Aff2">2</xref></contrib><aff id="Aff1"><label>1</label><institution-wrap><institution-id institution-id-type="GRID">grid.4514.4</institution-id><institution-id institution-id-type="ISNI">0000000109302361</institution-id><institution>Medical Inflammation Research,</institution><institution>Biomedical Center, Lund University,</institution></institution-wrap>22184 Lund, Sweden</aff><aff id="Aff2"><label>2</label><institution-wrap><institution-id institution-id-type="GRID">grid.4714.6</institution-id><institution-id institution-id-type="ISNI">0000000419370626</institution-id><institution>Medical Inflammation Research, Department of Medical Biochemistry and Biophysics,</institution><institution>Karolinska Institute,</institution></institution-wrap>17177 Stockholm, Sweden</aff></contrib-group><pub-date pub-type="epub"><day>31</day><month>7</month><year>2008</year></pub-date><pub-date pub-type="ppub"><year>2008</year></pub-date><volume>19</volume><issue>6</issue><fpage>420</fpage><lpage>428</lpage><history><date date-type="received"><day>23</day><month>5</month><year>2008</year></date><date date-type="accepted"><day>13</day><month>6</month><year>2008</year></date></history><permissions><copyright-statement>© Springer Science+Business Media, LLC 2008</copyright-statement><license><license-p>This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.</license-p></license></permissions><abstract id="Abs1"><p>The arthritis-susceptible DA rat is one of the most commonly used rat strains for genetic linkage analysis and is instrumental for the identification of many genetic loci. Even though DA rats were kept as inbred lines at different institutes and suppliers, it became obvious that the various breeding stocks differed genetically. To be able to compare the results from different linkage studies it is very import to verify the genetic background of the substrains used in those studies. We performed a genetic and phenotypic analysis of two DA substrains, DA/ZtmRhd and DA/OlaHsd, and found several genetic differences. One of the allelic differences between the DA/ZtmRhd and the DA/OlaHsd strain was located at rat chromosome 3, a 17-Mb large fragment, including the peak marker of a previously identified quantitative trait locus (QTL) for collagen-induced arthritis, <italic>Cia11</italic>. In addition, the substrains exhibited a significant difference in the susceptibility to pristane-induced arthritis (PIA) and disease severity of collagen-induced arthritis and PIA. However, by generating and testing a congenic line, we could demonstrate that phenotypic differences were not due to the contaminating fragment on chromosome 3. Nevertheless, we conclude that DA substrains show distinct genetic differences and caution should be taken when comparing arthritis data from different DA substrains.</p><sec><title>Electronic supplementary material</title><p>The online version of this article (doi:10.1007/s00335-008-9125-x) contains supplementary material, which is available to authorized users.</p></sec></abstract><kwd-group xml:lang="en"><title>Keywords</title><kwd>Quantitative Trait Locus</kwd><kwd>Pristane</kwd><kwd>Arthritis Severity</kwd><kwd>Ncf1 Gene</kwd><kwd>SSLP Marker</kwd></kwd-group><custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name><meta-value>© Springer Science+Business Media, LLC 2008</meta-value></custom-meta></custom-meta-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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