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Fragmentation of two quantitative trait loci controlling collagen-induced arthritis reveals a new set of interacting subloci

Ahlqvist, Emma LU ; Bockermann, Robert LU and Holmdahl, Rikard LU (2007) In Journal of Immunology 178(5). p.3084-3090
Abstract
Linkage analysis of F-2 crosses has led to identification of large numbers of quantitative trait loci (QTL) for complex diseases, but identification of the underlying genes has been more difficult. Reasons for this could be complications that arise from separation of interacting or neighboring loci. We made a partial advanced intercross (PAI) to characterize and fine-map linkage to collagen-induced arthritis in two chromosomal regions derived from the DBA/1 strain and crossed into the B10.Q strain: Cia7 on chromosome 7 and a locus on chromosome 15. Only Cia7 was detected by a previous F-2 cross. Linkage analysis of the PAI revealed a different linkage pattern than the F-2 cross, adding multiple loci and strong linkage to the previously... (More)
Linkage analysis of F-2 crosses has led to identification of large numbers of quantitative trait loci (QTL) for complex diseases, but identification of the underlying genes has been more difficult. Reasons for this could be complications that arise from separation of interacting or neighboring loci. We made a partial advanced intercross (PAI) to characterize and fine-map linkage to collagen-induced arthritis in two chromosomal regions derived from the DBA/1 strain and crossed into the B10.Q strain: Cia7 on chromosome 7 and a locus on chromosome 15. Only Cia7 was detected by a previous F-2 cross. Linkage analysis of the PAI revealed a different linkage pattern than the F-2 cross, adding multiple loci and strong linkage to the previously unlinked chromosome 15 region. Subcongenic strains derived from animals in the PAI confirmed the loci and revealed additional subloci. In total, no less than seven new loci were identified. Several loci interacted and three loci were protective, thus partly balancing the effect of the disease-promoting loci. Our results indicate that F-2 crosses do not reveal the full complexity of identified QTLs, and that detection is more dependent on the genetic context of a QTL than the potential effect of the underlying gene. (Less)
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author
organization
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Contribution to journal
publication status
published
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in
Journal of Immunology
volume
178
issue
5
pages
3084 - 3090
publisher
American Association of Immunologists
external identifiers
  • wos:000244734500064
  • scopus:33847364776
ISSN
1550-6606
language
English
LU publication?
yes
id
99bf140c-d8f6-41ad-bfeb-18db677b3b72 (old id 671622)
alternative location
http://www.jimmunol.org/cgi/content/abstract/178/5/3084
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=17312155&dopt=Abstract
date added to LUP
2007-12-11 12:48:21
date last changed
2017-01-01 07:06:26
@article{99bf140c-d8f6-41ad-bfeb-18db677b3b72,
  abstract     = {Linkage analysis of F-2 crosses has led to identification of large numbers of quantitative trait loci (QTL) for complex diseases, but identification of the underlying genes has been more difficult. Reasons for this could be complications that arise from separation of interacting or neighboring loci. We made a partial advanced intercross (PAI) to characterize and fine-map linkage to collagen-induced arthritis in two chromosomal regions derived from the DBA/1 strain and crossed into the B10.Q strain: Cia7 on chromosome 7 and a locus on chromosome 15. Only Cia7 was detected by a previous F-2 cross. Linkage analysis of the PAI revealed a different linkage pattern than the F-2 cross, adding multiple loci and strong linkage to the previously unlinked chromosome 15 region. Subcongenic strains derived from animals in the PAI confirmed the loci and revealed additional subloci. In total, no less than seven new loci were identified. Several loci interacted and three loci were protective, thus partly balancing the effect of the disease-promoting loci. Our results indicate that F-2 crosses do not reveal the full complexity of identified QTLs, and that detection is more dependent on the genetic context of a QTL than the potential effect of the underlying gene.},
  author       = {Ahlqvist, Emma and Bockermann, Robert and Holmdahl, Rikard},
  issn         = {1550-6606},
  language     = {eng},
  number       = {5},
  pages        = {3084--3090},
  publisher    = {American Association of Immunologists},
  series       = {Journal of Immunology},
  title        = {Fragmentation of two quantitative trait loci controlling collagen-induced arthritis reveals a new set of interacting subloci},
  volume       = {178},
  year         = {2007},
}