Mapping Data

Experiment

• Experiment
  TEXT-QTL
• Chromosome
  5
• Reference
  J:73060 Roper RJ, et al., Genetic control of susceptibility to experimental Lyme arthritis is polygenic and exhibits consistent linkage to multiple loci on chromosome 5 in four independent mouse crosses. Genes Immun. 2001 Nov;2(7):388-97
• ID
  MGI:5693828

Genes

Gene	Assay Type
Bbaa24	resistance/susceptibility
D5Mit431
D5Mit101
D5Mit98
Bbaa25	resistance/susceptibility
D5Mit214
Bbaa26	resistance/susceptibility
D5Mit30
D5Mit115
D5Mit31
D5Mit239
Bbaa2	resistance/susceptibility
D5Mit63
Bbaa3	resistance/susceptibility
D5Mit91
D5Mit24

Notes

• Experiment
  Composite interval mapping (CIM) was used for localization of QTL involved in modulating response to infection with Borrelia burgdorferi. Parental strains C3H/HeN and C3H/HeJ are susceptible to B.burgdorferi-induced arthritis whereas parental strains C57BL/6N and BALB/cAnN are resistant. Four different backcrosses and the reanalysis of a previous intercross were performed.
  
  In the (C57BL/6N x C3H/HeN) x C57BL/6N backcross authors state that previoulsy identified QTL Bbaa2 and Bbaa6, on Chrs 5 and 12 respectively, were reproduced.
  
  [10.28.2015 Curator Note: Because Bbaa2 and Bbaa6 were originally mapped in J:52017 in 1999 using an (C3H/HeNCr x C57BL/6NCr)F2 intercross which differs from the backcross used here, we consider the current study a separate mapping experiment and have named the Chr 5 QTL Bbaa24 and the Chr 12 QTL Bbaa27.]
  
  On Chr 5 Bbaa24 is linked to ankle swelling, mapping from 66-81 cM between markers D5Mit431 and D5Mit101 with an LRT of 31.7 accounting for 12.0% of trait variance. The QTLis also linked to histopathology, mapping from 66-78 cM between markers D5Mit431 and D5Mit98 with an LRT of 20.8 accounting for 8.8% of the trait variance. [Table 2.]
  
  In the (C57BL/6N x C3H/HeN) x C57BL/6N backcross another Chr 5 QTL linked to tendon sheath mapped to 70 cM with marker D5Mit214, LRT=16.1 accounting for 12.9% of the variance. Authors also equate this QTL with the previoulsy identified Bbaa2. [Curator Note: Since the cross used here also differs from the orginal mapping population for Bbaa2 we have named this QTL, Bbaa25.] [Table 2.]
  
  In the (C3H/HeJ x BALB/cAnN) x C3H/HeJ backcross another QTL that was also equated with Bbaa2 was mapped. [Curator Note: Since the cross used here also differs from the orginal mapping population for Bbaa2 we have named this QTL, Bbaa26.] [Table 2.]
  
  Bbaa26 maps to Chr 5 linked to ankle swelling at 72 cM with marker D5Mit30, LRT=47.1 accounting for 29% variance. It also linked to histopathology from 56-78 cM between markers D5Mit115 and D5Mit31, LRT=33.4 accounting for 20.6% of variance and to tendon histology from 58-72 cM between markers D5Mit239 and D5Mit30, LRT=24.7 accounting for 16.0% variance. [Table 2.]
  
  The reanalysis of the (C57BL/6N X C3H/HeN)F2 intercross also confirmed the previoulsy identified QTL Bbaa2 and Bbaa3 on Chr 5. Using CIM Bbaa2, linked to ankle swelling, mapped to 73.0 cM with marker D5Mit63, LRT=18.7. Bbaa3, linked to histopathology, mapped from 53.0 - 60.0 cM between markers D5Mit91 and D5Mit24, LRT=25.1 [Table 3.]
  
  
  C3H/HeN-derived alleles are associated with increased arthritis susceptibility and severity at all QTL mapped in this experiment.