Mapping Data

Experiment

• Experiment
  TEXT-QTL
• Chromosome
  4
• Reference
  J:114158 Ohtsuka Y, et al., Genetic linkage analysis of pulmonary fibrotic response to silica in mice. Eur Respir J. 2006 Nov;28(5):1013-9
• ID
  MGI:3690355

Genes

Gene	Assay Type
Slcs1	resistance/susceptibility
D4Mit9	PCR amplified length variant
Jun	reported elsewhere
Cdkn2a	reported elsewhere
Igfbpl1	reported elsewhere

Notes

• Experiment
  Linkage analysis was performed on 117 (C57BL/6J x CBA/J)F2 animals to identify QTLs associated with silica-induced pulmonary fibrosis susceptibility. 167 microsatellite markers were used for the genome scan. Parental strain C57BL/6J is susceptible to silicosis whereas parental strain CBA/J is resistant. Animals were exposed to silica at 6-8 weeks of age and assessed for lung fibrosis and lung hydroxyproline content 28 days after exposure.
  
  Significant linkage to silicosis susceptibility mapped to 44.5 cMon mouse Chromosome 4 near D4Mit9. This locus explains 9% of the phenotypic variance and is designated Slcs1 (silicosis susceptibility 1). Potential candidate genes mapping near Slcs1 include Jun (44.6 cM), Cdkn2a (42.7 cM), and Igfbpl1.
  
  Suggestive linkage to silicosis susceptibility mapped to 61.8 cM on mouse Chromosome 3 near D3Mit319 and to 21 cM on mouse Chromosome 18 near D18Mit177.1. The Chr 3 locus explains 7% of the phenotypic variance and the Chr 18 locus explains 6% of the phenotypic variance.Potential candidate genes mapping near the Chr 18 locus include Fgf1 (19 cM) and Spry4 (18 cM). Pas9 (43 cM) is a previously identified pulmonary adenoma susceptibility locus mapping to Chr 18.