Mapping Data

Experiment

• Experiment
  TEXT-QTL
• Chromosome
  2
• Reference
  J:237166 Everett ET, et al., Fine mapping of dental fluorosis quantitative trait loci in mice. Eur J Oral Sci. 2011 Dec;119 Suppl 1:8-12
• ID
  MGI:5904364

Genes

Gene	Assay Type
Dfs1	susceptibility/resistance

Notes

• Experiment
  Genetic factors underlie dental fluorosis (DF) susceptibility/resistance. The A/J (DF susceptible) and 129P3/J (DF resistant) inbred strains have been previously used to detect quantitative trait loci (QTL), Dfs1 and Dfs2 respectively, associated with DF on chromosomes Chr 2 and 11 [J:153399].
  
  In the present study increased marker density genotyping followed by interval mapping was performed to narrow the QTL intervals and improve the LOD scores. From an initial panel of 458 F2 mice (11) genomic DNAs from 140 mice representing DF phenotype extremes were selected for additional SNP genotyping. Among these 140 mice 75 were from the low DF group and 65 were from the high DF group. 112 SNPs representing Chrs 2 and 11 were selected and genotyped utilizing the Genetic Analysis service at The Jackson Laboratory (Bar Harbor, ME USA).
  
  The SNP assays selected detected polymorphisms between A/J and 129P3/J and increased the number of informative SNPs from 29 to 108 for Chr 2 and from 14 to 47 for Chr 11. Interval mapping was performed in R with R/qtl package. SNP datasets of the A/J and 129P3/J inbred strains from the Imputed Diversity Array, Build37 were used with the Mouse Strain Comparison Tool (The Center for Genome Dynamics at the The Jackson Laboratory, Bar Harbor, ME USA).
  
  Interval mapping using increased marker densities on Chrs 2 and 11 resulted in a modest narrowing of the respective QTL intervals and an improved estimation of maximum LOD scores with peak LOD = 8.252 located at marker rs4223510 (68 cM in an interval mapping between 65-74 cM) on Chr 2 for QTL Dfs1 and a peak LOD = 8.845 located at marker rs3694522 (35 cM in an interval mapping between 31-45 cM) on Chr 11 for QTL Dfs2.
  
  Accn1 residing at 80,693,67181,781,959 bp on Chr 11 was selected for further investigation. Following F treatment Accn1null mice developed DF that was not statistically different from the DF in similarly treatedC57BL/6J mice (Fig. 4)(Table 3). The data suggest that loss of function of Accn1 alone in the C57BL/6J strain is either insufficient (not a major effect gene) to contribute to DFsusceptibility, that Accn1 plays no direct role in DF susceptibility, or there is epistasis between other C57BL/6J alleles.