Twenty-four intact Tas2rs, along with three apparent Tas2r pseudogenes, have been identified in the distal chromosome 6 cluster of B6 mice [19] (Figure 4). We designed oligonucleotides to non-coding regions flanking the coding sequence of each intact Tas2r [see Additional file 2]. Using these oligos, we amplified each Tas2r coding sequence from D2 genomic DNA. PCR products were subcloned into cloning vectors and sequenced. Comparisons of the sequences of B6 and D2 orthologues revealed that only two of the twenty-four Tas2r alleles examined, Tas2r106 and Tas2r124, were identical across strains at the amino acid level (data not shown). A third, Tas2r120, could not be amplified from D2 genomic DNA (Figure 5) using either of two pairs of oligonucleotides (Additional file 2), suggesting that this Tas2r is deleted in D2 mice. Two D2 alleles, Tas2r103 and Tas2r117, contained numerous missense mutations and small deletions that create frame shifts and premature termination; these two genes may be pseudogenes in this strain. The remaining 19 Tas2rs contained between one and 16 missense mutations. All 24 Tas2rs examined have different alleles in B6 and D2 mice, and 307 single nucleotide polymorphisms are present within coding exons (data not shown). Although polymorphic residues between B6 and D2 Tas2rs are found in all regions of the receptors, 23% of the amino acid changes seen are within the first two extracellular loops of the T2Rs (data not shown).