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Gene Review:

Soa - sucrose octaacetate aversion

Mus musculus

Bachmanov, A.A. et al., Harder, D.B. et al., Capeless, C.G. et al., Lush, I.E. et al., Capeless, C.G. et al., et al.

Bachmanov, Li, Li, Neira, Beauchamp, Azen, Boughter, Whitney,

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High impact information on Soa

The results show that the Soa locus is contained in an approximately 1-cM (3.3-4.9 Mb) region including the Prp locus [1].
High-resolution genetic mapping of the sucrose octaacetate taste aversion (Soa) locus on mouse Chromosome 6 [1].
Three Soa alleles determine 'taster' (Soa(a)), 'nontaster' (Soa(b)), and 'demitaster' (Soa(c)) phenotypes of taste sensitivity to SOA [1].
Background genes not linked to Soa controlled avoidance differences for L-phenylalanine and ethanol [2].
Avoidance of bitter picric acid was influenced by the Soa locus, but avoidance of acetic acid was not [2].

Biological context of Soa

The Soa bitter-sensitivity and Prp salivary-protein loci map to distal mouse chromosome six [3].
The Soa bitter sensitivity locus exerts some influence on this phenotype, but an unknown number of other loci also contribute [4].
The genetics of tasting in mice. VII. Glycine revisited, and the chromosomal location of Sac and Soa [5].
The data are consistent with a position for the Soa locus on mouse chromosome 6, 62 cM from the centromere [6].
Thus the effect of the Soa genotype on SOA avoidance is mediated by peripheral taste responsiveness to SOA, involving taste receptor cells innervated by both the CT and GL nerves [7].

Associations of Soa with chemical compounds

The Soa locus controlled avoidance differences within the quartet for SOA, raffinose undecaacetate, glucose pentaacetate and brucine [2].
Calcium hydroxide and sodium hydroxide were used to hydrolyse sucrose octa-acetate (SOA) as a means of evaluating the taster (Soaa) and demitaster (Soac) allelic phenotypes of the genetic locus Soa [8].
The extensively characterized Soa (sucrose octaacetate) locus underlies one pattern [9].
Soa allelic variation had a major effect on sensitivity to 0.003-1.0 mM SOA and several concentrations of the bitter-tasting alkaloids brucine, strychnine, and quinine [10].
Haplotyping of 41 outbred CFW-Cr animals with a cDNA probe showed perfect cosegregation of Soa and Prp, a gene for salivary proline-rich proteins [6].

Other interactions of Soa

The bitterness tasting gene Soa is very closely linked to Prp on chromosome 6 (no recombinants among 67 backcross progeny) [5].

References

High-resolution genetic mapping of the sucrose octaacetate taste aversion (Soa) locus on mouse Chromosome 6. Bachmanov, A.A., Li, X., Li, S., Neira, M., Beauchamp, G.K., Azen, E.A. Mamm. Genome (2001) [Pubmed]
SW.B6-Soa(b) nontaster congenic strains completed and a sucrose octaacetate congenic quartet tested with other bitters. Harder, D.B., Gannon, K.S., Whitney, G. Chem. Senses (1996) [Pubmed]
Sucrose octaacetate avoidance in nontaster mice is not enhanced by two type-A Prp transgenes from taster mice. Harder, D.B., Azen, E.A., Whitney, G. Chem. Senses (2000) [Pubmed]
A common polygenic basis for quinine and PROP avoidance in mice. Harder, D.B., Whitney, G. Chem. Senses (1998) [Pubmed]
The genetics of tasting in mice. VII. Glycine revisited, and the chromosomal location of Sac and Soa. Lush, I.E., Hornigold, N., King, P., Stoye, J.P. Genet. Res. (1995) [Pubmed]
Chromosome mapping of Soa, a gene influencing gustatory sensitivity to sucrose octaacetate in mice. Capeless, C.G., Whitney, G., Azen, E.A. Behav. Genet. (1992) [Pubmed]
Soa genotype selectively affects mouse gustatory neural responses to sucrose octaacetate. Inoue, M., Li, X., McCaughey, S.A., Beauchamp, G.K., Bachmanov, A.A. Physiol. Genomics (2001) [Pubmed]
Hydrolysis of sucrose octa-acetate: qualitative differences in taster and demistaster avoidance phenotypes. Capeless, C.G., Boughter, J.D., Whitney, G. Chem. Senses (1994) [Pubmed]
Genetics of bitter perception in mice. Whitney, G., Harder, D.B. Physiol. Behav. (1994) [Pubmed]
Behavioral specificity of the bitter taste gene Soa. Boughter, J.D., Whitney, G. Physiol. Behav. (1997) [Pubmed]

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