Glycine tastes both bitter and sweet to mice but there are differences between strains in their ability to detect each taste. With respect to the bitter taste, fifteen strains were classified as tasters and twelve strains as non-tasters. The difference is due to a single gene, Glb (glycine bitterness). Cycloheximide tastes bitter to all mice at a concentration of 8 μM, but strain differences in sensitivity to the taste of cycloheximide can be detected at lower concentrations. The BXD RI strains can be classified into two groups with respect to sensitivity to cycloheximide. This is probably due to the segregation of two alleles of a single gene, Cyx. A comparison of the distribution in RI strains of alleles of four bitterness-tasting genes shows that the loci are all closely linked and are probably in the order Cyx–Qui–Rua–Glb.

Thirty strains of mice were tested for their ability to taste a 0·4 mM solution of raffinose undecaacetate (RUA). There were large strain differences. Some strains showed little or no ability to taste the RUA. Two strains, SWR and Schneider, could taste RUA because they possess the Soaa allele which enables them to taste a variety of acetylated monosaccharides. Three other strains, BALB/c, DBA/2 and C3H, could taste RUA because they possess the Ruaa allele which enables them to taste some larger structure which is a feature of the molecule as a whole. The gene Rua is tightly linked to the gene for quinine tasting. Qui, but the distribution of their alleles among the strains shows that they are different genes. It is suggested that there is in the mouse a cluster of tightly-linked genes, each one determining a taste receptor for a different bitter substance or chemical group. The relevance of these findings to the physiology of tasting is discussed.

Twenty-nine strains of mice were tested for their ability to taste a 0·8 mM solution of quinine sulphate. There were large strain differences, some strains (tasters) showing a strong aversion to the quinine and other strains (non-tasters) showing very little aversion. It was shown that the difference between strains 129/Sv and A2G is probably due to one gene. By using the CXB RI strains it was also shown that the difference between C57BL/6By and BALB/cBy is probably due to one gene. It is suggested that both differences may be due to the same gene, named Qui. In the progeny of a backcross involving both Soa and Qui there was evidence of an interaction between the genes which cannot be explained satisfactorily. Learning behaviour by the mice influenced their drinking habits, but this did not invalidate the results.

Twenty-six strains of mice were tested for their reaction to four different sweet substances; saccharin, acesulfame, dulcin and sucrose. There was considerable strain variation in the degree to which they found the sweet substances preferable to water. The variation in preference for any one sweet substance is very highly correlated with the variation in preference for the other sweet substances. This is interpreted to mean that there is only one sweetness receptor, although an alternative explanation in terms of variation in psychological motivation is not discounted. The difference between C57BL/6Ty and DBA/2Ty is largely due to a single gene, Sac.

Thirty-one inbred strains were tested for their reaction to drinking water which contained a low concentration (10−4 M) of sucrose octaacetate (SOA). One strain, SWR, showed a strong aversion to drinking the SOA solution. The other thirty strains, and two samples of wild-derived mice, tended to prefer the SOA solution to untreated drinking water. The pheno-typic difference between SWR and the other strains was shown to be determined by an autosomal gene. The allele present in SWR is dominant. The gene is not closely linked to jerker (je), pearl (pe) or waved-2 (wa-2).