Although the fungus Aspergillus nidulans has a multiplicity of phosphatases and of genes where mutations affect one or more phosphatases, we have succeeded in identifying structural genes for three phosphatases as well as one other gene which might encode a fourth. Using both conditional and non-conditional mutations, palD has been shown to be the structural gene for a phosphate-repressible alkaline phosphatase, palG to be the structural gene for a non-repressible alkaline phosphatase which apparently exists in two electrophoretically distinct forms (but whose rates of thermal inactivation are apparently very similar) and pacA to be the structural gene for both intracellular and secreted forms of a phosphate-repressible acid phosphatase. Colony staining techniques for the enzymes specified by palD and pacA have been described previously but we have now shown that the enzyme specified by palG can be detected by staining toluene-permeabilized colonies. Mutations in pacG lead to loss of non-repressible acid phosphatase as judged by colony staining and electrophoretic patterns but their effects on assays of activity in cell-free extracts are only marginal. Under phosphate-limited, but not phosphate-starved or phosphate-sufficient, conditions, pacG− mutations also affect the regulation of other, phosphate-repressible phosphatases. None of these phosphatases, alone or in combination, plays an essential role.

The regulation of the syntheses of a number of phosphatases in the fungus Aspergillus nidulans has been examined. Levels of the intracellular alkaline phosphatase P11 are increased by starvation for carbon, nitrogen, phosphorus or sulphur. There is, however, no evidence that any of the wide domain regulatory genes which mediate sufficiency-triggered repression for each of these elements involved. A possible interpretation is that all four forms of starvation result in accumulation of an inducing metabolite. The palcA gene has been identified as a wide domain, probably positive-acting regulatory gene mediating phosphate repression. The palcA product controls the syntheses of alkaline phosphatase PI, acid phosphatases PIII and PV, a phosphodiesterase lacking phosphomonoesterase activity and probably also a phosphate permease. Mutations resulting in derepression of phosphate-repressible activities at acid but not alkaline growth pH define a gene designated pacJ. pacJ mutations also confer arsenate resistance at low but not high pH. It is likely that phosphate derepression and arsenate resistance result from reduced uptake of H2PO4−. Finally, phosphatase regulation might be less complex than previously thought. Mutations designated r and mapping at several loci apparently have no effect on phosphatase. They enhance phosphatase colony staining but this occurs even if the phosphatase substrates are omitted from the staining mixtures. r mutations appear to promote reactions converting the diazonium salts used for phosphatase staining to coloured precipitates.

Structural genes for the leaf isozymes of peroxidases (E.C.1.11.1.7) have been located on chromosome arms 2BS, 2DS and probably 2AS of wheat, 2RS of cereal rye and on chromosome 2H of Hordeum vulgare. This character provides a useful genetic marker for these chromosome arms, and the results supports the notion of the conservation of gene synteny groups within the Triticinae.

Prior reports from this laboratory have described the experimental basis for our understanding of the rosy locus (ry: 3–52·0) of Drosophila melanogaster as a bipartite genetic entity consisting of a structural element that codes for the xanthine dehydrogenase (XDH) peptide and a contiguous cis-acting control element immediately to the left of the structural element. Although the left end (5′) of the structural element has been well defined, the right boundary (3′) has been given only casual treatment in our prior reports. In our recent studies of rosy locus expression we have been concerned with the production and identification of mutations in the non-structural regions immediately flanking the structural element. An improved definition of the right end of the structural element is essential to this analysis. In addition to producing a better definition of the right boundary of the structural element, this study produced several phenotypically novel mutations. These mutations were classified initially ascontrol element mutations, but upon analysis were found to map within the rosy structural element. No evidence was obtained for the existence of a control element contiguous with the right end of the structural element.

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.

A locus, Dlb-1, controlling the binding of the lectin from Dolichos biflorus to the intestinal epithelium and vascular endothelium of mice has been located on chromosome 11, 3.1 ± 1.4 centimorgans proximal to Rex, using recombinant inbred strains and conventional backcrosses with three-point linkage tests.

The two alleles so far discovered at this locus behave unusually. The Dlb-1a allele causes binding to the vascular endothelium but not to the intestinal epithelium while Dlb-1b induces the exact reciprocal binding pattern, and the heterozygote shows both patterns.

The histidine decarboxylase (HDC) gene complex, [Hdc], comprises the structural gene for mouse kidney HDC and closely linked regulatory elements which determine enzyme concentration and its response to hormones. One of these regulatory elements, Hdc-e, determines the response (induction or repression) of kidney HDC to oestrogen. HDC is oestrogen-inducible in C57BL/10 and oestrogen-repressible in DBA/2 and C57BL/6; alleles of Hdc-e segregate in crosses between C57BL/10 and DBA/2 and between the C57BL substrains. Two different haplotypes of[Hdc] have been defined previously, B.10 (Hdc-sb, Hdc-cb, Hdc-eb) in C57BL/10 and D (Hdc-sa, Hdc-cd, Hdc-ed) in DBA/2. C57BL/6 represents a third haplotype (B.6) (Hdc-sb, Hdc-cb, Hdc-ed) which differs from both B.10 and D. Hdc-e may therefore be a component of the complex independent of Hdc-s and Hdc-c.

The T/t–H-2 region on mouse chromosome 17 is known from complex natural variants (‘t-haplotypes’) to contain numerous genes, including some affecting the immune system and the development of the embryo. Rapid progress in the isolation of recombinant DNA clones for this 50 megabasepair region is generating the material for its complete molecular anatomy. A crucial step in revealing the biological functions controlled by the region is to obtain mutants in which genes are inactivated individually. We have used a pair of inbred mouse strains and a series of classical breeding schemes that permit the detection of recessive lethal and detrimental mutations in the T/t–H-2 region.

In this initial phase of our study, 280 gametes mutagenized in the male germ line by ethylnitrosourea (ENU) have yielded eleven independent pre-natal recessive lethal mutations. Four have been mapped against T mutations and have been shown to complement one another in all pairwise combinations.

A temporal survey of the alcohol dehydrogenase locus in a natural population of Drosophila melanogaster from the Canary Islands has revealed the existence of an electrophoretic Fast thermostable variant, mapped within 0.8 units of the structural Adh locus, and which persists over a 6-year period with a frequency ranging from 0.8 to 0.5%.

Data from foetal and weanling studies suggest that Oxford race metacentrics kq and no, but not pr, are transmitted preferentially from Robertsonian heterozygote common shrews collected from the Oxford area. These results suggest a possible mechanism for the maintenance of the Robertsonian polymorphism in that area.