The gene(s) controlling the high-molecular-weight glutelin subunits in rye (designated as Glu-Rl) was mapped with respect to the centromere using a 1RL-1DS wheat-rye translocation line and sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE). Analysis of 479 seeds from test-crosses between a 1R/1RL-1DS heterozygote and the cultivar India 115, revealed 14·6% aneuploid and 3·95% recombinant progeny. Excluding the aneuploids, this locus was calculated to be 4·65 ± 1·04 cM from the centromere on the long arm of chromosome 1R, which is comparable to the position of the homoeologous loci in wheat and barley.

A modifier locus is described that alters the level of phenotypic expression of the third chromosome mutant glass in a sex specific manner. Alternative alleles either confer a sexually dimorphic level of pigment in glass mutants, with the male being greater, or cause similar expression in the two sexes. The alleles are indistinguishable in females but produce the respective phenotypes in males. The gene maps to the tip of the X chromosome at position 0·96 ± 0·11. Cytologically, the locus is present between polytene bands 3A6–8 and 3C2–3 as determined by its inclusion in translocated X segments in w + Y, Dp(l;2)w70h31 and Dp(l;3)w67k27 The dimorphic allele is dominant to the nondimorphic condition in males heterozygous for an insertional translocation carrying the dimorphic allele and a normal chromosome carrying the nondimorphic form. The dimorphic allele in two doses in males does not exhibit a dosage effect. The modifier phenotype is unaffected in two X flies by the presence of the transformer mutation.

Females from different wild-type laboratory populations of Drosophila melanogaster differ genotypically in their degree of mating discrimination against mutant yellow males. The chromosomal organization of this difference was examined in two wild-type laboratory strains by experimental observation of the mating propensities of hybrid females in a mass-mating, multiple choice situation. The results indicate that the strain difference is polygenic in origin, involving loci on both the X-chromosome and autosomes. Reciprocal crosses revealed no maternal/cytoplasmic effects. The mating scores of parental, F1 and backcross females fit well to a model of additive chromosomal effects, with X-linked loci being recessive, and autosomal loci overdominant, for increased mating with yellow males. However, interactions, arising most probably from recombination, led to increased mating with yellow on the part of F2 females. In addition to the difference in female discrimination against yellow males, male/female interaction was found for the mating speed of flies from the two strains. These results are discussed in the light of previous studies of mating preferences in D. melanogaster. It is suggested that genetic variation in female mating preferences may be an important source of variation in the reported mating success of mutant yellow males.

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.

A new allele at the W-locus ( W19H), found in a mutagenesis experiment in which females were irradiated, involves a presumed deletion. The deletion covers the Ph locus (which forms part of a gene complex with the W, Ph and Rw loci), and the locus of a recessive lethal 2 cM distal to W. It does not extend distally to the bl locus; nor does it involve the Rw locus, W19H/Rw compounds being viable and fertile. Thus, the length of the deletion is 2–7 cM. The non-involvement of Rw shows that, in the gene triplet Rw, W, Ph, Rw must lie proximal to W and Ph, whose relative position remains unknown. Heteozygotes for W19H are not anaemic, show only minimal white spotting and no pigment dilution; they thus resemble heterozygotes for the original W mutant allele and differ from W/Ph trans heterozygotes, which have extensive white spotting. In addition W19H heterozygotes may be small and runted, many are believed to die prenatally, and some in the nest. Their radiosensitivity is increased. Homozygotes die at the pre-implantation stage.

The dimeric enzyme glucose phosphate isomerase (GPI-1) is regulated in oocytes by a cis-acting temporal gene (Gpi-1t) that maps close to the structural gene (Gpi-1s). Quantitative cellulose acetate electrophoresis of GPI-1 allozymes from unfertilized eggs produced by various Gpi-1sa / Gpi-1sb heterozygous females revealed a new Gpi-1t allele that we have designated Gpi-1tc. This allele is present in 101/H mice and a partially congenie stock that carries the Gpi-lsa gene derived from the AKR strain. We have confirmed that Gpi-1tc is closely linked to Gpi-1s and that it is cis-acting. It produces higher levels of GPI-1 in unfertilized eggs than the other two Gpi-lt alleles that are known (Gpi-1ta and Gpi-1tb) but has no effect on GPI-1 in somatic tissues or spermatozoa. This new Gpi-1t allele represents a third developmental programme for GPI-1 expression in oocytes.

Seventeen dominant cataract mutations of the mouse recovered in ethylnitrosourea mutagenesis experiments have been genetically characterized as to penetrance, fertility, and homozygous viability. Nine mutations were shown to be fully penetrant with no fertility effects, four mutations were classified as having reduced penetrance with no fertility effects, one mutation had reduced penetrance and reduced fertility, two mutations were shown to have a reduced frequency of mutant offspring due to penetrance and viability effects, and one mutation most likely has a reduced viability of carrier individuals. Of the eleven mutations for which definitive homozygous viability data were obtained, ten were shown to be homozygous viable and only one was shown to be homozygous lethal. In similar experiments in which dominant cataract, dominant skeletal or dominant visible mutations were recovered after radiation treatment, comparable frequencies of mutations with reduced penetrance were observed but there was a strikingly higher frequency of homozygous lethal mutations. These observations support the hypothesis of a qualitative difference in the mutations recovered after ethylnitrosourea as compared to radiation treatment. Finally, it is argued that a systematic comparison of the induced mutation rates to dominant and recessive alleles with subsequent genetic characterization of the recovered mutations provides a critical set of data necessary for an improvement in the indirect and direct procedures of genetic risk estimation.

A population with u deleterious mutations per genome per generation is considered in which only those individuals that carry less than a critical number of k mutations are viable. It has been shown previously that under such conditions sexual reproduction is advantageous. Here we consider selection at a locus that determines recombination frequency of the whole genome. The value v = u/ √ k has been found to play the decisive role. When v < 0·35 the direction of selection for recombination may be different for different cases, but the intensity of selection is always very small. The advantage of recombination becomes considerable when v > 0·5, its growth under increasing v being approximately linear. If v > 2 no less than 95% of the progeny are bound to die because of the selection against deleterious mutations. Since this seems to be too great a mutation load, we may assume 0·5 < v < 2·0 for any sexual population if mutation really maintains crossing-over. Results on selection at a locus which controls mutability provide evidence that v is located within the specified interval if the physiological cost of a twofold reduction of the mutation rate is within the range 10–80%. A number of consequences of this hypothesis about the mechanism of selection for sex and recombination are discussed.

Two male-sterile chromosome anomalies, the insertion Is(7; 1)40H and the tertiary trisomy, Ts(512)31H, were found to be associated with reduced ovarian volumes in immature females. Together with the reciprocal translocation, T(11; 19)42H, in which this effect was described previously, reduced ovaries have been found in all three male-sterile chromosome anomalies investigated so far, suggesting that ovarian involvement is likely to be common in these conditions. Assuming that the smaller ovarian size reflects a reduction in the number of oocytes, it is suggested that male-sterile chromosome anomalies may exert basically similar deleterious effects on meiotic germ cells in males and females, the difference in outcome being due to cell-physiological differences between spermatocytes and oocytes and to the small number of surviving oocytes required for fertility in females.

Postmeiotic segregation (PMS) of genetic variants occurs when a DNA heteroduplex formed during meiotic recombination goes undetected by repair enzymes and is transmitted unresolved to the meiotic products. PMS provides an alternative explanation for the origin of mosaics now attributed to half-chromatid mutation. In multicellular diploid eukaryotes, PMS could result in mosaic individuals with unusual migration patterns for proteins studied by gel electrophoresis. If the gonade were mosaic, complex progenies containing as many as six phenotypic classes at a single locus could be produced.

When males from a strain of Drosophila melanogaster which have multiple copies of the P family of transposable elements integrated into their genome (Bingham, Kid well & Rubin, 1982) (‘P’ strains) are crossed to females of strains lacking those elements (‘M’ strains), the F1 progeny manifest a number of aberrant traits known collectively as hybrid dysgenesis (Kidwell, Kidwell & Sved, 1977). Progeny of the reciprocal cross (P♀ × ♂M) are normal. The dysgenic syndrome is characterized by a high degree of genomic instability caused by enhanced transposition of P elements. Since mutations at visible loci and chromosomal rearrangements are frequently observed in dysgenic hybrids, it was hypothesized that this phenomenon could be used to investigate the effects of transposition on quantitative characters; therefore, the progeny of dysgenic and non-dysgenic crosses were artificially selected for high and low abdominal bristle number. The response to selection, phenotypic variation, and realized heritability were all increased in the dysgenic lines, relative to the non-dysgenic control. It is postulated that these features are the result of P element-induced mutations of loci affecting bristle number, and that future work should lead to the identification of these loci, as well as elucidating the role of transposition in population differentiation for metric traits