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.

When combinations of inhibitors acting on the subunit B of DNA gyrase were tested in Bac. subtilis strains, the growth-inhibiting effect of novobiocin was specifically antagonized by subinhibitory concentrations of coumermycin A1. An antagonism in the opposite direction was not observed.

Two alternative models are proposed, where the supercoiling decrease caused by novobiocin is antagonized by coumermycin.

This phenomenon seems to be characteristic of the Bac. subtilis species.

A non-transmissible plasmid, pAV5, was isolated from a hospital strain of Acinetobacter calcoaceticus, JC17. pAV5 confers resistance to the antibiotics tetracycline and neomycin in the genetically characterized strain of A. calcoaceticus EBF 65/65. Transfer of pAV5 can be mediated by the sex factors pAV1 and R751; transfer is occasionally associated with the segregation of the resistance determinants amongst the transconjugants. Phenotypic dissociation of pAV5 corresponds with the formation of two independent plasmids designated pAV51 and pAV52 mediating resistance to neomycin and tetracycline respectively.

Variable frequencies of unhatched eggs were observed to be produced by a number of F1 interstrain hybrids. This type of partial sterility resulting from F2 embryo death was found to be associated with the P-M system of hybrid dysgenesis. Dysgenic hybrid progeny of crosses between M strain females and P strain males may therefore have reduced fertility due to the disruption of development at two different stages: early F1 gonadal development and early F2 embryo development. These disruptions result in the previously described F1 gonadal dysgenesis (GD sterility) and F2 embryo lethality (EL sterility) respectively. The two morphologically distinct types of P-M-associated sterility differ in their patterns of response to F1 developmental temperature, and the temperature-sensitive period for EL sterility occurs considerably later in F1 development than for GD sterility. EL sterility is similar to SF sterility, which is associated with the I–R system of hybrid dysgenesis in that both result from death during early F2 embryogenesis. However, EL sterility differs from SF sterility in not being restricted to hybrids of the female sex and in showing different patterns of response to temperature and ageing in the F1 generation. Some implications of the existence of EL sterility for methods of strain classification in the I–R system are explored.

The ability of hybrid dysgenesis P factors to survive and multiply under conditions of strong negative sterility selection was studied in mixed P and M laboratory cultures. Eight populations were initiated with varying proportions of P and M strains. Mixed populations and controls were maintained for seventeen generations at 27 °C, a temperature sufficiently high to induce maximum frequencies of sterility in dysgenic hybrids. The two components of dysgenesis, P factor activity and cytotype, were monitored every generation for the first ten generations and intermittently thereafter. With one exception, all the mixed populations evolved to the P type indicating that P factors can survive and multiply, despite low initial frequency and strong negative selection against dysgenic hybrids. However, the average level of P factor activity attained at equilibrium was considerably lower than that of the P strain control population maintained under the same conditions. It was also lower than the equilibrium level of P factor activity attained in a similar experiment carried out at a lower temperature, suggesting that selection favoured P factors with weak rather than strong sterility potential.

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.

Expression of three wing-cell death mutants in Drosophila melanogaster was used to survey cryptic polygenic modifiers of cell death in wild type strains. Females carrying the X-linked mutants Beadex-3, notchoid and scalloped were crossed to males from each of 20 isofemale strains. Phenotypic variation in the amount of cell death was measured in F1 mutant males that were heterozygous for polygenic loci segregating in the wild strains. As expected, each mutant uncovered a broad range of polygenic variation among strains. Yet, when cluster analyses were used to evaluate the degree of correlation among the expressions of Bx3, sd and nd, the isofemale strains could be partitioned into a small number of groups that were similar in the effects they had upon the severity of cell death. Chromosome mapping of one cell death suppressor strain demonstrated that different polygenic loci could produce the same phenotype in different mutant backgrounds.

The protein and amino acid compositions of hair from mice carrying the naked (N) gene were compared with those of wild-type (+ / +) mouse hair using two-dimensional polyacrylamide gel electrophoresis and amino acid analysis. In samples obtained from N /+ mice, the numbers of positions of the low-sulphur (LS), high-sulphur (HS) and high tyrosine (HT) protein spots were indistinguishable from those observed in + / + samples but the amount of HT protein was reduced in N / + hair. In samples obtained from N /N mice the protein spots were fewer than, and perhaps different from, those in samples from the other two genotypes; all protein classes were represented but the HS and HT protein content appeared to be less than that in + / + and N / + hair. Amino acid analyses of hair samples showed that the HS contents of + / + and N / + hair were approximately the same, whereas the HT protein content of N / + hair was about half that in + / + hair. N / N hair contained less half-cystine and tyrosine than + / + and N / + hairs, but because the contents of proline, threonine and glycine were unexpectedly high, it appears that protein components of unusual composition are present in N / N hair. It was concluded that the gene at the N locus is involved only indirectly in the synthesis of the structural proteins found in mouse hair.

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.

Genetic similarities among 46 strains of rats based on published data involving 93 samples and 28 biochemical loci were assessed using principal coordinate and cluster analysis techniques. Seventeen strains were represented by more than one colony. In ten of these, nominally identical strains differed, and in four cases this was attributed to genetic contamination. A total of 52 genetically different strains were eventually identified. Strains BN and DA were most dissimilar, while strain BP was the most unusual strain over-all. The principal coordinate and cluster analysis showed three main clusters, which could be explained on the basis of linkage disequilibrium for some of the esterase loci in linkage group 5. Among six of these loci only 12 haplotypes were observed, with 24/52 strains having a single haplotype. Re-analysis of loci in linkage equilibrium failed to reveal any important clusters.

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.

Thirty-two t haplotypes were extracted from wild mice captured in Central Europe, Spain, the Soviet Union, Israel, Egypt, the Orkneys and South and North America, and tested for lethality in the homozygous state. Twenty-two proved to be homozygous lethals, 8 semilethals and 2 viables. The lethal t haplotypes were then tested by the genetic complementation test for identity with representatives of known complementation groups and with each other. Five of the 22 haplotypes proved to carry previously identified lethality factors (tw5, tw73, and tLub-1), while the rest carried new factors. The 17 haplotypes fell into 8 new complementation groups. Two of the new groups are partially overlapping in that they seem to share some lethality factors and differ in others. These tests raise the total number of known complementation groups to 16. The distribution of the individual t haplotypes among wild mice populations seems to reflect their differentiation from a common ancestor haplotype.

All four coat hair types were longer in mice homozygous for angora (go / go) than in wild-type mice ( + / +). This increase in hair length in mutant animals was due to an increase in the duration of the phase of hair growth (anagen VI). When skin recombinants incorporating mutant or wild-type epidermis and dermis were grafted to a nude host, the activity of the mutant was found to be confined to the epidermis.

Puberty was studied in mice of the ninth selected generation of the Q-strain. There were 6 replicate lines selected for large body size (6-week weight), 6 replicates selected for small size and 6 replicate unselected controls. Female puberty was assessed by the opening of the vagina and male puberty by the first copulation plug. The sexes differed in the mean age at puberty, males being older by 13 days in the large, 4 days in the control and 8 days in the small lines. The sexes differed also in the way size affected puberty. In males the large and small lines reached puberty at the same age and both were older than the controls. In females the large lines on average were heavier and younger at puberty than the controls, and the small lines were lighter and older than the controls, though not significantly older. The replicates within each size-group, however, reached puberty at about the same weight, irrespective of their differences in growth rate. Thus, the differences of growth between the large, control and small groups affected both the weight and the age of females at puberty, but the differences of growth between the replicate lines within each size affected only the age at puberty. No explanation was found for this inconsistency between size-groups and replicates. Several lines of evidence led to the conclusion that in females puberty is partly or mainly weight-dependent, whereas in males it is almost wholly age-dependent.

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.

Female reproductive performance is reported in mice selected for ten generations for one of three criteria: either appetite (A), fat percentage (F) or total lean mass (P). For each criterion lines were selected for high (H) or low (L) performance, with contemporary unselected controls (C). In the A and P lines, litter size changed in the direction of the selected criterion, the changes being larger and more rapidly established in the A than in the P lines. At generation 10, the differences in litter size between high and low lines were 2·6 live young born in the A lines, and 1·0 live young born in the P lines. The differences in 6-week weight between the high and low lines were 3·5 g in the A lines, 6·5 g in the P lines. Changes in ovulation rate were the primary reason for changes in litter size, the differences between the high and low lines being 3·8 corpora lutea for the A lines, and 3·1 corpora lutea for the P lines. Fitting body weight at mating as a covariate within lines in the analysis of ovulation rate and live foetus number removed the differences between the high and low selected P lines, but not those in the A lines. The high and low selected A and P lines did not differ in prenatal survival. There were no consistent differences in litter size, ovulation rate or pre-natal survival in the F lines.

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.

Mice gaining 3 or more standard deviations above the mean were noted beginning in generation 25 in a line selected for high 21–42 day weight gain. The exceptional growth rate appears to be due to an autosomal recessive gene, based on the following: (1) the exceptional individuals appeared suddenly, in only one of 2 closely related sublines; (2) mating high growth individuals to unrelated, normal size strains produces relatively uniform F1's with mean gains below the mid-parent average; (3) F2's have a distribution markedly skewed towards high gain and a coefficient of variation approximately double that of F1's; (4) true breeding high growth strains can be established in one generation by intermating the largest F2's; (5) intermating normal F2's produces progenies with a distribution similar to the F1 except for a few large segregates; (6) high growth segregates have been obtained in F2's from each of 4 successive backcrosses to the C57BL/6 inbred line. The symbol hg (high growth) is proposed for the postulated gene, which appears to be completely recessive. Frequency of positively identified segregates in F2's and backcrosses is on average less than 25 and 50%, due probably to some overlap of Hg- and hghg distributions. Gain of hghg individuals from 21–42 days is 30–50% higher than of Hg- contemporaries; mature weight is also much higher, while 21-day weight of hghg individuals in segregating litters is slightly lower. Fertility of homozygotes ranges from normal to as much as 40% lower than for comparable Hg- mice; hghg mice are not obese. The gene may provide a useful model for study of regulation of mammalian growth.

Mutation is modelled in two quantitative characters under separate genetic control in a large population. A bivariate pattern of selection acts to correlate the characters and, without pleiotropy, their genetic correlation is due entirely to linkage disequilibrium. Data on spontaneous mutation, the effective number of genes, and the intensity of natural selection on quantitative characters are used to evaluate the models. It is concluded that, even when selection favors a high correlation between the characters, with random mating and no linkage between loci influencing different traits the genetic correlation between characters is likely to be small in magnitude. A genetic correlation of large magnitude can be maintained only if the loci influencing different characters are tightly linked, or there is a high level of inbreeding in the population created by frequent mating between closely related individuals.

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.