Two mutant alleles of the meiotic locus, mei-9, have been examined for their effect on magnification of a rod Xbb chromosome and transmission of a ring Xbb chromosome under magnifying conditions. Our results indicate that the effects of these two mutations are allele-specific: mei-9a strongly inhibits both rod chromosome magnification and ring chromosome loss under magnifying conditions, while mei-9b has a smaller inhibitory effect on rod chromosome magnification and on the transmission of ring chromosomes under magnifying conditions. These observations can be explained by a difference in leakiness between the two alleles. Our results demonstrate that mutants defective in excision repair and repair replication inhibit ribosomal gene magnification. This suggests that a component of the excision repair pathway is involved in the process of magnification.

The frequency and distribution of P elements were investigated in the third chromosomes of two wild-type strains of Drosophila melanogaster using in situ hybridization of biotinylated probes to the polytene chromosomes. The relationship between these data and the extent of hybrid dysgenesis was determined through assays of egg production, egg hatchability (F2 embryo lethality), snw destabilization and male recombination along the third chromosome. The results suggest that P-element distribution, frequency and structure are all contributory factors in the regulation of hybrid dysgenesis. Texas 6 was shown consistently to be a stronger P strain than Texas 1, eliciting greater reductions in fertility, more extensive snw destabilization and higher frequencies of male recombination. Clustering of male recombination events, arising from pre-meiotic crossing over, was evident among the dysgenic progeny of each strain. Male recombination and snw destabilization were independently distributed among the dysgenic males studied, suggesting that these traits represent separate P-mediated functions. The third chromosome male recombination maps produced by the two strains differed significantly from each other and from the published female meiotic and polytene chromosome maps. Male recombination breakpoints were associated with the original distribution of P sequences in the two strains and the results suggest that this relationship may be closer for potentially complete P factors than for P sequences in general. An analysis of sub-lines derived from individual recombinant males revealed that chromosomal breakpoints could also be associated with novel insertions following P-element transposition.

Genome sizes (nuclear DNA contents) were documented spectrophotometrically from individuals of each of nine species of the North American centrarchid (sunfish) genus Lepomis. The distributions of DNA values within and among the nine species were essentially normal and continuous, suggesting that changes in DNA quantity in Lepomis are small in amount, involve both gains and losses of DNA, and are cumulative and independent in effect. Significant differences in mean genome size were found between individuals within populations in all nine species and between species. Nested analysis of variance and comparisons of average genome size difference or distance between individuals drawn from different levels of taxonomic organization revealed that the majority of genome size divergence in Lepomis occurs above the hierarchical level of individuals within populations. The Lepomis data when compared to similar data from North American cyprinid fishes appear to suggest that: (i) genome size evolution in these fishes at least follows a continuous rather than a discontinuous mode; (ii) the general predictions of hypothetical models relating genome size variation as a function of organismal position along adaptive continua may be oversimplified, or not applicable to complex, higher eukaryotes; and (iii) changes in genome size in these fishes may be concentrated in speciation episodes.

The chromosomal location of the mouse gene coding for vimentin, one of the intermediate filament subunits, was determined by in situ hybridization using specific H3-labelled DNA probes. There is only one copy of the vimentin gene and it is located on chromosome 2 region A2.

A divergent selection experiment with mice, using plasma concentrations of insulin-like growth factor-1 (IGF-1) at 42 days of age as the selection criterion, was undertaken for 7 generations. Lines were not replicated. To obtain sufficient plasma for the IGF-1 assay, blood from four individuals was volumetrically bulked to obtain a litter mean IGF-1 concentration. This necessitated the use of between family selection. Although inbreeding accumulated in a linear fashion in each of the high, control and low lines, the rates were different for each line (3·6, 1·6 and 5·3% per generation for the high, control and low lines, respectively). As a consequence, the effects of selection and inbreeding are confounded in this experiment. Divergence between the high and low lines in plasma concentrations of IGF-1 continued steadily until generation 5. In generations 6 and 7, there was a reduced degree of divergence and this contributed towards the low realized heritability value of 0.15 ± 0.12. Six-week liveweight showed a steady positive correlated response to selection for or against plasma concentrations of IGF-1 until generation 4 (high-low difference = 1·7 g = 12%). In generation 5, a substantial drop in 6-week liveweight in the low line relative to both the high and control lines occurred (high-low difference, 3·9; g, 25%). This difference was maintained until generation 7.

This experiment suggests that genetic variation exists at 6 weeks of age in plasma concentrations of IGF-1 in mice. Furthermore, genetic covariation between plasma IGF-1 concentrations and liveweight at 6 weeks of age is likely to be positive. Further experiments have been initiated to examine these theories.

The behaviour of the X- and Y-borne Sts locus has been studied in male and female mice. There was considerable heterogeneity in STS activity between inbred mouse strains, with a four fold difference in activity between the highest (101/H) and lowest (Ju/Ct) activity strains, which can be interpreted in terms of allelic differences. In all inbred strains male STS levels were higher than those of female STS levels and in the majority of strains tested male STS levels were nearly twice as high as female levels. Reciprocal crosses between C3H/HeH and the STS-deficient substrain, C3H/An, demonstrated that activities of the X- and Y-borne genes in males are essentially the same and this suggested that the lower STS level in females derives from X-inactivation of the locus. The possibility that hormonal differences could instead be responsible for the lower activity in females was ruled out by the findings that (a) castration of males did not reduce their STS levels and (b) sex-reversed males, X / X Sxr, had STS levels typical of females. Final proof that the mouse Sts locus can be subject to the X-inactivation process was provided by the observation that XX females had STS levels that were only slightly (20%) higher than those of XO females. The difference may indicate incomplete inactivation of the locus. Linkage data verifying the location of Sts on the distal end of the X chromosome are provided.

In total, the results of this study show that the murine Sts locus can be subject to the X-inactivation process and this, together with the existence of functional loci of near-equal activities on the X and Y chromosomes, results in an imbalance of STS levels between the sexes. X-inactivation does not therefore serve as a dosage compensation mechanism for the Sts locus in the mouse. All of these findings were made in C3H/HeH mice or in animals carrying C3H/HeH functional Sts alleles, and it is pointed out that the diverse results previously obtained by other investigators may be attributable to their use of different strains and crosses between strains but could also be complicated by technical factors.

Some HGPRT spontaneous revertants were isolated from a mutant line (E2) of V79 Chinese hamster cells and phenotypically characterized. Dot–Blot hybridization with a 32P-Iabelled HGPRT probe revealed an increase in the number of HGPRT sequences in some of these revertants, suggesting the occurrence of gene amplification. Cytogenetic analysis performed in three of these revertants showed a characteristic abnormally banding region (ABR) on the elongated p arm of the X chromosome. In Situ hybridization in one revertant (RHE2) showed that the amplified sequences reside on the p+ arm of the X chromsome in two different localizations. Because of the very probable clonal origin of the revertant, these features indicate that the amplified sequences might rearrange after their integration into the chromosome.

The number of children produced by a modern woman is usually below her total reproductive capacity and is determined by circumstances other than natural selection. It is, therefore, practically impossible to detect differences in natural fertilities associated with different types (e.g. phenotypes, genotypes) of women. This does not mean, however, that natural selection at the reproductive level cannot at all be detected today. If women of a particular type have high natural fertility, this usually means that they reproduce (become pregnant) at a higher rate than women of a type with lower natural fertility. Hence, when there is a limit on the number of children, women of the first type will reach the limit at an earlier age than women of the second type. As a result, types that have a higher natural fertility should be overrepresented among pregnant women of younger ages and, consequently, underrepresented among older ones, as compared to types with a lower natural fertility. Based on this notion, a model of age-related differences between distributions of types among pregnant women is suggested. The model is applied to data on MNSs-blood group and PGM1 (phosphoglucomutase) types in a sample of pregnant women and an evidence of natural selection at the reproduction level associated with these genetic markers is obtained.

Evolutionary consequences of natural selection, migration, genotype–environment interaction, and random genetic drift on interpopulation variation and covariation of quantitative characters are analysed in terms of a selection model that partitions natural selection into directional and stabilizing components. Without migration, interpopulation variation and covariation depend mainly on the pattern and intensities of selection among populations and the harmonic mean of effective population sizes. Both transient and equilibrium covariance structures are formulated with suitable approximations. Migration reduces the differentiation among populations, but its effect is less with genotype–environment interaction. In some special cases of genotype–environment interaction, the equilibrium interpopulation variation and covariation is independent of migration.