The cloning of the rpoB and rpoC genes in a high copy number vector in E. coli increased the amount of the encoded gene products, the β and β′ subunits of RNA polymerase. However, this unexpectedly caused a 30–50% decrease in RNA synthetic activity which alternatively induced a reduction of growth rate and enlargement of cell size, and decreased the DNA replication time. The results can be explained by autogenous regulation of the RNA polymerase genes by the ββ′ subunits. A relation between the decrease in number of transcription units and the observed higher rate of movement of DNA replication forks is discussed.

The transcriptional competence of the X-chromosome of a mutant strain of Drosophila melanogaster, [in(1)BM2 (reinverted)], and of hyperploid derivatives with different additional segments of the X-chromosome has been examined. The single X in the mutant male shows twice as much puffiness and RNA synthesis as does that in the normal male, revealing a level of X-coded activity in addition to the normal male and female levels. Feulgen cytophotometry reveals no duplication of DNA content in the mutant X. When duplication for the segments 1A-3E, 9A-20F, 11A-20F and 16A-20F of the X-chromosome are combined in the male with the mutant chromosome, the super-hyperactivity of the mutant X is completely abolished. In combination with the Bs. Y duplication, which contains 16A7-B2, the two-fold activity is also completely suppressed.

The mutant chromosome can appear in three discrete manifestations, namely, highly flabby, intermittently flabby and normal, suggesting a leaky nature of the mutant. The effect is also temperature-sensitive. Our results suggest that there may be a modulator gene complex (M+) in the 16A7-B2 region as well as regulators elsewhere on the X, which in combination influence the hyperactivity of the male X in Drosophila. We suggest that the In(1)BM2 (reinverted) chromosome carries a hypomorphic mutation of M+(Mm). The results presented here and earlier data on various X-chromosomal and autosomal hyperploids are discussed in the light of a model for dosage compensation in Drosophila.

P element mutagenesis was used to contaminate M strain second chromosomes with P elements. The contaminated lines were compared to uncontaminated control lines for homozygous and heterozygous fitness and its components. Mean homozygous fitness, viability and fertility of chromosome lines contaminated with P elements is decreased relative to the uncontaminated control lines by, respectively, 55, 28 and 40%. Variance among contaminated homozygous lines of total fitness increases by a factor of 1·5, variance of viability by a factor of 5·9, and variance of fertility by a factor of 1·9, compared to variance of these traits among the population of uncontaminated homozygous chromosomes. Estimates of P-element-induced mutational variance among second chromosome lines for homozygous fitness, viability and fertility are, respectively, 2 × 10−2, 5 × 10−2 and 2 × 10−2. This magnitude of mutational effect is equivalent, in terms of incidence of induced recessive lethal chromosomes and D:L ratio, to a dose of approximately 1·0–2·5 × 10−3 m EMS. The distributions of fitness traits among M-derived second chromosome homozygous lines contaminated with P elements are remarkably similar in many regards to distributions of fitness and viability of chromosomal homozygotes derived from natural Drosophila populations. It is possible that a proportion of the fitness variation previously observed (reviewed by Simmons & Crow, 1977) following homozygosis of wild chromosomes was not present in the natural populations, but was generated by P-element transposition during the chromosome extraction procedure. P-element-induced fitness mutations appear to be completely recessive. Implications for models of evolution of transposable elements are discussed.

Wild-type chromosomes of D. melanogaster mutagenized by passage through a single generation of hybrid dysgenesis have been compared against identical chromosomes passed through a reciprocal, non-dysgenic cross. Fitness of the chromosome in homozygous condition has been examined in population cages using the technique of balancer chromosome equilibration. The results indicate that amongst chromosomes with no lethal or visible mutation, more than 50% have suffered a measurable decline in fitness. The magnitude of this decline is estimated to be in the range 10–20%.

Crosses were made among 18 lines of mice, six previously selected for large 6-week weight, six for small 6-week weight, and six unselected controls, comprising a complete diallel cross among sizes and a partial diallel cross among replicate lines within sizes, and all purebred matings. Across all groups large size was associated with lower weight-specific food consumption and brown adipose tissue, and increased nest-building. Overall the crosses had lower weight-specific food consumption, and increased nest-building, body temperature, and brown adipose tissue than the purebreds. In general, heterosis in crosses between lines of different size, especially those involving large lines, tended to exceed that in crosses between lines of the same size.

After seven generations of selection, a line of mice selected for post-weaning (21–42 days) weight gain on full feeding (SF) showed significant increases of 49% in weight gain, 31% in efficiency and 14% in food intake, when compared with its control on full feeding between 21 and 42 days. After day 42, SF mice continued to eat more food and were 28% heavier than control mice at 91 days. Because SF mice were heavier than control mice at almost all ages, they were fatter on an age basis. There was, however, no change in the rate of deposition of fat, protein and ash relative to body weight. On restricted feeding between 21 and 42 days, SF mice showed a non-significant increase in weight gain, and hence in efficiency, of 12%. They deposited more fat than control mice during the feeding period but there was no significant difference when comparisons were made on a weight basis.

A contemporary line of mice selected for post-weaning (21–42 days) weight gain on restricted feeding (SR) had significant increases of 12% in weight gain, 17% in efficiency but no significant change in food intake, when compared with its control on full feeding between 21 and 42 days. SR mice were the same weight as control mice at all ages except day 21, when they were significantly lighter due to direct genetic effects rather than maternal effects. SR mice had a lower (P<0·10) rate of fat deposition per unit body weight and became less fat relative to their control as body weight increased. The rate of deposition of other components was not altered by selection. On restricted feeding, SR had a significant increase in weight gain, and hence in efficiency, of 37%. Changes in body composition were similar to those on full feeding.

It was concluded that the use of a restricted feeding regime had enabled the exploitation of heritable variation in the partitioning of energy for growth. This variation was independent of genetic variation for appetite and body weight.

Overall performance at each level of feeding was best improved by selection on that feeding level. The realized genetic correlation between post-weaning weight gain on full and restricted feeding was estimated to be 0·28 ± 0·08, indicating a very different genetic basis for the same character in the two feeding environments.

The probabilities of genetic identity between different members of the same family of transposable elements in a randomly mating host population are determined, under the assumption of statistical equilibrium between neutral mutations, random genetic drift, transposition and unbiased gene conversion. The method allows for variation in numbers of copies of the element between individuals within the host population, and for dependence of the probability of identity between a pair of elements on the frequencies of elements at the sites from which they were drawn. It is shown that, for the range of parameters under which the approximations used are valid, the effects of gene conversion on identity probabilities are relatively small, as are the effects of copy number variation and variation between sites in element frequencies.

By using a simple model of gene conversion, the actual number of alleles contained in a multigene family was theoretically studied. It was shown that the Ewens' sampling theory is applicable to predict the actual number in a gene family of a genome. However, the actual number of the gene family forming the total population becomes larger or smaller than the predicted value by the sampling theory, depending upon the relative magnitude of the rates of two homogenization processes, i.e. intra-genome and in the population.

The effects of mutation on mean and variance of response to selection for quantitative traits are investigated. The mutants are assumed to be unlinked, to be additive, and to have their effects symmetrically distributed about zero, with absolute values of effects having a gamma distribution. It is shown that the ratio of expected cumulative response to generation t from mutants, , and expected response over one generation from one generation of mutants, , is a function of t/N, where t is generations and N is effective population size. Similarly, , is a function of t/N, where is the increment in genetic variance from one generation of mutants. The mean and standard deviation of response from mutations relative to that from initial variation in the population, in the first generation, are functions of . Evaluation of these formulae for a range of parameters quantifies the important role that population size can play in response to long-term selection.