Chemostat cultures in which the limiting nutrient was lactose have been used to study the relative growth rate of Escherichia coli in relation to the enzyme activity of β-galactosidase. A novel genetic procedure was employed in order to obtain amino acid substitutions within the lacZ-encoded β-galactosidase that result in differences in enzyme activity too small to be detected by ordinary mutant screens. The cryptic substitutions were obtained as spontaneous revertants of nonsense mutations within the lacZ gene, and the enzymes differing from wild type were identified by means of polyacrylamide gel electrophoresis or thermal denaturation studies. The relation between enzyme activity and growth rate of these and other mutants supports a model of intermediary metabolism in which the flux of substrate through a metabolic pathway is represented by a concave function of the activity of any enzyme in the pathway. The consequence is that small differences in enzyme activity from wild type result in even smaller changes in fitness.

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.

Salmonella typhimurium phage P22 can recombine with a serologically and morphologically unrelated Salmonella phage Fels 2 to yield the hybrid phage F22 at a frequency of about 10−12. F22 has inherited the entire late genes (protein coat and tail structural genes) of Fels 2 but carries some P22 early genes. P22 genes in the F22 phage were indentified by marker rescue of various P22 mutants. The F22 genome carries the x-erf-c-18-12 segment of the P22 genome. A number of P22 amber mutants were also tested to support these data. The F22 region homologous to P22 was mapped by scoring the ratio of P22 backcross recombinant types in lysates of F22 lysogens superinfected with P22c2ts12. The ratio of the distances between these markers and the ends of the homologous region was determined. Furthermore a new F22 hybrid designated F22dis, containing both P22 immunity regions (c and Im), was isolated at a frequency of about 10−4 by superinfecting F22 lysogens with P22. F22dis phage has lost some Fels 2 gene(s) which have been replaced by the P22 segment containing the Im region, resulting in formation of a defective hybrid phage.

All major recombination pathways in the yeast Saccharomyces cerevisiae require the RAD52 gene product. We have examined the effect of the rad52-1 mutation on spontaneous mitotic recombination between heteroalleles, and found that prototrophs are produced at frequencies significantly above reversion. This residual recombination occurs at a relatively uniform level at all of the loci examined. To help understand the role that RAD52 plays in mitotic recombination, we examined recombination between all pairwise combinations of six mutant alleles of the LYS2 gene. The rad52-1 mutation decreased the variation in amount of recombination between the various pairwise combinations as well as lowering the overall frequency of recombination. The reduced variation results in a different pattern of recombination in rad52-1 cells than in wild type. One interpretation of these results is that the RAD52 gene product, directly or indirectly, plays a role in the formation or the resolution of mismatches in heteroduplex DNA.

The presence of a gene designated bncA which produces binucleate and trinucleate conidia in A. nidulans alters the instability of disomics, diploids, and strains with chromosome duplication. In disomics, the gene bncA increases instability. In duplicate and diploid strains, the bncA gene reduces instability by acting as a partial stabilizer. In the strain with chromosome duplication, the bncA gene produces increased percentages of bi- and trinucleate conidia, a fact that may be interpreted to be due to the larger conidial volume of this strain or to the combined effect of bncA and of the strain, which normally already exhibits a small amount of binucleate conidia.

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.

Populations of Drosophila melanogaster were subjected to selection for differing oviposition preference under allopatric and sympatric conditions. Flies were presented with the choice of a potato-based medium and a medium containing sugar and killed yeast on which to lay their eggs. Some gene flow was possible under sympatric conditions. In the allopatric lines selection was successful in rapidly generating an increased preference for sugar, and in the sympatric lines divergent oviposition preferences were generated in two cases out of four. A significant degree of reproductive isolation between one pair of allopatric lines was generated after eighteen months of selection.

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.

Ditelocentric accessions of the Chinese Spring cultivar of Triticum aestivum were analysed electrophoretically for peptidase (PEPT) and amino peptidase (AMP = LAP) activity. Isozymic activity was missing in the accessions CSDT6AS and CSDT6BS when stained for PEPT. This was taken as evidence that the structural genes encoding these isozymes are located on the long arms of chromosomes 6A and 6B. These genes have been named Pept-A1 and Pept-B1, respectively. Isozymic activity was missing in the CSDT6BL accession when stained for AMP. This result reconfirms the previously published location of the gene Amp-B1 on the short arm of chromosome 6B and demonstrates that the two sets of loci are clearly different.

We analyse the progression of linkage disequilibrium produced by random genetic drift in populations subject to cyclical fluctuations in size. Our model is applied to natural populations of Drosophila which show an annual demographic cycle of bottleneck (finite size) and demographic burst (size supposed to be infinite). In these populations, linkage disequilibrium stabilizes in such a way that, at equilibrium, the expected square of the correlation of gene frequencies E(r2) shows a stable cycle from year to year. If two loci are tightly linked, E(r2) barely varies during the annual cycle. Its values remain close to the value expected in a population of the same but constant effective size. If two loci are loosely linked, fluctuations in E(r2) are large. The maximum value, reached at the end of the bottleneck, is 10 to 100 times greater than the value obtained at the end of the burst. Our results show that the interpretation of observed linkage disequilibrium, by means of statistical tests, requires an accurate knowledge of population demography.

In a series of Lacerta vivipara samples from southern France's central mountains, the distribution of genotypes at the mannose phosphate isomerase (MPI) locus has only been accountable as due to sex linkage in female heterogamety, provided the W chromosome carries only one of the two observed alleles in the populations sampled. This is in perfect accordance with cytogenetical data. Reasons are presented that seem to limit acceptable hypotheses for the recent origin of this sex-linked polymorphism to three: a founder effect, a point mutation in Z chromosomes after crossover suppression, or hitch-hiking with the translocation involved.

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%.

Genetic variation in 40 domestic rabbits (Oryctolagus cuniculus) from eight different strains was investigated by horizontal starch gel electrophoresis. Twenty nine enzyme systems were examined in different tissues, 10 isoenzymes were found to be polymorphic. Indices of genetic variation show values comparable to those found in most other mammalian species. Thus the unusually high values reported previously by other authors may be due to a limited and not randomly chosen set of enzymes studied.

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.

In Drosophila melanogaster a large number of the genes coding for 18S and 28S rRNA are interrupted in the 28S region by insertions of two types. Ribosomal insertion transcripts were compared in wild-type and bobbed strains. We found that the level of insertion transcripts increased in bobbed mutants after deletion of 50% of INS− genes, and inversely decreased in revertants when more than 50% of wild-type levels. Among type II insertion transcripts we found a predominant 3·5 kb RNA, precisely of the most frequent insertion size. No primary insertion transcript has been found, although it could be undetected if very fast splicing leads to mature 28S occurs.

Linkage crosses were used to determine the gene order of aminoacylase-1, beta-galactosidase, and transferrin on mouse Chromosome 9. The most likely gene order, which was more than 107 times more likely than the next most likely order, was transferrin, aminoacylase-1, beta-galactosidase. These results demonstrate that aminoacylase-1 and beta-galactosidase mark a chromosomal segment that has been conserved since divergence of lineages leading to man and mouse. The length of this segment is about 11 cM and the estimate of the true length of the conserved segment marked by these two genes is 33 cM. A second aminoacylase allozyme, which requires MgCl2, is described.

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.

DK/Lm is a new inbred mouse strain with over 20 generations of brother–sister mating. The genotype of the DK/Lm mouse at the black-brown locus is b/b and heterozygosity at the agouti locus (Ay/a) is maintained. DK/Lm-Ay/a mice become sable in phenotype at the first moult, whereas C57BL/6J-Ay/a mice do not. The sable phenotype is defined as that of a mouse whose basic colour is yellow (phaeomelanic) but whose dorsal aspect is more or less darkened by the presence of nonyellow (eumelanic) pigment. At about 6 months of age the DK/Lm mouse gradually reverts to yellow in phenotype.

Mice of the two strains are compared. Observations are discussed and related to hypotheses regarding gene action at the a and e loci. The new strain is a useful experimental model for study of the relationship between gene action at the agouti locus and the important pleiotropic effects influenced by this locus.

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.

The effects of population size and selection intensity, which are in the breeder's control, are investigated for ranges of values of quantities outside his control, namely the number, initial distribution of frequencies and effects of genes influencing the trait. Two alleles are assumed to be initially segregating at each locus, with no linkage, dominance or epistasis. The effects are assumed to follow a gamma distribution, using a wide range of its two parameters which specify both mean gene effect or selective value and the shape of the distribution, or the ratio of Wright's effective number to actual number of genes. The initial gene frequencies (q) are assumed to be either 0·5 at all loci, uniformly distributed over the range 0–1, or to have a U-shaped distribution, proportional to [q(1 − q)]−1 such as derives from neutral mutation, with gene effect and frequency distributions independent. The mean and variance of selection response and limits, in the absence of new mutation, are derived.

The shape of the distribution of effects is not usually important even up to the selection limit. With appropriate parametrization, the influence of the initial frequency distribution is small over a wide range of parameters. For reasonable choices of parameters, the effects of changing population size from those typically used in animal breeding programmes are likely to be small, but not negligible. For the initial U-shaped frequency distribution, further increases in population size are always expected to give a greater limit, regardless of present value, but not for the other distributions.