A method based on the animal model is described which allows the estimation of continuous changes in variance components over time using restricted maximum likelihood (REML). The method was applied to the analysis of a selection experiment in which a foundation population formed from a cross between two inbred strains of mice (C57BL/6J and DBA/2J) was divergently selected for 6 week body weight over 20 generations. The analysis suggested that there was an increase in phenotypic variance of about 50% in the low selected lines over the course of the experiment which was attributed to increases in the environmental and additive variance components. Variance changes in the High selected lines were generally smaller than in the Low lines, although there was an estimated 20% increase in the environmental variance. Simple models to explain these effects involving dominance, linkage and epistasis were explored. Testing which of these was responsible for the variance changes noted in this experiment (if any) is difficult, although the epistasis and dominance models require less stringent conditions than the linkage model, and the dominance model is supported by evidence of heterosis in the F1.

Theoretical models of the effects of selection against deleterious mutations on variation at linked neutral sites (background selection) are used to predict the relations between chromosomal location and genetic variability at the DNA level, in Drosophila melanogaster. The sensitivity of the predictions to variation in the mutation, selection and recombination parameters on which they are based is examined. It is shown that many features of the observed relations between chromosomal location and level of genetic diversity in D. melanogaster can be explained by background selection, especially if the weak selective forces acting on transposable elements are taken into account. In particular, the gradient in diversity in the distal portion of the X chromosome, and the lack of diversity on chromosome 4 and at the bases of the major chromosomes, can be fully accounted for. There are, however, discrepancies between predicted and observed values for some loci in D. melanogaster, which may reflect the effects of forces other than background selection.

1. Techniques were developed to facilitate genetic analysis of a Myxomycete, Physarum polycephalum. The uninucleate cells that form part of the life-cycle (the ‘amoebae’), in two-membered culture with Pseudomonas fluorescens, were found to be suitable for handling by some of the standard techniques of microbial genetics, including plating.

2. As reported previously, a single-factor (+/−) mating-type system was discovered in P. polycephalum controlling the formation of plasmodia by the amoebae. Plasmodia are formed only when amoebae of different mating-type are mixed together. A single spore gives a culture of amoebae of one mating-type only, which may be assumed to be a clone.

3. A strain of amoebae resistant to emetine hydrochloride was isolated and was found to maintain its resistance through many subcultures in the absence of the drug.

4. A cross was made between the emetine-resistant strain (mating-type −) and an emetine-sensitive strain (mating-type +). Spores obtained from the hybrid plasmodium were plated and four sets of isolates of amoebae were made from these spores, and separately tested for mating-type and for emetine resistance.

5. The results of testing these isolates agree with the hypothesis that mating-type and emetine resistance are determined by pairs of alleles at two unlinked loci provided that factors disturbing the segregation for emetine resistance are assumed to be present.

6. Consideration of factors that could have disturbed the segregation for emetine resistance shows that selfing did not occur in the cross but that some misclassification for emetine resistance probably did occur.

Strains with altered properties of host-induced modification (HIM) have been isolated. Someof these variants were stable on first isolation but the majority of them are unstable. They segregate during many generations two different stable HIM phenotypes and a third type which continues to segregate. Usually this instability disappears during repeated serial single colonyisolation, but in one case it still persisted after nine such single colony isolation steps. Evidence suggesting that they are unstable partial diploids is discussed.

The gene (dw) causing hypopituitary dwarfism was transferred by repeated backcrosses into strains of mice differing genetically in growth-rate through previous selection. The dwarf mice lack growth hormone, and the purpose was to find out if the differences in growth-rate between the strains were in any part due to differences in their growth hormone status – amount of hormone or tissue sensitivity. In the absence of growth hormone, i.e. in the dwarfs, the strains still grew at different rates, proving that growth hormone status was not the only cause of their differences. The effect of substituting the dw gene was, however, greater in the large strain than in the unselected control, and less in the small strain than in the control. The growth differences between the strains were therefore in part due to growth hormone. Tissue sensitivity in the three strains was compared by their responses to graded doses of exogenous growth hormone. The large and control strains did not differ, but the small strain had a lower sensitivity. The results suggest that the increased growth-rate of the large strain is partly due to an increased amount, or activity, of its circulating growth hormone, while the reduced growth-rate of the small strain is in part due to a reduced sensitivity of its target organs to growth hormone.

The frequency of adjacent-2 disjunction in mice carrying the reciprocal translocation T(9; 17)138Ca was studied by mating together animals heterozygous for the translocation and carrying different recessive marker genes, using Tt for chromosome 17 and cwcw for chromosome 9. The proportion of marked young arising from adjacent-2 disjunction varied according to the markers carried in the two parents. When the female carried Tt the frequencies of marked young were always higher than when non-T females were used, and when Tt and cwcw were carried in the same parent there was a shortage of marked young obtaining both copies of the proximal region of chromosome 17 from the father. Both these effects were regarded as probably another example of the phenomenon discovered by Johnson, of inviability of young lacking a maternal homologue of a certain region of chromosome 17. There were other variations in frequency of marked young, among crosses using non-T females, which may have been due to differences in transmission ratio of male gametes carrying various t-haplotypes or to true variations in frequency of adjacent-2 disjunction.

In this study we genetically analyse a large autosomal region (23 map units) in Caenorhabditis elegans. The region comprises the left half of linkage group V [LGV(left)] and is recombinationally balanced by the translocation eT1(III; V). We have used rearrangement breakpoints to subdivide the region from the left end of LGV to daf-11 into a set of 23 major zones. Twenty of these zones are balanced by eT1. To establish the zones we examined a total of 110 recessive lethal mutations derived from a variety of screening protocols. The mutations identified 12 deficiencies, 1 duplication, as well as 98 mutations that fell into 59 complementation groups, significantly increasing the number of available genetic sites on LGV. Twenty-six of the latter had more than 1 mutant allele. Significant differences were observed among the alleles of only 6 genes, 3 of which have at least one ‘visible’ allele. Several deficiencies and 3 alleles of let-336 were demonstrated to affect recombination. The duplication identified in this study is sDp30(V;X). Lethal mutations covered by sDp30 were not suppressed uniformly in hermaphrodites. The basis for this non-uniformity may be related to the mechanism of X chromosome dosage compensation in C. elegans.

A series of six bones from samples of mice from eleven inbred strains and one F1 hybrid were measured using a simple apparatus. The bones examined were the mandible, os coxae, femur, tibia–fibula, scapula and humerus. Considerable variation in the shape of each bone was found and successful discrimination between the strains was obtained. Correct strain classification ranged from 87% for the scapula to 98% for the os coxae. Gross abnormalities and quantitative variants were identified.

As the pattern of discrimination is different for each bone, the use of other bones in addition to the mandible may improve resolution in the identification and quality control of mouse stocks. The objective and precise identification of abnormal and variant bones suggests that the method may be useful for population studies and for the detection of induced skeletal abnormalities in toxicological investigations.

Mouse chimaeras made by aggregating embryos homozygous for nine recessive genes with embryos carrying the corresponding dominants were mated with partners of the recessive strain. Progeny were either of the recessive type for all loci examined, or showed the dominant characters at all loci. Tail length in homozygous vestigial-tail progeny was unaffected by whether the fertilizing spermatozoon had undergone maturation in a chimaera or in a control vestigial-tail male. There was thus no indication that the germ cells had been in any way modified by their intimate association with germ cells and somatic tissue of contrasting genotype in the chimaeras.

Thirty-nine enzyme loci and seven non-enzymic protein loci have been screened for electrophoretically detectable variation in a population of Pleuronectes platessa, a marine flatfish. The mean heterozygosity per individual is 0·102 ± 0·026, or 0·118 ± 0·030 if the non-enzymic proteins are excluded. The distributions of allele frequencies and single locus heterozygosities are given, and the results discussed with reference to current theories concerning the nature of protein variation.

The interaction of three neurogenic loci viz. Delta, Enhancer of split and Notch, and a related gene, Hairless, of Drosophila melanogaster was investigated at the adult morphology level by measuring the effects of the mutations of the three other genes on the expression of the recessive lethal antimorphic Abruptex mutations of the Notch locus. The Abruptex mutations were also coupled in cis or trans with facet-glossy or split mutations of the Notch locus. In some of the experiments, the genotype of the fly was homozygous for either facet-glossy or split mutation or their wild type alleles but heterozygous for the Abruptex. Facet-glossy is located in a large intron of the locus, whereas split is located in the same exon as Abruptex. In all compounds studied, Delta suppressed the expression of Abruptex while Hairless and Enhancer of split enhanced it. The interactions of the four genes studied were allele specific, suggesting an interaction at the protein level. The comparison of the results presented in this study on the interaction of the neurogenic genes with other results on the same subject suggests that the interactions are similar in embryonic and imaginal development.