This paper examines the hypothesis that the associations between alleles at allozyme loci and gene arrangements, which are observed in many Drosophila populations, result from inversions remaining associated with the alleles contained in the gametes in which they originally occurred. The effects of double crossing over in heterokaryotypes and of selection at loci linked to the allozyme loci, which are themselves assumed to be neutral, are studied theoretically. It is concluded that selection at linked loci is unlikely to have an important effect in retarding the decay of this type of association. The literature on associations between allozymes and gene arrangements is surveyed, and it is concluded that a ‘neutralist’ explanation of this sort cannot be excluded, except possibly in some cases where the allozyme locus is outside the inversion breakpoints and crosses over with measurable frequency in heterokaryotypes.

The number of loci which are potentially able to produce sterility genes was estimated for Drosophila melanogaster. There appear to be, on the second chromosome, about 80 loci capable of producing male sterility and about 60 loci capable of producing female sterility. These figures seem to be considerably less than (400–500) loci responsible for lethal genes.

An experimental evaluation of Robertson's (1970) theory concerning optimum intensities of selection for selection of varying durations has been carried out using published results from a long term selection study in Drosophila. Agreement of predicted rankings of treatments with expectations was excellent for low values of t/T (generations/total number scored) but poor for larger values of t/T. This was due to the 20% selection intensity treatments responding worse than expected and the 40% treatments relatively better than expected. Several possible reasons for the discrepancies exist but the most likely explanation is considered to be the greater reduction in effective population size due to selection in treatments with more intense selection.

The development of a set of two-locus descent measures is reviewed. The three digenic measures, inbreeding coefficient and parental and recombinant descent coefficients, are considered in detail. The derivations of these three in pedigrees, fixed mating systems, and random mating in monoecious or dioecious populations are given. General expressions for digenic frequencies and disequilibria functions at any time are found by applying the three digenic descent measures to two types of initial populations. The final or equilibrium status of the population is also given. As the inbreeding coefficient is the same as the recombinant descent coefficient in the case of complete linkage, avoidance or promotion of early inbreeding has similar effects on the two coefficients. Estimable components of linkage disequilibrium and other measures of association within and among populations are elaborated.

Growth relations of lines selected for fast or slow larval feeding rate have been compared with those in the genetically heterogeneous control base population from which they were derived. Larvae of the slow strain have reduced growth rate and reach their critical weight for pupation later than unselected larvae. Larvae of the fast strain attain their critical weight at the same time as the unselected control larvae, suggesting that growth rate in the precritical period of development is already maximized in the base population and cannot be improved by increasing food intake. This constraint does not apply to the fixed period of post-critical growth however, since fast feeding larvae give rise to larger adult flies than the controls.

Larval feeding rate is affected by genes located on all three major chromosomes. The small fourth chromosome has negligible effect. Selection for slow feeding rate has led to an increase in the frequency of recessive genes affecting the character. High scores of larvae selected for fast feeding rate depend upon interactions between non-homologous selected chromosomes which individually have little effect. Larval feeding rate in the control unselected population appears to be buffered, firstly by epistatic interactions against the effects of chromosomes tending to promote ‘supra-optimal’ feeding rate and, secondly, by dominance against chromosomes promoting a lowering of feeding rate.

Under conditions of scramble type competition between the selected lines for limited resources, fast feeding larvae have a higher survival rate, and complete their period of larval development earlier to give larger adult flies than their slow feeding competitors. The contribution of larval feeding rate to competitive ability at different levels is discussed, and it is suggested that the effects of change in this behavioural character may be far reaching.

Primary genes, designated as NYSA, NYSD, NYSE, NYSF (dominant) and nysB, nysC (recessive) are responsible for resistance to nystatin ranging from 30 to 80 u/ml. A dominant modifier gene increases the resistance conferred by NYSF from 80 to 140 u/ml and a recessive modifier gene enhances resistance due to NYSA by 20 u/ml (from 40 to 60 u/ml). One nystatin-resistant mutant is apparently cytoplasmic and this ‘mutation’ suppresses specifically the action of modifying factors which increase the level of resistance conferred by the NYSA gene. Interaction resulting in additive levels of resistance is shown by gene NYSD in combination with each of the genes nysB, nysC and NYSE. A model of step-wise increases in resistance due to polygenic primary genes and nuclear and cytoplasmic modifying factors is proposed.

The R factors, R56 and R64, interfere with the growth of several otherwise unrelated phages, including λ, P22 and T7. In addition, λvir is inhibited more strongly in λ lysogens carrying either R factor when the prophage has an intact O – P region. Interference does not occur in certain str A R+ hosts but may reappear if they also carry other mutations affecting ribosomal proteins. Host mutants not permitting interference were isolated but were not strA. Non-interfering plasmid mutants were also isolated, of which some also failed to cause interference after transfer to a different host genus.

Five loci have been identified in Saccharomyces cerevisiae whose function reduces suppressor activity in strains carrying ochre super-suppressor mutations. Recessive mutations which allow an increased level of suppression occur at these loci. In such mutants, termed allosuppressors, the serine-inserting suppressor SUPQ5 suppresses ochre mutations in a [psi−] background and Class I tyrosine-inserting suppressors are lethal or have a reduced viability. Mutations at two allosuppressor loci, sal3 and sal4, have a lethal interaction with one another and with the extrachromosomal determinant [psi+]. This interaction is expressed in the absence of any suppressor mutation. All the mutant alleles of one allosuppressor locus sal3 are cold sensitive. One allosuppressor mutation, sal4.2, is temperature-sensitive for growth, as well as for other aspects of its phenotypic expression; namely the expression of SUPQ5 and the lethal interactions with Class I super-suppressors, with [psi+] and with sal3. At low temperature (24 °C), sal3-sal4.2 double mutants weakly suppress the ochre mutation ade2.1, but do not suppress his5.2 or lys1.1. It is argued that the site of function of the products of these loci is ribosomal and that they are involved in chain termination at UAA codons. It is inferred that the [psi+] factor or its product affects protein synthesis by interaction with the ribosome.

sF− mutants of Aspergillus nidulans are subject to toxicity by a metabolite derived from sulphate but are not blocked in cysteine biosynthesis. Bearing in mind the unavoidable presence of sulphate in agar-solidified media, their apparent auxotrophy for thiosulphate, L-cysteine or L-methionine stems from the ability of these reduced sulphur-containing metabolites to repress, directly or indirectly, the syntheses of sulphate permease and the enzymes of sulphate assimilation, thereby preventing synthesis of the toxic metabolite.