Within-line heterogeneity has been found in the mitochondrial DNA (mtDNA) in two isofemale lines of D. simulans. The co-existing types, S and M, were typical of the mtDNA in D. simulans and in D. mauritiana, respectively, their nucleotide divergence per site being ca. 2·1%. Segregation analysis confirmed that some individuals in these lines were heteroplasmic and suggested incomplete maternal inheritance of mtDNA in Drosophila. Examination of other lines of D. simulans revealed that the M type of D. mauritiana occurs at 71% in Réunion, 38% in Madagascar and 0% in Kenya. This finding and interspecific sequence comparisons of both M types indicate that D. mauritiana diverged from D. simulans probably less than 240000 years ago.

Restriction site analysis revealed a variant growth hormone gene haplotype fixed within growth-selected mice (High line-3; HL-3) exhibiting growth rates 1·5 times greater than those of unselected Foundation population (FP-3) mice. Relative to the FP-3 haplotype, the HL-3 haplotype exhibited restriction fragment length polymorphisms for each of seven different restriction enzymes. Three of the polymorphic sites lie within 1·1 kb of the 5′ end of the structural gene; a fourth polymorphism exists within the structural gene. The HL-3 haplotype was also fixed within an additional three growth-selected lines (including a replicate of HL-3). This identification of an association, between the natural variant of a growth regulating gene and a growth-related phenotype, is the prototype of experiments that could lead to the isolation of variant genes which enhance livestock production characters.

In this study we estimate the frequency at which P-element insertion events, as identified by in situ hybridization, generate lethal and mild viability mutations. The frequency of lethal mutations generated per insertion event was 0·004. Viability dropped an average of 1% per insertion event. Our results indicate that it is deletions and rearrangements resulting from the mobilization of P elements already in place and not the insertions per se that cause the drastic effects on viability and fitness observed in most studies of P–M dysgenesis-derived mutations. Elements of five other families (I, copia, 412, B104, and gypsy) were not mobilized in these crosses. Finally, we contrast the density of P elements on the X chromosome with the density on the four autosomal arms in a collection of thirty genomes from an African population. The relative number of P elements on the X chromosome is too high to be explained by either a hemizygous selection or a neutrality model. The possible reasons for the failure to detect selection are discussed.

A recessive autosomal mutation has been found in the CXBI/ByEss recombinant-inbred line but in neither of the parental strains, C57BL/6ByEss and BALB/cByEss. Its presence in the CXBI/ByJax and CXBI/ByLac sublines suggests an origin early in inbreeding. The locus, seminal vesicle shape (svs), appears to be linked to the albino locus on chromosome 7. The homozygote has seminal vesicles with a smooth tubular external appearance. In segregating crosses homozygotes had slightly lighter seminal vesicles but the weights of other androgen target organs were not reduced. Exogenous testosterone increased the size of the seminal vesicles but did not alter their shape. The mutation did not affect the pattern of proteins on SDS–acrylamide gel electrophoresis, which did differ between the parental strains. The locus affecting a 27000 Da protein has provisionally been assigned the symbol svp-4.

Models of variability in quantitative traits maintained by a balance between mutation and stabilizing selection are investigated. The effects of mutant alleles are assumed to be additive and to be randomly sampled from a stationary distribution. With a two-allele model the equilibrium genetic variance in an infinite population is independent of the distribution of mutant effects, and dependent only on the total number of mutants appearing per generation. In a finite population, however, both the shape and standard deviation of the distribution of mutant effects are important. The equilibrium variance is lower when most of the mutational variance is contributed by few genes of large effect. Genes of small effect can eventually contribute substantially to the variance with increasing population size (N.) The equilibrium variance can be higher in a finite than an infinite population since near-neutral alleles can drift to intermediate frequencies where selection is weakest. Linkage leads to a reduction in the maintained variance which is small unless linkage is very tight and selection is strong, but the reduction becomes greater with increasing N since more mutants segregate. A multi-allele model is simulated and it is concluded that the two-allele model gives a good approximation of its behaviour. It is argued that the total number of loci capable of influencing most quantitative traits is large, and that the distribution of mutant effects is highly leptokurtic with the effects of most mutants very small, and such mutants are important in contributing to the maintained variance since selection against them is slight. The weakness of the simple optimum model is discussed in relation to the likely consequences of pleiotropy.

Mice which are either homozygous or heterozygous for the CatFraser mutation have ocular cataracts accompanied by selective reduction of the γ-crystallins, a homologous family of proteins present in the lens and encoded by a family of tightly linked genes. We measured the concentrations of four different mRNAs, each encoding a different γ-crystallin, in the lenses of homozygous CatFraser mice and in normal controls at various stages of development by preparing Northern blots from lens RNA, probing with RNAs complementary to each of the four messages and densitometry of the bands thus generated. The results show that, for each of these messages, the ontogenetic patterns observed in normal mice are retained in the mutant, but at much lower concentrations.

A mutant strain of Drosophila melanogaster with five markers on the X-chromosome was found to be more sensitive than the wild type when infected with an insect-pathogenic strain of Serratia marcescens. Two of the five mutations in this fly strain, cut and miniature, were found to be responsible for this sensitivity. A double-mutant, with both cut and miniature, was as sensitive to Serratia infection as was the original sensitive Drosophila strain with all five mutations. Recombinant flies with other alleles of cut and miniature were also sensitive. A revertant of cut was found to be less sensitive than the parental flies. Our insect pathogenic strain of Serratia produces several proteases and a chitinase. A bacterial mutant, lacking proteases and chitinase, was found to be less virulent than wild-type bacteria. When pupal shells from resistant and cut-miniature flies were incubated with a mixture of protease and chitinase there was a release of N-acetyl glucosamine, and 50% more material was liberated from pupal shells of sensitive flies. Sensitive flies reared on sucrose infected with Serratia showed bacteria in their hemolymph earlier than wild-type flies. We conclude that Drosophila genes for cut and miniature are associated with the sensitivity to Serratia infection, presumably because the gut peritrophic membrane is more susceptible to bacterial proteases and chitinase.