A genetic analysis was made of the Female-lethal (Fl) locus of Drosophila melanogaster. This is an X-linked mutation which causes lethality only in females. Other alleles do not complement Fl and are either lethal or sterile when homozygous in females. Complementation studies on Fl alleles demonstrate that there is no simple ranking of these alleles in terms of severity of phenotypic effect. Dosage manipulation of Fl alleles indicates that the sex-specificity is not a consequence of gene dosage effects. Viability studies on males carrying Fl alleles show that Fl alleles have no effect on viability regardless of the presence or absence of a Y chromosome. The Fl locus is therefore sex-specific. The hypothesis that Fl+ is involved in the establishment of imaginal phenotypic sex cannot be substantiated on the basis of experiments utilizing sex-change mutations.

A quite specific kind of sterile F1 female, called SF females, arises only when females of strains denoted reactive are crossed with males of the other class (inducer). It was previously shown that this sterility results from a nucleocytoplasmic interaction between the maternal reactive cytoplasm and a factor, called I, which may be born by any one of the paternal chromosomes. In SF females, but not in their brothers, a varying proportion of reactive chromosomes are able to acquire irreversibly the I factor, independently of any classical genetic recombination with the inducer chromosome(s). During this process, called chromosomal contamination, the contaminating chromosome(s) do not undergo any apparent change. The present paper deals with the efficiency of both original inducer and contaminated chromosomes to yield a more or less intense SF sterility. The Otanu inducer laboratory strain contains at least two types of X chromosomes (called strong and weak) which differ genetically with respect to their inducer efficiency. Reactive third chromosomes were contaminated by these strong or weak X chromosomes and their inducer efficiencies compared. Results show that they are on average stronger when they have been contaminated by strong X chromosomes than when contaminated by weak ones. Such a correlation favours the hypothesis that chromosomal contamination is due to the insertion of some genetic element(s) into reactive chromosomes.

Experiments were carried out to see if rare male mating advantage could be detected when males differ at only one locus. The eye colour mutant sepia was inserted into a strain of Drosophila melanogaster homozygous for a first, second, and third chromosome from the Canton-S strain. Tests for the rare male advantage were conducted using ratios of 4:1, 1:1, and 1:4 of the coisogenic wild-type and sepia males. No deviations from expected types of matings were observed. The results are discussed with respect to possible conditions necessary for the rare male effect to occur.

Preliminary investigation of the genetic basis of diapause in the gypsy moth, Lymantria dispar, involved a comparison of reciprocal crosses between wild-type moths and a selectively bred ‘non-diapause’ strain with the parental stocks, where half of the eggs resulting from each of the four mating types were exposed to one month of chill at 5 °C. The presence of chill dramatically altered the phenotypic expression of diapause-dependent characteristics. Early hatching was completely recessive in unchilled eggs, while hatching time was intermediate in chilled eggs, and there was no difference between reciprocal hybrids. Proportion of eggs hatching and, therefore, number of larvae produced was also influenced by chill. Unchilled hybrids did not differ substantially from wild-type eggs, while chilled hybrids were closer to the performance of the selected line. In this case, a significant reciprocal difference indicated some involvement of sex-linkage in the inheritance of diapause.

An inherited exencephaly in the mouse is described, using embryos at 11–17 days gestation. The cephalic portion of the neural tube remains open on the dorsal surface, the bony vault of the brain fails to develop, and the tissues of the brain are exposed; the development of these tissues, which is somewhat variable, is described. There is strong evidence that the condition is due to a single recessive gene, xn, with full viability until birth. Penetrance is twice as high in females as in males, and it varies overall according to the genetic milieu studied, from 33% to 84%. These features, and the absence of pleiotropic effects and of genetic evidence of associated chromosomal anomalies, make its inheritance different from that of exencephalies so far described.

The multi-locus systems expressing non-epistatic and generalized symmetric selection lend themselves to the study of the stability of certain central polymorphic equilibria. These equilibria persist when any form of migration connects demes which share a common equilibrium. The analysis of the stability of the equilibrium in the global system is tractable, thus supplementing known protection results for two alleles at one locus with stability conditions on an internal equilibrium involving an arbitrary number of loci, each with an arbitrary number of alleles. Two of the principal findings are that stability of central Hardy–Weinberg type equilibria increase with ‘more’ migration and ‘more’ recombination. As a corollary, local stability in each deme implies stability in a system with migration superimposed; but instability in each deme when isolated does not imply instability when migration is superimposed.

A haploid strain of Saccharomyces cerevisiae has been described which, on glucose medium, segregates vegetatively a high frequency of mutants with different degrees of respiratory impairment. The range of mutants seemingly encompasses both non-revertible ρ- petites and revertible point mutations resembling leaky mit- mutations. The segregants have aberrant cytochrome contents and reduced growth capabilities on fermentable sugars other than glucose; these defects apparently correlate with the degree of respiratory impairment. Genetic analysis of this mutator phenomenon has implicated a nuclear gene which appears to show specificity of interaction with the mitochondrial genome as well as a requirement for glucose repression. The mutator effect seems to extend also to the loci in mitochondrial DNA for resistance to the antibiotics erythromycin and oligomycin.

Ten glycosidases were measured in suspensions of spermatozoa from the vasa deferentia of two inbred mouse strains and their intercrosses. Eight of these glycosidases were associated with the sperm cells and all of these showed genetical variation between the strains except α-l-fucosidase with optimal activity at pH 5·4. In contrast liver enzyme activities showed no significant variation except α-l-fucosidase. Genetic studies indicated that the variation of spermatozoal β-d-hexosaminidase, α-d-mannosidase, α-l-fucosidase and β-d-galactosidase are inherited at autosomal loci and α-d-galactosidase variation shows X-linked inheritance. We propose a new provisional gene symbol (Afuc-2) for a spermatozoal variant of α-l-fucosidase.

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.