For 29 generations, populations of Drosophila melanogaster were offered one favourable (standard) and one suboptimal (salt-supplemented) medium, either singly or simultaneously. Egg-to-adult viability, fecundity and choice of oviposition medium were measured at regular intervals on both resources up to 17 generations after initiation of the salt treatment. Except for a decrease in viability on salt medium in the single-resource populations (SRPs) maintained on the optimal medium, these fitness components remained unchanged. Estimation of a more inclusive measure of fitness, productivity, obtained at generations 27–29, revealed that: (1) the SRPs maintained on salt medium were more adapted to salt medium; (2) the mixed-resource populations (MRPs) were intermediate in their adaptation to salt medium between either type of single-resource population. These results support Levins' model of optimal strategy for populations living in a coarse-grained environment when the fitness set is convex. Family selection for increased and decreased resistance to salt in the medium, carried out for the viability component at generations nine and 19, showed that: (1) genetic variation with respect to this component was present in all populations; (2) the SRPs maintained on salt medium had responded to the salt treatment by eliminating sensitive genotypes; (3) in the first selection experiment, the MRPs had a greater amount of additive genetic variance with respect to viability than either type of SRP; in the second experiment, this difference was not significant, but it was in the predicted direction. The latter finding provides some evidence in favour of the hypothesis repeatedly presented in the literature that environmental heterogeneity could promote the maintenance of genetic variability in populations.

Isofemale lines of Drosophila melanogaster from six localities along the east coast of Australia, spanning 2900 km and 26 degrees of latitude, were assayed for their gonadal dysgenesis characteristics in the P–M system of hybrid dysgenesis. A strong clinal pattern with latitude was discovered. From north to south, the first two populations were typical strong P populations, and the next population was moderate P. The next population to the south was neutral (Q), with some weak P and weak M characteristics. The two southernmost populations were typical M populations. Much variance in P activity in P populations and in susceptibility to P activity in M populations was detected among isofemale lines. This clinal pattern with latitude of the P–M system is paralleled by similar clinal patterns for frequencies of common cosmopolitan inversions and of certain allozymes in Australia. A model of introductions of flies with different characteristics in the north and south could account for the P–M clinal pattern, but cannot account for an intermediate Q population, nor establish the inversion and isoenzyme dines at the same time. Current models of transposable element population dynamics are limited to single population dynamics, and are therefore inadequate for these clinal data.

A significant excess of female offspring resulted when pregnant females of the D. simulans species were left to lay their eggs on food containing quinacrine. The same result occurred in a subsequent experiment in which male parents were injected with quinacrine. This was the first time that a chemical compound showing an affinity with DNA in vitro altered the sex ratio in a consistent manner. This effect had been predicted based on the unique quinacrine fluorescent staining pattern in D. simulans, in which only the Y stains intensely in mitotic chromosomes. It seems that treatment acts on spermatids or spermatozoa causing decreased functioning of the Y-bearing ones, resulting in an excess of female offspring. Interestingly, the species D. mauritiana and D. melanogaster, although very closely related to D. simulans, do not have its staining pattern and as predicted did not respond to treatment; therefore, the important parameter appears to be related to the staining pattern of mitotic chromosomes and not to the phylogenetic relationship.

Restriction enzymes were used to search for genetic variability at 162 cleavage sites in mitochondrial DNA (mtDNA) purified from 22 mice caught at seven Swedish localities. Although all of these mice bear the nuclear genes of Mus musculus, they bear the mtDNA of M. domesticus exclusively. Yet, some of the Swedish localities are 750 km away from the hybrid zone between these two species. Furthermore, only one type of mtDNA was found at the seven Swedish localities; this type was found before at an eighth locality in Sweden as well as in Jutland north of the hybrid zone. The apparent lack of mtDNA divergence in the mouse population of Sweden contrasts with the extensive divergence usually found within other geographic areas in Europe, Africa and North America. Electrophoretic analysis of proteins encoded by nuclear genes indicates that the Swedish mice have lower average heterozygosity than Danish and Central European populations of musculus mice. These findings lead us to suggest that the source of the commensal mouse population in Sweden was a small propagule that originated from a population situated only a few kilometres to the east of the point at which the hybrid zone on the European mainland meets the Baltic Sea, namely on East Holstein. Such a founder event may have been associated with the spread of farming from north Germany into Sweden about 4000 years ago.

The numbers of members of three families of copia-like elements were counted on twenty X, 2nd and 3rd chromosomes collected from a natural population of Drosophila melanogaster. Theoretical predictions were computed for two models of copy number stabilization: (1) element frequencies are regulated by a simple genetic process such as copy number dependent transposition or excision, independent of chromosomal location; (2) elements are eliminated by natural selection against mutational effects of their insertion into the chromosome. Since insertions into the X can be expected to suffer more selection than autosomal insertions, due to expression of mutant phenotypes in the hemizygous state, hypothesis 2, called the disproportional model, predicts that the proportion of elements on the X will be smaller than the proportion of the genome contributed by the X, while hypothesis 1, called the equiproportional model, predicts that this proportionality will be unaffected. Two of the elements, 297 and roo, showed no evidence for deficiency of X-linked elements, but the data for a third element, 412, were consistent with the prediction based on the selective model.

These results indicate that simple selection against mutational effects of insertions of transposable elements is not generally adequate to account for their distribution within populations. We argue that a mechanism such as recombination between elements at different chromosomal sites, leading to rearrangements with highly deleterious, dominant effects could play a role in stabilizing copy number. This process would lead to a higher abundance of elements in genomic regions with restricted crossing over. We present some data indicating such an effect, and discuss possible interpretations.

In a search for genetic differences in susceptibility to cleft lip with or without cleft palate [CL(P)], congenic and recombinant inbred strains of mice were treated with phenytoin or control injections. Of six loci tested, five were found to affect susceptibility to phenytoin-induced and/or sporadic CL(P): (1) the major histocompatibility locus, H-2; (2) the locus controlling β2-microglobulin, B2m; (3) a locus controlling β-glucuronidase, Gus; (4) the locus controlling N-acetyl transferase, Nat; and (5) the locus for brown pigmentation, b. B2m and Gus only affected the sporadic incidence of CL(P), while the b locus only affected phenytoin-induced incidence of CL(P). Three of these loci are also known to affect glucocorticoid-induced isolated cleft palate (CP), but different alleles of the loci are involved. Phenytoin did not affect levels of adenosine 3′,5′-cyclic monophosphate (cAMP) in palates and tongues of day 15 fetuses. A comparison of glucocorticoid receptor parameters with the incidence of phenytoin-induced CL(P) found no correlation.

Mouse t haplotypes have been divided into nine subregions that are each defined by one or more molecular markers. In previous studies, three of these subregions were shown to contain ‘distorter loci’ that interact to effect the transmission-ratio distortion phenotype characteristic of all complete t haplotypes. To determine which of the remaining six subregions also play a role in this phenotype, we analysed the accumulated data on transmission ratio distortion from males that carried one of 26 different combinations of two partial t haplotypes. We have obtained evidence for the association of two additional subregions with distorter loci. First, we present further evidence for the existence of a previously postulated distorter locus, Tcd-3, and describe its mapping to the T66C subregion. Secondly, we describe the identification of a new distorter locus, Tcd-4, in association with the subregion defined by the structural gene for the TCP-1 protein. Further studies indicate that two doses of the Tcd-4 locus are equivalent in effect to a single dose each of Tcd-4 and a second distorter locus, Tcd-1. This result suggests that different distorter locus products could have a common mode of action.

Male mice heterozygous for two distorter genes, Tcd-1 and Tcd-2, of the mouse t-complex but homozygous wild type for the responder, were generated by crossing animals carrying the partial t-haplotypes th51 and th18 to inbred strains. The fertility of these males was then compared with that of their brothers carrying normal chromosome 17s. On three of the inbred backgrounds used, C3H/HeH, C57BL/6J and TFH/H, the th51th18 + / + + + males were significantly less fertile than their normal sibs. With the fourth inbred strain used, SM/JH, both types of male were nonnally fertile. This confirmed earlier preliminary findings that when both homologues of chromosome 17 carry wild-type alleles of the responder, heterozygosity for the distorter genes is sufficient to impair fertility, but the effect varies with genetic background. These results are consistent with the concept that both the transmission ratio distortion and the male sterility caused by the t-complex are due to harmful effects of the distorter genes on wild-type alleles of the responder.

The level of histidine decarboxylase in mouse kidney normally differs between the sexes with females higher than males. In a strain derived from feral Danish mice (DAN), however, both males and females have the same, high, HDC activity due to the males being insensitive to repression by testosterone. Genetic analysis indicates that this insensitivity is caused by a variant allele of a new gene in the histidine decarboxylase gene complex, Hdc-a; the Hdc-ab allele in C57BL/10 confers high sensitivity to testosterone whereas the Hdc-aw allele in the DAN strain confers low sensitivity. In addition, the DAN strain has a novel haplotype for the other three known elements of [Hdc]: the allele Hdc-sd of the structural gene, the Hdc-cd allele of the gene determining enzyme concentration, and the oestrogen-inducible allele Hdc-eb.

The average effect and average excess both measure the phenotypic effects of gametes in a population. A matrix notation is introduced that provides a general analytical solution for the average effects at a single locus with k alleles that can be solved for any population regardless of its genotype frequencies. This same notation also provides an easy way of deriving and generalizing to k alleles the well-known relationships between average effects and average excesses that exist under random-mating and regular deviations from Hardy–Weinberg equilibrium due to inbreeding.

The widespread use of restriction endonucleases and DNA sequencing provides a wealth of data on the genetic structure of natural populations. From such data, detailed phylogenies can be constructed and qualitatively different kinds of mutational and substitutional processes can be studied. A neutral model can be constructed to describe the frequencies of sequence haplotypes according to the haplotypes from which they arose and the types of substitution that distinguish them. One feature of such a model is that it examines the ancestors of various sequences. Deleterious selection against a character has a distinct effect on descendant sequences. Individuals containing many deleterious characters leave few or no descendants because these individuals are quickly eliminated by selection. Hence, such a model lends itself to the study of deleterious selection. It is possible to determine if selection is required by searching for any set of mutation rates that can explain an observed set of data. Simulations of artificial populations without selection suggest that this method seldom indicates selection when none is present. Furthermore, recent recombination events between the sequences do not induce false indications of deleterious selection. The method may, however, require relatively large simple sizes in order to accurately reflect the true nature of populations. The method is often very conservative and may not indicate selection when it is, in fact, present.