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.

A study of α-amylase isozyme patterns from gibberellin-induced endosperms of wheat-alien genotypes (amphiploid, addition and substitution lines) resolved by flat-bed isoelectric focusing identified homoeoloci for α-Amy-1 (malt α-AMY-1 genes) on chromosomes 6H of Hordeum vulgare, 6RL of Secale cereale, 6Rm of S. montanum and 6E of Agropyron elongatum. Homoeoloci for α-Amy-2 (green α-AMY-2 genes) were identified on chromosomes 7HchL of Hordeum chilense, 7RL of Secale cereale, 7Sb of Aegilops bicornis, 7U of Ae. umbellulata and 7EL of Agropyron elongatum. Analysis of mature grain β-amylase identified β-Amy-1 loci on chromosomes 4H of H. vulgare, 4Hch of H. chilense, 4S1 of Ae. sharonensis and Ae. longissima and β-Amy-2 loci on chromosomes 5RL of S. cereale and 5U of Ae. umbellulata. These gene locations provide further evidence for the homoeology of the alien chromosomes with wheat and for the conservation of gene synteny among wheat and its relatives.

The selective advantage of sexual reproduction is widely regarded as a major unsolved problem in biology. Recently, it has been proposed that the fundamental selective advantage of sex is its promotion of recombinational repair and hence survival of DNA in the germ line of organisms. A bacteriophage T4 system was set up to test this theory. After a phage T4 injects its DNA into an Escherichia coli cell it quickly establishes a barrier, through its immunity function, to infection by a second phage T4, arriving at a later time. This barrier causes phage T4 to reproduce asexually. The immunity barrier has a selective advantage in preserving the host cell as a sole resource for the first phage. If the first phage's DNA is damaged by UV irradiation, however, it has a reduced probability of being able to survive in the host cell when it is there alone. It was found that UV irradiation, in addition to reducing the first phage's viability, also prevents the first phage from raising an effective immunity barrier. This UV-induced reduction in immunity now allows sexual interaction with later-arriving secondary phage or sexual reproduction. It was found that these secondary phage enhanced survival of genes of the UV-damaged first phage. This supports the theory that under DNA-damaging conditions, which should be prevalent in nature, sex would have a selective advantage.

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.

Cold-resistant revertants of the cold-sensitive, ribosomal suppressor suaC109 have been isolated, with a view to obtaining mutations in new ribosomal protein genes. Many revertants had reduced suppressor activity and were classified as antisuppressor mutants. Both intragenic and extragenic reversions were found. In seven strains the extragenic reversion to cold resistance segregated with the antisuppressor phenotype, and these were designated asu mutations. Three of the five asu genes, C, B and D were mapped to linkage groups, I, II and V respectively. The antisuppressors are not gene-specific, although they mainly antagonize the activity of ribosomal suppressors. The antisuppressors altered all aspects of the phenotype of suppressor suaC109 including sensitivity to aminoglycoside antibiotics, and are therefore thought to be mutations in ribosomal protein genes.

Wild-type Caenorhabditis elegans fails to reach adulthood if L1 larvae are incubated in the presence of 30 mM or greater concentrations of caffeine. Eleven mutants have been isolated in which caffeine has a less pronounced effect on development. The mutations are recessive, define two genes, and have been mapped. The mechanism(s) of resistance is unknown.

The inheritance of alleles at ten enzyme loci of Stagnicola elodes (Lymnaeidae) was analysed by laboratory crosses. Alleles for alanine aminopeptidase (2 alleles), leucine aminopeptidase (2 alleles), aspartate aminotransferase (2 alleles), β-hydroxybutyrate dehydrogenase-1 (4 alleles), 6-phosphogluconate dehydrogenase (2 alleles), esterase-2 (2 alleles), esterase-3 (2 alleles), esterase-7 (2 alleles), esterase-13 (2 alleles) and esterase-18 (2 alleles) segregate in the F2 generation according to Mendelian expectations. Contingency X2 tests for linkage done on F2 progeny from crosses between strains homozygous for alternate alleles at two loci showed that β-hydroxybutyrate dehydrogenase-1, esterase-13 and esterase-18 are presumably linked.

The glue proteins are products of a developmentally regulated gene family. These genes are transcriptionally active during the third larval instar and code for the major protein products of salivary glands. The activity of several of the genes can be visualized as intermoult puffs in the polytene salivary gland chromosomes. The amount of one of these proteins, P5, varies widely among wild-type strains. We have used biochemical and genetic methods to investigate the source of this variation. The results of in vitro translation of salivary gland RNA suggest that the variation occurs pretranslationally. Genetic mapping experiments showed that sites on several chromosomes can modulate the amount of P5, but that one site on the third chromosome determines the absence and presence of this protein. We have mapped this glue protein gene, called GP5, to the interval between bx (3–58·8) and sr (3–62·0) which also includes the intermoult puff at 90BC. We discuss the relationship between P5 and the glue protein gene Sgs-5 which is also located at 90BC.

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.

In order to increase our understanding of the evolutionary dynamics of transposable genetic elements we have studied the chromosal location of copies of 2 element families in 20 X chromosomes extracted from a natural population of Drosophila melanogaster from Spain. The I element was localized at a total of 64 chromosomal sites and copia at 45 sites in this sample with a mean copy number of 3·2 and 2·3 elements/chromosome respectively. Both elements were highly variable in location, with no site reaching a higher frequency than 4/20 in either case. Comparisons with other data sets suggest that insertion frequencies can be used to detect population structuring.

In this paper we describe the use of a free duplication, sDp2 (I;f), for the recovery, maintenance, and analysis of mutations defining essential genes in the left third of Linkage Group I of Caenorhabditis elegans. The lethals were induced in a strain of genotype (sDp2) + /dpy-5 + unc-13/ dpy-5 unc-15 +, using either 12 mM ethylmethane sulphonate or 1500 r of gamma radiation. Lethal mutations linked to the dpy-5 unc-13 chromosome were recognized by the absence of Dpy-5 Unc-13 individuals amongst the self progeny and were maintained by isolating Unc-13 hermaphrodites. These strains – which have two mutant alleles of the essential gene and a wild-type allele on the duplication – are balanced, since crossing-over does not occur between sDp2 and the normal homologues. Using this sytem we have recovered 58 EMS-induced mutations. These have been characterized with regard to map position and complementation. Twenty-nine of the EMS-induced mutations lie to the left of dpy-5 and define 20 complementation groups; 3 were inseparable from dpy-5 and define 3 complementation groups; 21 were to the right and define 17 complementation groups. Among a set of 29 gamma radiation-induced lethal mutations, 17 appear to be single gene mutations or are very small deletions. We estimate that we have identified from one-sixth to one-half of the essential genes in the sDp2 region.

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 ability of restricted selection indices to prevent genetic change in a restricted trait over several generations of selection was studied using deterministic computer models. Four loci, two affecting each trait independently, and two pleiotropic loci, one affecting each trait in the same direction, and one with opposite effects, were modelled. In general, continued effectiveness of the restriction was achieved only when the restricted trait was affected by only one locus. In some conditions (equal gene frequencies), an independent locus and one pleiotropic locus affecting the restricted trait allowed maintenance of the restriction. The results suggest that long-term restriction may be very difficult without re-estimation of parameters.

Two separate, but interacting, genetic systems underlie the variation in seasonal cycles among members of the Chrysoperla carnea species-complex. The two systems are expressed as all-or-none reproductive responses to photoperiod and prey (i.e. short-day/long-day requirement for reproduction versus long-day reproduction and prey requirement for reproduction versus reproduction without prey). In each case the alternative to reproduction is reproductive diapause. The photoperiodic responses are determined by alleles at two unlinked autosomal loci. The expression of dominance by the alleles at these loci varies among geographical populations. The genes that determine the photoperiodic responses also act as suppressors of the genes that govern responsiveness to prey. An autosomal, polygenic system, with a threshold for the expression of diapause, determines responsiveness to prey. The two genetic systems are important to seasonal diversification and speciation within the C. carnea species-complex.

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.

The accumulation of beneficial and harmful mutations in a genome is studied by using analytical methods as well as computer simulation for different modes of reproduction. The modes of reproduction examined are biparental (bisexual, hermaphroditic), uniparental (selfing, automictic, asexual) and mixed (partial selfing, mixture of hermaphroditism and parthenogenesis). It is shown that the rates of accumulation of both beneficial and harmful mutations with weak selection depend on the within-population variance of the number of mutant genes per genome. Analytical formulae for this variance are derived for neutral mutant genes for hermaphroditic, selfing and asexual populations; the neutral variance is largest in a selfing population and smallest in an asexual population. Directional selection reduces the population variance in most cases, whereas recombination partially restores the reduced variance. Therefore, biparental organisms accumulate beneficial mutations at the highest rate and harmful mutations at the lowest rate. Selfing organisms are intermediate between biparental and asexual organisms. Even a limited amount of outcrossing in largely selfing and parthenogenetic organisms markedly affects the accumulation rates. The accumulation of mutations is likely to affect the mean population fitness only in long-term evolution.

P-element mutagenesis was used to contaminate M-strain second chromosomes with P elements. The effect of P-element transposition on abdominal and sternopleural bristle scores and on female productivity was deduced by comparing the distributions of these quantitative traits among the contaminated second-chromosome lines with a control population of M-strain second-chromosome lines free of P elements. Estimates of P-element-induced mutational variance, Vm, for these characters are very high, and mutational ‘heritabilities’ (Vm/Ve, the ratio of mutational variance to environmental variance) are of the same order as heritabilities of these traits from natural populations. P-element-induced mutational variance of abdominal bristle score is roughly two orders of magnitude greater than spontaneous and X-ray-induced Vm/Ve for this trait.

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.

Classical population genetic models show that disruptive selection in a spatially variable environment can maintain genetic variation. We present quantitative genetic models for the effects of disruptive selection between environments on the genetic covariance structure of a polygenic trait. Our models suggest that disruptive selection usually does not alter the equilibrium genetic variance, although transient changes are predicted. We view a quantitative character as a set of character states, each expressed in one environment. The genetic correlation between character states expressed in different environments strongly affects the evolution of the genetic variability. (1) If the genetic correlation between character states is not ± 1, then the mean phenotype expressed in each environment will eventually attain the optimum value for that environment; this is the evolution of phenotypic plasticity (Via & Lande, 1985). At the joint phenotypic optimum, there is no disruptive selection between environments and thus no increase in the equilibrium genetic variability over that maintained by a balance between mutation and stabilizing selection within each environment. (2) If, however, the genetic correlation between character states is ± 1, the mean phenotype will not evolve to the joint phenotypic optimum and a persistent force of disruptive selection between environments will increase the equilibrium genetic variance. (3) Numerical analyses of the dynamic equations indicate that the mean phenotype can usually be perturbed several phenotypic standard deviations from the optimum without producing transient changes of more than a few per cent in the genetic variances or correlations. It may thus be reasonable to assume a roughly constant covariance structure during phenotypic evolution unless genetic correlations among character states are extremely high or populations are frequently perturbed. (4) Transient changes in the genetic correlations between character states resulting from disruptive selection act to constrain the evolution of the mean phenotype rather than to facilitate it.

Animal models which emulate defects similar to those in man are required for medical research. Many investigations on the cellular, developmental and molecular aspects of cataractogenesis use the cataract Fraser (CatFr) mouse. This report shows that the CatFT and Lop lens abnormalities are linked, and are probably allelic genes on chromosome 10. It also shows that the CatFT gene is maintained on an inbred genetic background which differs from 79 other strains; it is proposed that this strain be named CAT.