Using the Ewens sampling distribution of selectively neutral alleles in a finite population, it is possible to develop an exact test of neutrality by finding the probability of each configuration with the same sample size and observed number of allelic classes. The exact test provides the probability of obtaining a configuration with the same or smaller probability as the observed configuration under the null hypothesis. The results from the exact test may be quite different from those from the Ewens—Watterson test based on the homozygosity in the sample. The advantages and disadvantages of using an exact test in this and other population genetic contexts are discussed.

Genet. Res., Camb. (1982), 39, pp. 157–168

The relationship between heterochromatic homology and meiotic segregation of compound second autosomes during spermatogenesis in Drosophila melanogaster

By Arthur J. Hilliker, David G. Holm and R. Appels

Several errors occurred in the headings of Table 4, on p. 162: the table should read as follows:

Two triplications induced in a normal halpoid chromosome complement by TEM (Tr-I) and by mustard gas (Tr-II) are described. Two models which may lead by successive steps to the formation of a triplication are suggested. The induction of two latent breaks is essential in both of them. The origin of repeats in general is discussed. It is concluded that chromosome breaks rather than non-homologous crossing-over constitute the major source of repeats.

Genetic analysis of hybrids between Drosophila simulans and D. sechellia shows that sexual isolation in females is caused by at least two genes, one on each major autosome, while the X chromosome has no effect. These results are similar to those of a previous study of hybrids between D. simulans and another sibling species, D. mauritiana. In this latter hybridization, each arm of the second chromosome carries genes causing sexual isolation in females, implying a total divergence of at least three loci. The genetic similarity between the D. simulans/D. mauritiana and D. simulans/D. sechellia hybridizations probably results from independent evolution and not phylogenetic artifacts, because the dominance relationships and behavioural interactions differ between the two hybridizations. The lack of an X-chromosome effect on sexual isolation contrasts with genetic studies of post-zygotic reproductive isolation, which invariably show strong effects of this chromosome.

Quantitative variation in traits that change with age is important to both evolutionary biologists and breeders. We present three new methods for estimating the phenotypic and additive genetic covariance functions of a trait that changes with age, and illustrate them using data on daily lactation records from British Holstein—Friesian dairy cattle. First, a new technique is developed to fit a continuous covariance function to a covariance matrix. Secondly, this technique is used to estimate and correct for a bias that inflates estimates of phenotypic variances. Thirdly, we offer a numerical method for estimating the eigenvalues and eigenfunctions of covariance functions. Although the algorithms are moderately complex, they have been implemented in a software package that is made freely available.

Analysis of lactation shows the advantages of the new methods over earlier ones. Results suggest that phenotypic variances are inflated by as much as 39 % above the underlying covariance structure by measurement error and short term environmental effects. Analysis of additive genetic variation indicates that about 90 % of the additive genetic variation for lactation during the first 10 months is associated with an eigenfunction that corresponds to increased (or decreased) production at all ages. Genetic tradeoffs between early and late milk yield are seen in the second eigenfunction, but it accounts for less than 8 % of the additive variance. This illustrates that selection is expected to increase production throughout lactation.

The probability of fixation of a mutant gene in a finite population was investigated by taking into account the effect of random fluctuation of selection intensity. It was shown that not only the product of the effective population number and average selection coefficient (Nes) is important, but also the ratio of the mean and the variance of selection coefficient (s/ Vs) has an important influence on fixation probability. In particular, when this ratio is small, a mutant gene, even if selected against, becomes fixed in the population like a selectively neutral mutant. In general, when random fluctuation of selection intensity is not negligible it may be convenient to use ‘effective selection coefficient’. The bearing of the present findings on the neutral mutation-random drift theory of evolution and variation at the molecular level was discussed.

In this study, five separate alleles at the agouti locus in house mice were tested for potential effects on a battery of 13 minor skeletal variants. Six genotypes (aa, ata, atat, Aa, Avya, and Aya) were compared on a standard congenic background (C57BL/6). In log-linear analyses, three of the 13 characters showed significant genotype differences (another three were close to significance), and genotypes also exhibited overall significance in a multivariate randomization test. Both multidimensional scaling and clustering showed an association of aa with ata, Aa with Avya and Aya, and a general separation of atat from the other genotypes. Genotype differences averaged 0·63 in probit standard deviations, 0·09 when assessed by the mean measure of divergence. Since the general magnitude of effects of these major genes was quite similar to those previously estimated for presumptive polygenes from subline divergence studies, it was concluded that major genes may often act as polygenes and make important contributions to the variation in minor skeletal variants.

The short-term response to artificial selection in a wild-type population for increased scutellar bristle number, has been interpreted in terms of two alternative threshold models. Both models have been shown to give a satisfactory transformation of the scale of measurement, in that the underlying variable shows an effectively linear response in terms of the accumulated selection differential, and the pheno-typic variance on the underlying scale remains virtually unchanged over a period of generations sufficient to increase the incidence of extra-bristles to almost 100%.

A genetic analysis based on the bivariate model, which to a large extent takes account of the location of the supernumerary bristles, has shown the phenotypic variance on the underlying scale to have the following composition: the additive genetic variance is 27·2 ± 0·9% of the total, and the developmental error or ‘chance’ variance accounts for a further 63·8 ± 2·6%, so that the remaining 9·0 ± 2·7% of the variance must be due to environmental differences among individuals and to non-additive genetic effects.

The relative magnitudes of these parameters are remarkably similar to those observed for two quasi-continuous variables in the same population, viz. abdominal and sternopleural hair number. In view of the ease with which scutellar bristles may be scored, the character can therefore serve as an extremely useful model character for quantitative genetic experiments.

Thymineless strains of Escherichia coli C600 were constructred harbouring both an R factor of the N incompatibility group (R46 or R447b) and a compatible plasmid (Plac- of the A-C group or the Iα plasmid R62), which contained a segment of N group DNA. Selection was made for the transferred plasmid and dislodgement phenomena were manifest either as loss of an entire plasmid or as deletions of a region of plasmid DNA. Even after the two R factors had become established as separate replicons, the N group R factor but not the other plasmid exhibited instability.

Thymine starvation of strain C600 thy (R447b/R62) increased the elimination rate of the N group plasmid R447b but no elimination of R62 was observed. However, thymine starvation of strain C600 thy (R46/Plac-) not only increased the rate of elimination of R46 but also increased the rate of loss of Plac-. There was no detectable increase in nuclease activity in unstarved R46/Plac- strains and it is concluded that dislodgement of R46 from these strains is not due to induction of the nuclease that has been proposed to be responsible for the elimination of N group plasmids during thymine starvation.

Two variants of Plac- were isolated. These did not dislodge R46 from unstarved R46/Plac- strains and were not lost during thymine starvation even though thymineless elimination of R46 occurred at normal frequency.

The number of children produced by a modern woman is usually below her total reproductive capacity and is determined by circumstances other than natural selection. It is, therefore, practically impossible to detect differences in natural fertilities associated with different types (e.g. phenotypes, genotypes) of women. This does not mean, however, that natural selection at the reproductive level cannot at all be detected today. If women of a particular type have high natural fertility, this usually means that they reproduce (become pregnant) at a higher rate than women of a type with lower natural fertility. Hence, when there is a limit on the number of children, women of the first type will reach the limit at an earlier age than women of the second type. As a result, types that have a higher natural fertility should be overrepresented among pregnant women of younger ages and, consequently, underrepresented among older ones, as compared to types with a lower natural fertility. Based on this notion, a model of age-related differences between distributions of types among pregnant women is suggested. The model is applied to data on MNSs-blood group and PGM1 (phosphoglucomutase) types in a sample of pregnant women and an evidence of natural selection at the reproduction level associated with these genetic markers is obtained.

Using polarography the uptake of oxygen by intact and homogenized mycelium of a wild-type strain and strains of slow-growing non-perithecial (sgp) mutants was compared. It was found that whilst the oxygen uptake of intact, wild-type mycelium increased on the addition of glucose or succinate as substrate, uptake of oxygen by mutant mycelium increased only when glucose was used as substrate and was unaffected by succinate. When, however, homogenates of mutant mycelium were used oxidation of the succinate occurred. It was concluded that the inability of the mutants to utilize succinate was due to their impaired ability to take up the compound across the hyphal wall and this was confirmed using radioactively labelled substrates. It is tentatively suggested that the abnormal growth of the sgp mutants on glucose medium and their impaired permeability to tricarboxylic acid cycle intermediates may be due to reduced availability of high energy compounds caused by a lesion in their oxidative phos-phorylation system.

A cross of a leopard frog heterozygous for the dominant Burnsi gene (B/ +) with a wild-type (+ / +) resulted in a large excess of B/ + progeny. Two descendent lines established by these B/ + progeny are characterized by excess +/ + progeny. These seemingly contradictory data are reconciled by postulating the existence of a dominant subvital gene (Sbv) linked to the + allele of Burnsi in the initial cross. Progeny used to establish subsequent lines were recombinants with Sbv linked to B. This proposed linkage would constitute the first case of linkage between two mutant loci in anuran amphibians.

The model, suggested by Ohta & Kimura, of an infinite number of selectively neutral alleles, in which alleles can only mutate to neighbouring alleles, has been extended to include a migratory pattern. The stepping-stone and island models of migration have been considered. In the latter case, it has been found that as the number of colonies becomes large, the expected number of alleles, ne, becomes approximately equal to

where m is the migration rate, v is the mutation rate and Ne is the effective size of each population. This solution tends to that of Ohta & Kimura as m → 0 but one can see that for any appreciable value of Nem, a large increase in ne is obtained. In order to check the validity of iterative results, models with a finite number of alleles have been considered, and their solutions have been found to converge quickly to those of the infinite case. The results exemplify the great power of migratory structure and neutral alleles to maintain a large amount of heterozygosity. Double step mutation and the finite time solution have also been considered.

Selective differences among male Drosophila melanogaster due to differences in ability to compete for mates may often have been under-estimated in the past because, under the test procedure used, females did not represent a limited resource. In the experiment reported here, no difference was detected between inbred and outbred males ‘competing’ to mate with an equal number of females. When the receptive female: male ratio was halved a large reduction in male mating ability due to inbreeding became apparent.

The properties of the t haplotypes, specific mutant states of the proximal region of chromosomes 17 in the house mouse, are of continuing interest. One such property is increased transmission of the t haplotype by heterozygous t/ + males to offspring. Using the reciprocal translocation T(16; 17)43H we have constructed males with tertiary trisomy of chromosome 17 (+ T43/+ +/Rb7 + ) carrying the Robertsonian translocation Rb(16.17)7Bnr. Only the progeny of these males which had inherited either T43/ + or Rb7 from their male parent were viable. The segregation patterns in the offspring of t-bearing trisomics were analysed on days 16–18 of embryonic development. It was found that, when the t12 haplotype is in the normal acrocentric (♂♂ + + T43/ + t12 + /Rb7 + +), its presence in the gamete + t12 + / + + T43 does not produce meiotic drive. However, when t6 is in Rb7, meiotic drive was observed: 80% of offspring carried the t haplotype. It is concluded that the meiotic drive is probably inhibited by the presence of a normal homologue of chromosome 17 in the same sperm. Possible mechanisms for the t haplotype effect are discussed.