McLaren & Monk (1982) and Cattanach et al. (1982) reported that T(X; 16)16H/X Sxr mice, in which the X chromosome bearing Sxr is the inactivated X chromosome, can develop as fertile females. By mating such females to X/Y Sxr males it has been possible to produce mice homozygous for Sxr. Two X Sxr / Y Sxr males were identified which together fathered 141 sons and 1 daughter. The single daughter proved to be XO, indicating a non-disjunctional event with neither paternal sex chromosome being transmitted. It is concluded that X Sxr / Y Sxr mice are viable and fertile, and that all their progeny, provided they receive a paternal sex chromosome, develop as males.

Populations of the slug Arion ater rufus sampled from several localities in England and the Netherlands are polymorphic for different electro-phoretic variants of digestive-gland esterase and salivary-gland tetra-zolium oxidase. Samples of Arion ater ater, which is endemic to the British Isles, were found to be monomorphic for these enzymes. Localized populations of A. a. rufus in Britain could have originated from specimens imported accidentally from continental Europe. There is evidence for gene flow between overlapping populations of the two subspecies. In one of the English populations of A. a. rufus, studied in detail, polymorphism for esterase and tetrazolium oxidase is shown to be balanced. Heterosis may be an important factor contributing to the maintenance of balanced polymorphism for tetrazolium oxidase in this population.

Segregation-distorting t-sperm show a specific increase in N-acetylglucosamine: galactosyltransferase activity over wild-type (+/+) due to a deficiency of a wild-type galactosyltransferase inhibitor (Shur & Bennett, 1979). Eight other enzymic activities are indistinguishable between +- and t-sperm suspensions. In this study, three additional points are analysed. First, galactosyltransferases are assayed on sperm homozygous for a semilethal haplotype (tW2/tW2), relative to heterozygous (+ /tw2) and wild-type (+/+) controls. tW2/tW2 assays circumvent the +-sperm inhibition of t-sperm galactosyltransferases that occurs in heterozygous + /t-assays and show that t-sperm are actually four times as active as wild-type. Second, sperm which are compound heterozygotes for two complementing lethal t-haplotypes (tlx/tly), have nearly twice the theoretical enzyme level of tlx/tly sperm. Thus, in either homozygous (tW2/tW2) or double heterozygous (tlx/tly) form t-haplotypes act synergistically on sperm galactosyltransferase activity.

Third, and most interesting, sperm bearing either recombinant, viable t-haplotypes (+/tv, tvx/tvy), or one of three dominant T/t-complex mutations, were assayed to determine which portions of the T/t-complex are responsible for elevated galactosyltransferase activity. Results show that sperm bearing recombinant, non-segregation-distorting, viable tv-haplotypes no longer show elevated transferase activity. Therefore, the elevated t1-sperm galactosyltransferase activity strictly correlates with the increased transmission frequency of t1-sperm. These studies strengthen further the hypothesis that sperm surface galactosyltransferases are involved in egg binding during fertilization, and that t1-sperm segregation-distortion results, at least in part, from increased galactosyltransferase activity.

A mouse antigen, MuB1, has been shown by the study of backcrosses to be inherited in a unifactorial dominant manner. Its inheritance is not linked with gamma globulin allotypes, but has been shown to be linked with the presence of the haemolytic complement system. The concentration of MuB1 in the serum of several inbred strains of mice showed sex-associated differences; however, the presence of MuBl did not depend on the sex of the parents or on the sex of the offspring. The inheritance of antibody responsiveness is discussed in terms of the inheritance of the antigen, MuB1.

Females from different wild-type laboratory populations of Drosophila melanogaster differ genotypically in their degree of mating discrimination against mutant yellow males. The chromosomal organization of this difference was examined in two wild-type laboratory strains by experimental observation of the mating propensities of hybrid females in a mass-mating, multiple choice situation. The results indicate that the strain difference is polygenic in origin, involving loci on both the X-chromosome and autosomes. Reciprocal crosses revealed no maternal/cytoplasmic effects. The mating scores of parental, F1 and backcross females fit well to a model of additive chromosomal effects, with X-linked loci being recessive, and autosomal loci overdominant, for increased mating with yellow males. However, interactions, arising most probably from recombination, led to increased mating with yellow on the part of F2 females. In addition to the difference in female discrimination against yellow males, male/female interaction was found for the mating speed of flies from the two strains. These results are discussed in the light of previous studies of mating preferences in D. melanogaster. It is suggested that genetic variation in female mating preferences may be an important source of variation in the reported mating success of mutant yellow males.

We have developed molecular markers that distinguish between several inbred and congenic mouse strains using polymerase chain reaction (PCR) amplification of genomic DNA repeat sequences. Mouse genomic DNA, digested with four base recognition site-restriction endonucleases, was amplified by PCR using primers for the following repeat sequences: Bl (Alu homolog), LINE, LLR3, IAP, human Alu and myoglobin. Amplification products analysed by agarose gel electrophoresis and stained with ethidium bromide produced unique DNA fragments, some of which are specific for each of 12 strains tested. This method can be used for molecular analysis of the mouse genome, including genetic monitoring.

We have investigated the interchromosomal effect of the naturally-occurring paracentric inversions In(2L)t and In(3R)P on meiotic recombination in two regions of the X chromosome in Drosophila melanogaster. Previous authors have suggested that the rate of recombination at the tip of the X chromosome may be substantially higher in some natural populations than values measured in the laboratory, due to the interchromosomal effect of heterozygous autosomal inversions. This suggestion was motivated by observations that transposable elements are not as common at the tip of the X chromosome as predicted by recent research relating reduced meiotic exchange to increased element abundance in D. melanogaster. We examined the effects of heterozygous In(2L)t and In(3R)P on recombination at both the tip and base of the X chromosome on a background of isogenic major chromosomes from a natural population. Both inversions substantially increased the rate of recombination at the base; neither one affected recombination at the tip. The results suggest that the presence of inversions in the study population does not elevate rates of crossing over at the tip of the X chromosome. The relevance of these results to ideas relating transposable element abundance to recombination rates is discussed.

The maintenance of polygenic variability by a balance between mutation and stabilizing selection has been analysed using two approximations: the ‘Gaussian’ and the ‘house of cards’. These lead to qualitatively different relationships between the equilibrium genetic variance and the parameters describing selection and mutation. Here we generalize these approximations to describe the dynamics of genetic means and variances under arbitrary patterns of selection and mutation. We incorporate genetic drift into the same mathematical framework.

The effects of frequency-independent selection and genetic drift can be determined from the gradient of log mean fitness and a covariance matrix that depends on genotype frequencies. These equations describe an ‘adaptive landscape’, with a natural metric of genetic distance set by the covariance matrix. From this representation we can change coordinates to derive equations describing the dynamics of an additive polygenic character in terms of the moments (means, variances, …) of allelic effects at individual loci. Only under certain simplifying conditions, such as those derived from the Gaussian and house-of-cards approximations, do these general recursions lead to tractable equations for the first few phenotypic moments. The alternative approximations differ in the constraints they impose on the distributions of allelic effects at individual loci. The Gaussian-based prediction that evolution of the phenotypic mean does not change the genetic variance is shown to be a consequence of the assumption that the allelic distributions are never skewed. We present both analytical and numerical results delimiting the parameter values consistent with our approximations.

Pawns are behavioural mutants which show impairment in membrane excitability and are, therefore, devoid of normal avoiding reactions. We obtained 103 lines of Pawns through mutagenesis and screening. Among those that yielded to breeding studies, 59 lines belonged to the pwA complementation group and 38 lines belonged to the pwB group. No other genic loci were found in this extensive analysis. Mutants of the pwA locus showed various degrees of phenotypic leakiness. Based on the pheno- and genotypic differences, we estimated that at least 45 independent mutational events were represented in these 103 Pawn lines.

Four inbred strains of mice were used, differing in the total percentages of spermatozoa with abnormal heads (KE, 22·1%; C57, 26·4%; KP, 7·7%; CBA, 5·5%) and in the frequency distribution of abnormality types, as divided into four arbitrary classes. The most variable class 2 (narrow heads with canals inside the nuclear material) accounted for 47% of all abnormalities in KE strain, was common in CBA (29%) and almost missing in KP and C57 strains. F1 hybrids from the diallel crosses of these strains exhibited highly significant heterosis effects and significant reciprocal differences in the total percentage of abnormalities. The relative frequency of class 2 ranked in F1 hybrids in a similar order as calculated from the mid-parental values. After seven generations of backcrosses performed to introduce the Y chromosome from CBA to the genetical background of the KE strain, the total percentage of abnormalities was significantly reduced, although the relative proportion of class 2 was similar to that in KE strain. Also the Y chromosome from C57 strain, introduced into the genetical background of KE strain, caused a significant reduction of total abnormalities, but again the relative frequency of class 2 was not affected. It is concluded that the Y chromosome plays an important role in determining the total percentage of sperm head abnormalities, but does not seem to be involved in influencing specific abnormality types.

The phenomenon of X-chromosome inactivation in female mammals, whereby one of the two X chromosome present in each cell of the female embryo is inactivated early in development, was first described by Mary Lyon in 1961. Nearly 30 years later, the mechanism of X-chromosome inactivation remains unknown. Strong evidence has accumulated over the years, however, for the involvement of a major switch or inactivation centre on the mouse X chromosome. Identification of the inactivation centre at the molecular level would be an important step in understanding the mechanism of X-inactivation. In this paper we review the evidence for the existence and location of the X-inactivation centre on the mouse X-chromosome, present data on the molecular genetic mapping of this region, and describe ongoing strategies we are using to attempt to identify the inactivation centre at the molecular level.

An Arg− conditionally streptomycin (Sm)-dependent strain of E. coli B that carries an R factor mediating Sm adenylation cannot grow on minimal agar containing 20 μg Sm/ml unless the strain either becomes Arg+ or loses the ability to adenylate Sm (Harwood & Smith, 1969b). We have therefore studied the efficacy of this selection with respect to enriching for SmS mutants of such R factors. Following u.v. mutagenesis, cells were plated on the selective medium; of the clones which were examined, Arg− R-SmS colonies were found up to 3000 times more frequently than Arg+ R-SmR colonies.

Three new autosomal mutants of the milkweed bug, Oncopeltus, obtained by treatment with ethylmethane sulphonate, are described and compared with the two other previously known variants. Preliminary data are given on the results of testcrosses and of chromatographic analysis of some pteridene pigments.