The importance of atherosclerosis in public health has generated a vast literature relating to epidemiology of the disease, clinical descriptions of symptoms and records of variation of serum concentration of cholesterol, triglyceride or lipo-protein fractions in normal or affected persons. Such evidence has led to a number of hypotheses as to the origins of the disease, and although rival theories may be espoused with fervour or may fluctuate in popularity, a familial predisposition to coronary disease is a recurring theme. In this brief review, which does not aim to be exhaustive and is not concerned with hypertension, we shall focus attention on the more important aspects and attempt to set the conflicting evidence in perspective.

Two hundred and two house mice (Mus musculus L.) from 29 populations in Europe and North Africa were typed for 16 H-2K and 17 H-2D antigens, each antigen defining a different allele. Among the 13 best characterized populations, 1 to 4 common and 3 to 20 rare antigens were observed. However, an average of 37% of the H-2K and 39% of the H-2D antigens remain to be identified. Ninety-four percent of the 50 mice tested were heterozygous for H-2K antigens and 89% for H-2D antigens. In 4 of the 8 populations tested, the most common H-2K and H-2D antigens occurred in the same individual more often than if randomly associated. Associations between common H-2K and H-2D antigens and excess heterozygosities may be the consequence of the small size and instability of populations composed primarily of related individuals. Estimates of the genetic distances between populations revealed that Danish, Egyptian, and several of the Orkney Island populations were related. These were the only populations in which metacentric chromosomes were not found. In contrast, populations which were antigenically different were also karyotypically different, regardless of taxonomic status of allozymic similarity.

Robertson, 1978, addressed the interesting problem of ascertaining the distribution of the time to detection of a recessive homozygote in a finite population. He was motivated in part by breeding and artificial selection practices. The same problem arises in the context of evolutionary processes and medical genetics since it refers to the time of first appearance as a homozygote of a new crossover event or a mutant gene.

Retarded development of females (Symbol: Rf) has arisen spontaneously as a new trait in a chromosome mutant strain, which has an autosome fused to the original W chromosome. Female imagines with this trait emerge 1–3 weeks later than the males, due to retarded larval development. The proportion of female imagines is low. Rf is maternally inherited, it is neither expressed in nor transmitted through males. The evidence suggests that it is a dominant or epistatic factor on the autosomal part of the W chromosome-autosome fusion.

Linkage data and revised maps for 52 autosomal loci in L. cuprina are presented. Examination of the linkage relationships of biochemically and morphologically similar mutations in L. cuprina, Musca domestica L. and Drosophila melanogaster (Mg) suggests that the major linkage groups have survived largely intact during the evolution of the higher Diptera.

The model of Lyon & Mason (1977) which defines three subregions of the t complex (T, tail-determining; A, abnormal transmission ratio; L, lethal) has been extended in an interpretation of male fertility data obtained from the combination of TOrl with different t haplotypes. The results demonstrate: (1) the T region of most t haplotypes (t12, t0, tw18 and tw2) possess gene(s) that interact with the L region to give quasisterility; (2) the T region of t6 lacks the allele(s) that result in quasisterility; and (3) the T region interacts with the A region to modify the transmission ratios of t haplotypes. The results were discussed in terms of an interacting genetic system controlling male fertility.

In order to assess the relationship between genetic and environmental variability, a large natural population of Drosophila melanogaster was replicated as eight subpopulations, which were subjected to four different patterns of environmental variation. The environmental variable imposed was presence of 15% ethanol in the culture medium. Experimental treatments of the populations were intended to simulate constant environmental conditions, spatial heterogeneity in the environment, and two patterns of temporal environmental variation with different periodicity (long- and short-term temporal variation). Additive genetic and phenotypic variation in sternopleural and abdominal chaeta number, and body weight, were estimated in two successive years, and measurements were taken of the genotype–environment correlation of body weight and sternopleural bristle score with medium type.

Additive genetic variance of sternopleural chaeta number and of body weight was significantly greater in the three populations experiencing environmental heterogeneity than in the control population, but additive genetic variance of abdominal bristle score was not clearly affected by exposing populations to varying environments. Temporal environmental variation was equally, if not more, efficient in promoting the maintenance of genetic variation than spatial heterogeneity, but the cycle length of the temporal variation was of no consequence. Specific genotype–environment interactions were not present, therefore adaptation to heterogeneous environments is by selection of heterozygosity per se, rather than by differential survival of genotypes in the alternate niches.

A spontaneous autosomal mutation in C57BL/Tb mice, provisionally called reduced pigmentation, symbol rp, has pronounced effects on three kidney lysosomal glycosidase activities. Homozygous rprp mice have significantly higher activities of β-galactosidase, β-glucuronidase and N-acetyl-β-hexosaminidase than their heterozygous litter-mates. Homozygotes have light ears and tails, diluted fur and dark eyes. The mutation is not allelic to any known to affect lysosomal functions, or to a number of pigmentation variants with similar phenotypic effects. The locus is on chromosome 7.

Michie's hypothesis of ‘affinity’ is invoked to explain how fertility might theoretically be achieved in a female mule or hinny. Chromosomally balanced haploid gametes could be produced in these inter-specific hybrids by movement of centromeres of similar ancestry to opposite poles at anaphase I of meiosis. Male hybrids could probably never be fertile on account of the low numbers of spermatozoa produced; females, on the other hand, might occasionally achieve fertility by the ovulation of a chromosomally balanced egg.

The title of the paper by Bailey et al. (Genetical Research 36, 167–180, 1980) should read:

‘A third gene affecting GABA transaminase levels in Aspergillus nidulans’