An amber mutation was created in the CAT gene of plasmid vector pACYC184 and this modified plasmid was fused with the Streptomyces vector pIJ702 for use as an indicator for the identification of Streptomyces strains carrying nonsense suppressor tRNA mutations. The resulting hybrid plasmid pGM1109 was introduced into the chloramphenicol-sensitive mutant M252 of Streptomyces lividans. Chloramphenicol-resistant colonies were isolated and characterized. None of them was a nonsense suppressor mutant. The failure to obtain such mutants is discussed on the basis of codon usage in streptomycetes.

The DNA structures around the G6PD coding region in three high-G6PD activity mutants and their low-activity revertants of Drosophila melanogaster were analysed by Southern blot using a cloned G6PD gene as a probe. As a result, two kinds of insertion sequences were found; one was present just 5′ to exon I (Ins1), and the other within the intron (Ins2). The Ins1 sequence was 3·5 Kb in two mutants and 2·9 Kb in one mutant. In both cases, it consisted of a core sequence either 1·2 or 0·6 Kb long flanked by terminal repeats. On the other hand, low-activity revertants possessed either a defective Ins1 or no Ins1. The Ins2 sequence was found in all mutants and revertants, but not in Canton S. Although a recombinant phage carrying the DNA fragment spanning the entire Ins1 has not been obtained, sequencing data of the clone containing only the terminal repeats demonstrated that the repeats are defective P elements. Comparison of the genomic DNA structures of mutants and revertants suggested that the element responsible for the positive regulation of the G6PD gene in the mutants would probably be the core sequence, but not the flanking defective P elements. It was also conjectured that the 1·2 Kb core sequence might be composed of two identical elements, which might transpose independently.

The role of epistatic interaction of allozymes in the determination of variation in larval ethanol tolerance of Drosophila melanogaster was examined. Isofemale lines from the Tahbilk Winery were made homozygous for different common alleles of alcohol dehydrogenase (Adh) and sn-glycerol-3-phosphate dehydrogenase (Gpdh). When fed 6% ethanol, all the lines had reduced survival and, in the survivors, reduced body weight and lengthened development time. A strong positive correlation between tolerance and development time suggested that alleles responsible for slowing development on ethanol also increased ethanol tolerance. Analysis of larval ethanol tolerance over four generations showed that larvae of the AdhffGpdhff, and AdhssGpdhss allelic combinations were more tolerant than larvae with the other combinations. However, these genotypes were not associated with the slowing of development nor the weight loss on ethanol. Hence, larvae with certain combinations of Adh and Gpdh allozymes may have a greater capacity to metabolize ethanol and be more tolerant to its toxic effects.

One hundred and ninety-eight mice trapped along a south–north transect through the Danish hybrid zone between Mus musculus domesticus and M. m. musculus were typed for mitochondrial DNA (mtDNA), the Y chromosome and ten autosomal loci encoding diagnostic proteins. The southern (domesticus) populations display two mtDNA variants (S1 and S2) and the northern (musculus) have a third mtDNA variant (N) of domesticus origin. Across the hybrid zone defined by ten autosomal loci, there is a steep dine between the southern and northern types of mtDNA. As well as confirming an earlier finding that Danish musculus all have a domesticus mtDNA (Ferris et al. 1983a, & b), our results show that this mtDNA takeover is not the result of a persistent mitochondrial gene flow between the two subspecies. While the coincident dines for the ten autosomal loci and the abrupt dine for the Y chromosome can be explained by selection, it is less likely to be the case for the mtDNA exchanges. We discuss the possible role of sex-linked migration and genetic drift to account for the distribution of the mitochondrial variants.

A low activity mutant of glucose-6-phosphate dehydrogenase, G6pda-m1Neu has been used to position G6pd in the mouse X chromosome. Linkage tests with tabby, Ta and harlequin, Hq, indicate a likely gene order of Hq–G6pd–Ta. Muscular dystrophy, mdx, has been located by two-and three-point crosses using Hprt, Pgk-1 and Moblo and suggest a gene order of Hprt–mdx–Pgk-1–Moblo. Together with existing linkage data a tentative order for the seven loci is Hq–Hprt–G6pd–mdx–Ta–Pgk-1–Moblo. The relative positions of G6pd and mdx have not been directly tested and G6pd is assigned provisionally proximal to mdx. In the three point test using Hq, G6pd and Ta the recombination frequency found between Hq and Ta was 9·9 ± 2·6%, substantially less than the value of 20·5 ± 2·1% reported by Isaacson et al. (1974).

Two hitherto unmapped recessive autosomal mutations, ‘arrested development of righting response’ (adr) and ‘myotonia’ (mto, now adrmto), were found to be allelic, so that preliminary linkage data on adr and adrmto can now be combined. No linkage was found to the glucose phosphate isomerase (Gpi-1) locus on Chr 7 that marks a region of homology between mouse Chr 7 and human Chr 19, and in man is closely linked to the myotonic dystrophy (DM) gene. The adr gene was expressed on diverse genetic backgrounds including the athymic nude mouse.

Glycine tastes both bitter and sweet to mice but there are differences between strains in their ability to detect each taste. With respect to the bitter taste, fifteen strains were classified as tasters and twelve strains as non-tasters. The difference is due to a single gene, Glb (glycine bitterness). Cycloheximide tastes bitter to all mice at a concentration of 8 μM, but strain differences in sensitivity to the taste of cycloheximide can be detected at lower concentrations. The BXD RI strains can be classified into two groups with respect to sensitivity to cycloheximide. This is probably due to the segregation of two alleles of a single gene, Cyx. A comparison of the distribution in RI strains of alleles of four bitterness-tasting genes shows that the loci are all closely linked and are probably in the order Cyx–Qui–Rua–Glb.

The n0 coalescent of Kingman (1982a, b) describes the family relationships among a sample of n0 individuals drawn from a panmictic species. It is a stochastic process resulting from n0 − 1 independent random events (coalescences) at each of which n (2 ≤ n ≤ n0) ancestral lineages of a sample are descended from n − 1 distinct ancestors for the first time. Here a similar genealogical process is studied for a species consisting of two populations with migration between them. The main interest is with the probability density of the time length between two successive coalescences and the spatial distribution of n − 1 ancestral lineages over two populations when n to n − 1 coalescence takes place. These are formulated based on a non-linear birth and death process with killing, and are used to derive several explicit formulae in selectively neutral population genetics models. To confirm and supplement the analytical results, a simulation method is proposed based on the underlying bivariate Markov chain. This method provides a general way for solving the present problem even when an analytical approach appears very difficult. It becomes clear that the effects of the present population structure are most conspicuous on 2 to 1 coalescence, with lesser extents on n to n − 1 (3 ≤ n) coalescence.This implies that in a more general model of population structure, the number of populations and the way in which a sample is drawn are important factors which determine the n0 coalescent.

A population genetics model of the role of asymmetric pairing and unequal exchange in the stabilization of transposable element copy number in natural populations is proposed and analysed. Monte Carlo simulations indicate that the approximations incorporated into the analysis are robust in the relevant parameter ranges. Given several simple assumptions concerning transposition and excision, equal and unequal exchange, and chromosome structure, predictions of the relative numbers of transposable elements in various regions of the Drosophila melanogaster genome are compared to the observed distribution of roo/B104 elements across chromosomal regions with differing rates of exchange, and between X chromosomes and autosomes. There is no indication of an accumulation of elements in the distal regions of chromosomes, which is expected if unequal exchange is reduced concomitantly with normal crossing over in the distal regions. There is, however, an indication of an excess of elements relative to physical length in the proximal regions of the chromosomes, which also have restricted crossing over. This observation is qualitatively consistent with the model's predictions. The observed distribution of elements between the mid-sections of the X chromosomes and autosomes is consistent with the predictions of one of two models of unequal exchange.

There are a number of reports of gametic disequilibrium between alleles causing segregation distortion (e.g. t alleles in M. musculus and SD alleles in D. melanogaster) and linked loci. These observations have resulted in the conclusion by some researchers that segregation distortion may cause gametic disequilibrium. In this manuscript I have shown that (1) segregation distortion cannot generate gametic disequilibrium de novo and (2) because segregation distortion results in an excess of heterozygotes, the rate of decay of disequilibrium is faster than if segregation distortion were absent. Other factors, such as mutation or selection, appear to generate the observed disequilibrium, and extremely low recombination appears important in retarding its decay.