Population genetics of extranuclear genomes is further developed under the neutral-mutation random-drift hypothesis, and the characteristic evolutionary aspects are summarized. Several formulae derived here are concerned with the variances of genetic variability (gene identity) at a single extranuclear locus and the evolutionary distance between two isolated populations which is estimated from a comparison of homologous linked nucleotide sites. Two types of variance are considered; one is the variance in the entire population (VQ) and the other is the variance within a single germ cell (VH). When compared with a Mendelian genetic system in a panmictic population, an extranuclear genetic system has the following equilibrium properties: (1) the mean genetic variability is low if, despite the high multiplicity of the genome in a cell, the proportion of the cytoplasmic contribution from the male's gamete is small, (2) the effect of recombination is small and a large amount of variance of linkage disequilibrium tends to be maintained, (3) the overall relationship between the mean and variance of genetic variability does not much differ but VQ (VH) is expected to be small if the paternal contribution is small, and (4) the evolutionary distance estimated depends on the extent of intrapopulational variation in a common ancestor population which in turn depends on within-cell variation. I argue that there is an analogy between the model of extranuclear genomes in a finite population and that of nuclear genes in a subdivided population. The analogy helps our understanding of some properties in an extranuclear genetic system.

We studied the evolutionary dynamics of extranuclear genes taking into account simple kinds of selection, two modes of inheritance and the multiplicity of genomes within a cell. Particular attention was paid to the accumulation of advantageous or deleterious mutations in an extranuclear genome. Within-generation drift due to multiplicity of genome and non-Mendelian segregation promotes the fixation of advantageous mutations and prevents deleterious mutations from accumulating. We show also that the extent of paternal contribution makes little difference in the rate, but, in contrast, the configuration of the genome and the mode of transmission both makes a large difference. These results are compatible with what is known about extranuclear genomes.

A complete genetic map has been established for the P22 clear plaque forming mutations cir4-l, cir5-l and cir6-l. These are located within or closely linked to the immI region of P22 and represent a new class of clear plaque forming mutants located outside and rather distant from the immC region. They were mapped with respect to the markers mnt, vy and ant of the immI region and to genes 16 and 9 which span it. The three cir mutations complement each other and – with one possible exception – the cl, c2 and c3 mutations of the immC region. P22 cir6-l – like P22 cir5-l (Harvey et al. 1981) – is suppressed by the ant−am19 allele, whereas P22 cir4-l is not. The results are discussed in terms of the regulation of early ant expression.

Haploid amoebae of Physarum polycephalum may form plasmodia sexually by ‘crossing’, which involves cellular and nuclear fusion, or asexually by ‘selfing’, which occurs without nuclear fusion. In most amoebal strains, selfing is seen in clonal cultures only at very low frequency. In the present study, we have shown that selfing occurs at a similarly low frequency in mixtures of crossing-incompatible amoebae, but is stimulated in crossing-compatible mixtures. In certain compatible mixtures involving mutant strains, where crossing is temperature-sensitive, selfing may be stimulated even at a temperature that largely or wholly abolishes crossing. The extent to which selfing is stimulated appears to be influenced by matB, a locus which is known to affect the frequency of amoebal fusion. We have failed to detect any filter-transmissible factor that might be responsible for the effects we have observed. We suggest a sequence of events that might bring about ‘stimulated selfing’ as a consequence of abortive crossing.

Two spontaneously arising chromosome rearrangements were isolated in Sordaria brevicollis from one perithecium. These were detected through increased production of black spores in intercrosses of complementing buff spore colour mutants. One was a reciprocal translocation between linkage groups I and II; the other a reciprocal translocation between linkage groups II and VI. In the former case the translocation resulted in frequent non-disjunction generating black spores which were either tertiary or interchange disomics. The frequency of premature centromere division was also increased. In the case of the translocation involving linkage groups II and VI the black spores were formed as a result of adjacent-1 segregation and were probably duplication/deficiency products.

In both rearrangements the breakpoint in linkage group II was, as far as could be judged, in an identical place. This and the fact that they were isolated from a single fruiting body, suggests that the chromosome breakage event arose as a potential lesion, which replicated before the potential break was either restituted, to restore a normal chromosome, or opened, to form the rearrangements.

Houseflies collected from eight pig-breeding farms were used to investigate the nature of sex determinants in fly populations of South-East England. Earlier observations had shown that their sex determination mechanism was not of the standard (XX females, XY males) type.

Most flies of both sexes were XX; the male determining Y chromosome of standard populations was rare. Test-crosses to females of standard multimarked strains and crosses using aneuploid (OX) flies identified two dominant male determinants, one on autosome 3 (M III) and another on the X chromosome (Xm), and provided the first demonstration in this species of an active involvement of the X chromosome in sex determination. A small secondary constriction on X appeared to indicate reliably the presence of Xm. Most individuals in field populations were Xm homozygotes, implying the presence of an unlocated female determinant F,† epistatic to Xm and M III.

M III was less common and differed in frequency between samples. Its increased frequency in a strain selected in the laboratory with the pyrethroid insecticide permethrin might be due either to genetic drift, or to linkage between M III and a gene on autosome 3 that confers resistance to pyrethroids in houseflies.

To determine the extent of gametic disequilibrium between loci linked to the t-complex in house mice, alleles of four allozyme-encoding loci associated with eleven t-complexes recently found in wild mice and sixteen t-complexes maintained in laboratory colonies were identified. The allozyme-encoding loci included in the survey were complement component-3, kidney catalase, glyoxalase-1 and phosphoglycerate kinase-B. In contrast to published surveys showing strong disequilibrium between the H-2 complex, t-complex protein-1 and the t-complex, disequilibrium between the t-complex and linked allozyme-encoding loci was not detected. This result is discussed in terms of several hypotheses concerning the structure of mouse populations and the mechanisms maintaining gametic disequilibrium between the H-2 complex, t-complex protein-1 and the t-complex.

Recombination between two mouse t–haplotypes, tw12tf and tLub-1, was investigated by screening the tailless progeny of the cross ♀ tw12tf/tLub-1 + × ♂Ttf/+tf for the segregation of tufted phenotype, tw12 and tLub-1 lethal factors, and metacentric chromosome (since tLub-l haplotype is associated with a Robertsonian fusion involving chromosomes 4 and 17). The results give a 17% estimate of the recombination frequency between centromere and tf, with tLub-l lethal factor mapping about two-thirds of the distance from centromere to tf and the tw12 lethal factor behaving as if closely linked to tf. This further extends the findings of Silver & Artzt (1981) and of Artzt, McCormick & Bennett (1982), and shows that two t–haplotypes with quite independent laboratory histories recombine at a normal level, supporting the notion that all t–haplotypes basically share the same structure.

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.