Bulinus truncatus, one of the intermediate hosts of the genus Schistosoma is an hermaphrodite freshwater snail species occupying a variety of environments over almost all Africa. These environments are subjected to large variations in water availability. B. truncatus is allotetraploid and its populations exhibit various frequencies of aphallic individuals (unable to reproduce as male). Both traits probably favour a reproduction by self-fertilization. Here we investigate the genetic structure of populations of B. truncatus of Niger and Ivory Coast using protein electrophoresis to analyse the influence of the environment and of both the last traits. To obtain an estimate of the true heterozygosity in this allotetraploid species, we analyse independently the two diploid loci at each tetraploid locus. Our study indicates (i) an extremely low intrapopulation polymorphism with most alleles fixed and the total absence of heterozygotes and (ii) low differentiation between populations. These results indicate high gene flow between populations. However, the existence of private alleles sometimes at high frequency, the low polymorphism and the lack of heterozygotes point to the role of both genetic drift and self-fertilization, the second amplifying the genetic consequences of the first.

Linkage disequilibrium between molecular polymorphisms in a 10 kb region in the white locus of Drosophila melanogaster, revealed with a battery of four-cutter restriction enzymes, was investigated in 266 lines sampled from seven natural populations around the world. A total of 73 (35 restriction site, 37 insertion/deletion and 1 inversion) polymorphisms were detected, of which 55 non-unique polymorphisms were analysed for linkage disequilibrium. Clustering of significant linkage disequilibrium was observed in the transcriptional unit of the white locus as in Miyashita & Langley (1988). It was shown that about two thirds of the 2-locus combinations showing significant linkage disequilibrium have similar degree and direction of association over different populations. Despite lower divergence in allelic frequencies of molecular polymorphisms among populations, an increase in the proportion of 2-locus pairs showing significant linkage disequilibrium is observed in the transcriptional unit. Large values of Ohta's D measure ratio (1982 a, b) cluster in the transcriptional unit, and correspond to significant linkage disequilibria. Although the exact molecular mechanism is not clear, these results suggest that epistatic selection is responsible for significant linkage disequilibrium in the transcriptional unit of this locus

Three Harwich P sublines with different P-element activity potential were used to investigate the influence of P-derived chromosomes on snω mutability and vg suppression and to relate the induction of these dysgenic traits to the number and structure of P elements. Destabilization of the snω allele, a measure of P transposase activity, was differentially influenced by the major autosomes. Chromosome 2 of the standard Harwich subline, Hw, induced only 60% of the level of mutability relative to chromosome 3, whereas chromosome 3 of the weakest Harwich subline, Hf, induced only 50% of the mutability relative to chromosome 2. In somatic suppression of the vg21–3 allele, chromosome 3 of the Hf subline produced a lower level of complete suppression as compared to chromosome 3 of the Hw or the Hs subline (the high hybrid-dysgenesis-inducing subline). The level of these dysgenic traits and GD sterility, was not correlated with the number of P elements per individual (67–68) or per chromosome arm which was very similar among the sublines. The number of complete P elements per genome, based on Southern blot analysis of the X and major autosomes, ranged from 15 to 19. Destabilization of the snω allele and vg suppression by chromosome 3 was correlated with a greater number of complete P elements. Two novel unexpected observations emerged from these studies: both snω mutability and vg suppression data demonstrated high P-element activity in hybrids derived from non-dysgenic crosses irrespective of Harwich subline, indicating a lack of P-cytotype regulation. Mutability in non-dysgenic males ranged from 40 to 60% of the level found in dysgenic males. The high snω mutability and low GD sterility in non-dysgenic hybrids suggests that these traits may arise by a different mechanism.

Hitch-hiking of dispersed mobile elements serving as molecular markers was used as a new tool for mapping quantitative trait loci in Drosophila melanogaster. Two Drosophila strains with high fitness (HA) were backcrossed repeatedly to a closely related strain with low fitness (LA) to initiate experimental populations with expected HA gene frequencies of 1/32. The frequencies of 19 insertion sites of the retrotransposons mdg1 and copia were analyzed after 11 to 17 generations. Frequencies of sites from the HA line increased substantially in the pericentromeric region, indicating that one or more loci responsible for the fitness difference between the strains were located there. A maximum likelihood (ML) procedure was applied to estimate selection coefficients associated with the markers, and this indicated a broad, strongly selected region of the chromosome. At least one additional locus was localized in the middle of the 2L arm. Possible applications of this method are discussed.

A novel central partial t haplotype was generated by screening for a recombination event between overlapping distal and proximal partial haplotypes. This haplotype contains just two elements Tcrt and Tcd-3t —involved in the t-specific transmission ratio distortion phenotype. Breeding analysis of males that carry this chromosome provides evidence that Tcd-3 is, indeed, a distorter locus and not a second responder. Furthermore, the data indicate that a single well-defined distorter locus is insufficient to overcome completely the self-destructive, low transmission ratio distortion phenotype expressed by the t allele at the t complex responder locus, although a small, but highly significant, effect was observed.

To examine the effects of X-chromosome imprinting during early mouse embryogenesis, we attempted to produce XM0, Xp0, XMXMY, XMXPY and XMXMXP (where XM and Xp stand for the maternally and the paternally derived X chromosome, respectively) making use of mouse strains bearing the translocation Rb(X.2)2Ad and the inversion In(X)1H. Unlike XMXPY embryos, XMXMY and XMXMXP conceptuses suffered from severe growth retardation or abnormal development characterized by deficient extra-embryonic structures at 6.5–7.5 days post coitum (dpc). A cytogenetic study suggested that two XM chromosomes remaining active in certain non-epiblast cells were responsible for the serious developmental abnormality found in these embryos disomic for XM. Although matings involving females heterozygous for Rb(X.2)2Ad hinted at the paucity of XP0 embryos relative to those having the complementary karyotype of XMXMXP, further study of embryos from matings between females heterozygous for In(X)1H and Rb2Ad males did not substantiate this observation. Thus, the extensive peri-implantation loss of XP0 embryos shown by Hunt (1991) may be confined to XO mothers. Taken together, this study failed to reveal a parentally imprinted X-linked gene essential for early mouse embryogenesis other than the one most probably corresponding to the X-chromosome inactivation centre.

In a stably subdivided population with symmetric migration, the chance that a favoured allele will be fixed is independent of population structure. However, random extinction introduces an extra component of sampling drift, and reduces the probability of fixation. In this paper, the fixation probability is calculated using the diffusion approximation; comparison with exact solution of the discrete model shows this to be accurate. The key parameters are the rates of selection, migration and extinction, scaled relative to population size (S = 4Ns, M = 4Nm, Λ = 4Nλ); results apply to a haploid model, or to diploids with additive selection. If new colonies derive from many demes, the fixation probability cannot be reduced by more than half. However, if colonies are initially homogeneous, fixation probability can be much reduced. In the limit of low migration and extinction rates (M, Λ ≪ 1), it is 2s/{1 + (Λ/MS)(1 −exp(−S))}, whilst in the opposite limit (S ≪ 1), it is 4sM/{Λ(Λ + M)}. In the limit of weak selection (M, Λ ≫ 1), it is 4sM/{Λ(Λ + M)}. These factors are not the same as the reduction in effective population size (Ne/N), showing that the effects of population structure on selected alleles cannot be understood from the behaviour of neutral markers.