Many species of insects bear maternally inherited bacteria which contribute to the physiology and metabolism of their host whereas others bear inherited bacteria which are regarded as parasitic. Parasitic behaviours centre on disruption of the production, survival or fertility of male hosts, through which the microbe is not transmitted. One of the most common of these is early male-killing, where the bacteria kill male embryos they enter. The question arises as to why all inherited symbionts are not male-killers. The male-killing agents identified to date derive from two groups: the Proteobacteria and the Mollicutes. However, bacteria from other groups (Spirochaetes, Flavobacteria) are found to be inherited in insects, but contain no incidence of male-killing. We show here an association of male-killing with a bacterium from one of these groups. The bacterium causing male-killing behaviour in the ladybird Coleomegilla maculata is most closely related to Blattabacterium, a host-beneficial Flavobacteria found in cockroaches and some termites. This result indicates there is little if any taxonomic bar to the evolution of male-killing behaviour. This pattern severely contrasts with the evolution of two other parasitic symbiont behaviours, cytoplasmic incompatibility and the induction of host parthenogenesis, which have been found to be associated exclusively with bacteria from one group: Wolbachia. The result is briefly discussed in the light of the incidence of parasitic and beneficial cytoplasmic elements among insects.

Non-recombining populations should suffer from four classic population genetic disadvantages: (1) they cannot reverse Muller's Ratchet, the accumulation of deleterious mutations caused by genetic drift and mutation; (2) whenever the fix a favourable mutation they lose all unlinked favourable variants; (3) they tend to lose favourable mutations that are linked to deleterious mutations; and (4) their genetic loads can be quite high when deleterious mutations have synergistic effects. It is commonly assumed that inter-chromosomal recombination (independent assortment) can counter these phenomena, but this has been studied only for the genetic load case. In contrast, many studies have shown that recombination via crossing over can counter these phenomena. Here we first show that segregation alone can strongly decelerate Muller's Ratchet in diploids, i.e. that recombination is not the only way to do so. We then show that inter-chromosomal recombination can indeed deal with phenomena (1) to (3) above very effectively if the genome consists of a moderate number of chromosomes. Therefore, if the above advantages of genetic recombination played a large role in the initial success of eukaryotic sex, the crucial moment in the origin of sex might have been the evolution of inter-chromosomal recombination, i.e. the evolution of genome segmentation, segregation, and syngamy. Crossing over might have become established as a major recombinational device only later, eliminating the disadvantages of extensively segmented genomes.

We studied the dominance of the effects of chromosomes carrying unselected mutations on five life-history traits in Drosophila melanogaster. Mutations were accumulated on the second chromosome for 44 generations in the absence of natural selection. Traits studied were female fecundity early and late in adult life, male mating ability, and male and female longevity. Homozygous effects were estimated for 50 mutant lines, and heterozygous effects were estimated by crossing these lines in a partial diallel scheme. Direct estimates of dominance showed that the effects of mutants are at least partially recessive. Heterozygotes had higher trait means than homozygotes in all five cases, and these differences were significant for late fecundity and female longevity. For all traits, genetic variance was larger among homozygous crosses than among heterozygous crosses. These results are consistent with those of many other studies that suggest that both unselected mutations and those found segregating in natural populations are partially recessive.

Eight isofemale lines of Drosophila melanogaster were raised at four temperatures and at four yeast concentrations in their food. Temperature and food show a significant interaction in determining wing length and thorax length, affecting mean size per line and genetic variation between lines. The combination of low temperature and poor food conditions leads to a sharp increase in the genetic variation over lines of both body size characters. The increase in genetic variation in wing length under less favourable conditions is due to an increase in genetic variation of both cell size and cell number. Changes in wing area in response to both temperature and food level follow a common cell size/cell number trajectory. Changes in wing size are obtained by line-specific changes in the cellular composition of the wing, rather than by changes specific for the environmental factor.

It is known that genetic polymorphisms can be maintained in populations without superiority of the heterozygote subject to constant but non-linear selection through periodic and higher-order behaviour. In this paper we explore evolutionary paths from single equilibria to higher-order attractors and the existence of polymorphisms that do not arise from equilibria. We explore whether there is a continuous range of allelic types that can create such polymorphisms. We use a single-locus genetic model with exponential density-dependent fitness functions and show that there are large parameter ranges in regions of both overdominance and partial dominance where polymorphic attractors exist.

We consider using microsatellites for paternity checking and parent identification in different population structures, and allowing for possible typing errors or mutations. Statistical rules derived from the Bayesian and the sampling approaches are discussed in the case involving the choice of the true father–mother pair among a finite set of possible parental pairs. General situations are investigated by means of random simulations, in order to characterize the joint influences of the number and polymorphism of typed loci, the population structure and size, and error rates. Approximate expressions are provided that give the efficiency of a set of markers for identifying the parents in various mating schemes. The importance of a non-zero value for the typing error rate in the likelihood is highlighted.

Theoretical arguments are presented which suggest that each advance of Muller's ratchet in a haploid asexual population causes the fixation of a deleterious mutation at a single locus. A similar process operates in a diploid, fully asexual population under a wide range of parameter values, with respect to fixation within one of the two haploid genomes. Fixations of deleterious mutations in asexual species can thus be greatly accelerated in comparison with a freely recombining genome, if the ratchet is operating. In a diploid with segregation of a single chromosome, but no crossing over within the chromosome, the advance of the ratchet can be decoupled from fixation if mutations are sufficiently close to recessivity. A new analytical approximation for the rate of advance of the ratchet is proposed. Simulation results are presented that validate the assertions about fixation. The simulations show that none of the analytical approximations for the rate of advance of the ratchet are satisfactory when population size is large. The relevance of these results for evolutionary processes such as Y chromosome degeneration is discussed.

The influence of gamma-irradiation on P element excision and excision-site repair mechanisms was directly tested by embryonic somatic excision assays. Preblastoderm P[ry+, Δ2–3](99B) embryos, having a stable source of somatically active P transposase, were irradiated previous to injection with P excision indicator plasmids. Frequencies of precise or nearly precise P excision increased with gamma-ray doses ranging from 0·5 to 3·5 Gy. Higher doses resulted in frequencies close to that in unirradiated embryos, though considerable embryonic lethality was also evident at these doses. A direct positive interaction between gamma-irradiation and P element activity is concluded.