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 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.

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.

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.

This paper reports the first direct molecular evidence that X chromosome loss during determination of male aphids (XO) is random. Clonal and sexual females, and males, of the species Sitobion near fragariae were screened using three polymorphic microsatellite loci. Two loci, Sm10 and Sm17, showed the same heterozygous genotypes in all three aphid morphs. The third, Sm11, was heterozygous for the same two alleles in clonal and sexual females, but of the 25 males screened 11 showed the ‘160’ allele and 14 showed the ‘156’ allele. This result indicates X-linkage of locus Sm11, with random loss of the X chromosome during the formation of male embryos. The possible implications of this result are discussed with respect to aphid sex determination, recombination and chromosome evolution.

Genetic instability is associated with aging in many species. One of the initiating factors for genetic instability is the movement of transposable elements (TEs), which occur in all prokaryotic and eukaryotic organisms. The hypothesis that TEs could be involved in the aging process is discussed and the correlation between aging and activity of TEs is analysed in a variety of biological systems.

Until now, with regard to the hobo system of hybrid dysgenesis, natural populations of Drosophila melanogaster have been investigated using only two criteria: at the molecular level, the presence or absence of XhoI fragments 2·6 kb long or smaller; and/or at the genetic level, the ability to induce gonadal dysgenesis sterility in crosses A (females of an E reference strain crossed with males under test) and A* (females under test crossed with males of an H reference strain). Recently, analyses of laboratory strains using these criteria as well as the mobilization of two reporter genes, the male recombination and the number of ‘TPE’ repeats in the S region, revealed a lack of correlation between the different dysgenic parameters themselves, and also between these parameters and the molecular characteristics of the strains. Thirteen current strains derived from world populations were therefore investigated with regard to all these dysgenic traits, to determine discriminating criteria providing a robust method of classifying natural populations and deducing the dynamics of hobo elements in these populations. We show, as in laboratory strains, a lack of correlation between the parameters studied. Therefore, the significance of each of them as well as the nature of hobo hybrid dysgenesis are discussed, to propose an analysis method of the hobo system applicable to natural populations. According to the geographical distribution of hobo activities in world populations and to the variable polymorphism of the number of ‘TPE’ repeats, we propose a new scenario for the invasion of D. melanogaster by hobo elements.

To assess the role of genetic changes in sensitivity to leptin hormone in contributing to responses to long-term selection for fatness, leptin was administered to a long-term fat selected (F) and a control line (C) of mice. These lines differ almost three fold in their percentage of fat (fat%) at about 15 weeks of age. Treated (T) animals received twice-daily intraperitoneal injections of 5 mg/kg leptin from 91 to 105 days of age; untreated (U) animals received equivolume injections of phosphate-buffered saline. Treated compared with untreated animals in both lines had significantly (P<0·05) lower mean body weight, food intake and fatness at the end of test (fat%: CT 3%, CU 7·4%, FT 14·9%, FU21·1%). The differences in response between the lines [(CT−CU)−(FT−FU)] were all non-significant (P>0·05), however. There was a very wide range of fatness (estimated from dry matter content) among FT animals (3–29%), much higher than in FU (15–31%), CT (0·7–6·4%) and CU (2–15%) animals. While sensitivity to leptin remains in the fat line, response appears to vary among animals at the dose level used.