Aedes (Stegomyia) aegypti (L.) and Aedes (Stegomyia) albopictus (Skuse) are the most important vectors of the dengue and yellow-fever viruses. Both took advantage of trade developments to spread throughout the tropics from their native area: A. aegypti originated from Africa and A. albopictus from South-East Asia. We investigated the relationships between A. aegypti and A. albopictus mosquitoes based on three mitochondrial-DNA genes (cytochrome b, cytochrome oxidase I and NADH dehydrogenase subunit 5). Little genetic variation was observed for A. albopictus, probably owing to the recent spreading of the species via human activities. For A. aegypti, most populations from South America were found to be genetically similar to populations from South-East Asia (Thailand and Vietnam), except for one sample from Boa Vista (northern Amazonia), which was more closely related to samples from Africa (Guinea and Ivory Coast). This suggests that African populations of A. aegypti introduced during the slave trade have persisted in Boa Vista, resisting eradication campaigns.

We have isolated the clock gene period (per) from the medfly Ceratitis capitata, one of the most economically important insect pest species. The overall pattern of conserved, non-conserved and functional domains that are observed within dipteran and lepidopteran per orthologues is preserved within the coding sequence. Expression analysis from fly heads revealed a daily oscillation in per mRNA in both light[ratio ]dark cycles and in constant darkness. However PER protein levels from head extracts did not show any significant evidence for cycling in either of these two conditions. When the Ceratitis per transgene under the control of the Drosophila per promoter and 3′UTR was introduced into Drosophila per-null mutant hosts, the transformants revealed a low level of rescue of behavioural rhythmicity. Nevertheless, the behaviour of the rhythmic transformants showed some similarities to that of Ceratitis, suggesting that Ceratitis per carries species-specific information that can evidently affect the Drosophila host's downstream rhythmic behaviour.

Sequence polymorphisms result in phenotypic variation through the pathways of interacting genes and their products. We focused on transcript-level variation in the splicing pathway for sex determination – a model network defining downstream morphological characters that are dimorphic between males and females. Expression of Sex lethal, transformer, transformer2, doublesex, intersex and hermaphrodite was assayed with quantitative RT-PCR in 0- to 1-day-old adult males and females of 36 Drosophila melanogaster inbred lines. Abundant genetic variation in the transcript levels was found for all genes. Sex-specific splices had high concentrations in the appropriate sex. In the other sex, low but detectable concentrations were also observed. Abundances of splices strongly co-varied between sexes among genotypes, with little genetic variation strictly limited to one sex. The level of sexually dimorphic Yolk protein1 expression – an immediate downstream target of the pathway – was modelled as the target phenotype of the upstream sex determination pathway. Substantial genetic variation in this phenotype in males was explained by leaky splicing of female-specific transcripts. If higher transcript levels of the appropriate isoform of sex determination genes are beneficial in a sex, then stronger leakiness of the inappropriate transcript might be deleterious, perhaps contributing to the fitness trade-offs previously observed between the sexes.

The fate of lethal alleles in populations is of interest in evolutionary and conservation biology for several reasons. For instance, lethals may contribute substantially to inbreeding depression. The frequency of lethal alleles depends on population size, but it is not clear how it is affected by population structure. By analysing the case of the infinite island model by numerical approaches and analytical approximations it is shown that, like population size, population structure affects the fate of lethal alleles if dominance levels are low. Inbreeding depression caused by such alleles is also affected by the population structure, whereas the mutation load is only weakly affected. Heterosis also depends on population structure, but it always remains low, of the order of the mutation rate or less. These patterns are compared with those caused by mildly deleterious mutations to give a general picture of the effect of population structure on inbreeding depression, heterosis, and the mutation load.

The mechanism underlying the maintenance of adaptive genetic variation is a long-standing question in evolutionary genetics. There are two concepts (mutation–selection balance and balancing selection) which are based on the phenotypic differences between alleles. Mutation – selection balance and balancing selection cannot properly explain the process of gene substitution, i.e. the molecular evolution of quantitative trait loci affecting fitness. I assume that such loci have non-essential functions (small effects on fitness), and that they have the potential to evolve into new functions and acquire new adaptations. Here I show that a high amount of neutral polymorphism at these loci can exist in real populations. Consistent with this, I propose a hypothesis for the maintenance of genetic variation in life history traits which can be efficient for the fixation of alleles with very small selective advantage. The hypothesis is based on neutral polymorphism at quantitative trait loci and both neutral and adaptive gene substitutions. The model of neutral – adaptive conversion (NAC) assumes that neutral alleles are not neutral indefinitely, and that in specific and very rare situations phenotypic (relative fitness) differences between them can appear. In this paper I focus on NAC due to phenotypic plasticity of neutral alleles. The important evolutionary consequence of NAC could be the increased adaptive potential of a population. Loci responsible for adaptation should be fast evolving genes with minimally discernible phenotypic effects, and the recent discovery of genes with such characteristics implicates them as suitable candidates for loci involved in adaptation.

To study the effects of maternal and endosperm quantitative trait locus (QTL) interaction on endosperm development, we derive a two-stage hierarchical statistical model within the maximum-likelihood context, implemented with an expectation-maximization algorithm. A model incorporating both maternal and offspring marker information can improve the accuracy and precision of genetic mapping. Extensive simulations under different sampling strategies, heritability levels and gene action modes were performed to investigate the statistical properties of the model. The QTL location and parameters are better estimated when two QTLs are located at different intervals than when they are located at the same interval. Also, the additive effect of the offspring QTLs is better estimated than the additive effect of the maternal QTLs. The implications of our model for agricultural and evolutionary genetic research are discussed.

Effectiveness of marker-assisted selection (MAS) and quantitative trait loci (QTL) mapping using population-wide linkage disequilibrium (LD) between markers and QTL depends on the extent of LD and how it declines with distance in a population. Because marker–QTL LD cannot be observed directly, the objective of this study was to evaluate alternative measures of observable LD between multi-allelic markers as predictors of usable LD of multi-allelic markers with presumed biallelic QTL. Observable LD between marker pairs was evaluated using eight existing measures and one new measure. These consisted of two pooled and standardized measures of LD between pairs of alleles at two markers based on Lewontin's LD measure, two pooled measures of squared correlations between alleles, one standardized measure using Hardy–Weinberg heterozygosities, and four measures based on the chi-square statistic for testing for association between alleles at two loci. In simulated populations with a range of LD generated by drift and a range of marker polymorphism, marker–marker LD measured by a standardized chi-square statistic (denoted χ2′) was found to be the best predictor of useable marker–QTL LD for a group of multi-allelic markers. Estimates of the level and decline of marker–marker LD with distance obtained from χ2′ were linearly and highly correlated with usable LD of those markers with QTL across population structures and marker polymorphism. Corresponding relationships were poorer for the other marker–marker LD measures. Therefore, when LD is generated by drift, χ2′ is recommended to quantify the amount and extent of usable LD in a population for QTL mapping and MAS based on multi-allelic markers.