Depression and risk of type 2 diabetes: the potential role of metabolic factors.

The aim of the present study was to evaluate the interaction between depressive symptoms and metabolic dysregulations as risk factors for type 2 diabetes. The sample comprised of 2525 adults who participated in a baseline and a follow-up assessment over a 4.5-year period in the Emotional Health and Wellbeing Study (EMHS) in Quebec, Canada. A two-way stratified sampling design was used, on the basis of the presence of depressive symptoms and metabolic dysregulation (obesity, elevated blood sugar, high blood pressure, high levels of triglycerides and decreased high-density lipoprotein). A total of 87 (3.5%) individuals developed diabetes. Participants with both depressive symptoms and metabolic dysregulation had the highest risk of diabetes (adjusted odds ratio=6.61, 95% confidence interval (CI): 4.86-9.01), compared with those without depressive symptoms and metabolic dysregulation (reference group). The risk of diabetes in individuals with depressive symptoms and without metabolic dysregulation did not differ from the reference group (adjusted odds ratio=1.28, 95% CI: 0.81-2.03), whereas the adjusted odds ratio for those with metabolic dysregulation and without depressive symptoms was 4.40 (95% CI: 3.42-5.67). The Synergy Index (SI=1.52; 95% CI: 1.07-2.17) suggested that the combined effect of depressive symptoms and metabolic dysregulation was greater than the sum of individual effects. An interaction between depression and metabolic dysregulation was also suggested by a structural equation model. Our study highlights the interaction between depressive symptoms and metabolic dysregulation as a risk factor for type 2 diabetes. Early identification, monitoring and a comprehensive management approach of both conditions might be an important diabetes prevention strategy.

Linkage disequilibrium and recombination in hominid mitochondrial DNA.

The assumption that human mitochondrial DNA is inherited from one parent only and therefore does not recombine is questionable. Linkage disequilibrium in human and chimpanzee mitochondrial DNA declines as a function of the distance between sites. This pattern can be attributed to one mechanism only: recombination.

Recombination and selection at Brassica self-incompatibility loci.

In Brassica species, self-incompatibility is controlled genetically by haplotypes involving two known genes, SLG and SRK, and possibly an as yet unknown gene controlling pollen incompatibility types. Alleles at the incompatibility loci are maintained by frequency-dependent selection, and diversity at SLG and SRK appears to be very ancient, with high diversity at silent and replacement sites, particularly in certain "hypervariable" portions of the genes. It is important to test whether recombination occurs in these genes before inferences about function of different parts of the genes can be made from patterns of diversity within their sequences. In addition, it has been suggested that, to maintain the relationship between alleles within a given S-haplotype, recombination is suppressed in the S-locus region. The high diversity makes many population genetic measures of recombination inapplicable. We have analyzed linkage disequilibrium within the SLG gene of two Brassica species, using published coding sequences. The results suggest that intragenic recombination has occurred in the evolutionary history of these alleles. This is supported by patterns of synonymous nucleotide diversity within both the SLG and SRK genes, and between domains of the SRK gene. Finally, clusters of linkage disequilibrium within the SLG gene suggest that hypervariable regions are under balancing selection, and are not merely regions of relaxed selective constraint.

Identification and characterization of a polymorphic receptor kinase gene linked to the self-incompatibility locus of Arabidopsis lyrata.

We study the segregation of variants of a putative self-incompatibility gene in Arabidopsis lyrata. This gene encodes a sequence that is homologous to the protein encoded by the SRK gene involved in self-incompatibility in Brassica species. We show by diallel pollinations of plants in several full-sib families that seven different sequences of the gene in A. lyrata are linked to different S-alleles, and segregation analysis in further sibships shows that four other sequences behave as allelic to these. The family data on incompatibility provide evidence for dominance classes among the S-alleles, as expected for a sporophytic SI system. We observe no division into pollen-dominant and pollen-recessive classes of alleles as has been found in Brassica, but our alleles fall into at least three dominance classes in both pollen and stigma expression. The diversity among sequences of the A. lyrata putative S-alleles is greater than among the published Brassica SRK sequences, and, unlike Brassica, the alleles do not cluster into groups with similar dominance.

Microsatellite variation and evolution in the Mimulus guttatus species complex with contrasting mating systems.

Mutational variability at microsatellite loci is shaped by both population history and the mating system. In turn, alternate mating systems in flowering plants can resolve aspects of microsatellite loci evolution. Five species of yellow monkeyflowers (Mimulus sect. Simiolis) differing for historical rates of inbreeding were surveyed for variation at six microsatellite loci. High levels of diversity at these loci were found in both outcrossing and selfing taxa. In line with allozyme studies, inbreeders showed more partitioning of diversity among populations, and diversity in selfing taxa was lower than expected from reductions in effective population size due to selfing alone, suggesting the presence of either population bottlenecks or background selection in selfers. Evaluation of the stepwise mutation model (a model of DNA replication slippage) suggests that these loci evolve in a stepwise fashion. Inferred coalescent times of microsatellite alleles indicate that past bottlenecks of population size or colonization events were important in reducing diversity in the inbreeding taxon.

Flowering plant self-incompatibility: the molecular population genetics of Brassica S-loci.

Self-incompatibility systems in different angiosperm families are reviewed, and the evidence that incompatibility has arisen several times is outlined. New data on the sequence polymorphism of self-incompatibility loci from two different angiosperm families are compared with results from other highly polymorphic loci, particularly MHC loci. We discuss what molecular genetic analyses of these sequences can tell us about the nature and maintenance of the polymorphism at self-incompatibility loci. We suggest that there is evidence for recombination at the Brassica self-incompatibility loci, so that it may be possible to discern regions that are particularly functionally important in the recognition reaction, even though the long-term maintenance of polymorphisms in these amino acid residues has caused the evolution of many other sequence differences between alleles.

Does human mtDNA recombine?

In this article we review the evidence for and against recombination in human mtDNA. If recombination occurs, there needs to be a route by which genetic material can incorporate itself into the mitochondrial genome, and hence between mitochondrial lineages. We review the evidence for possible routes and then review the current state of the population genetic evidence for recombination. We conclude that there is no firmly established route by which recombination can occur, and that while some of the population genetic evidence is suggestive of recombination, it is far from conclusive.

Local differentiation in Plasmodium falciparum drug resistance genes in Sudan.

Studies of population genetic structure of parasites can be used to infer which parasite genes are under selection. Here, the population structure of 4 genes associated with drug resistance of Plasmodium falciparum (the chloroquine resistance transporter, pfcrt, dihydrofolate reductase, dhfr, dihydropteroate synthase, dhps, and multi-drug resistance, pfmdr-1) were examined in parasite populations in 3 villages in eastern Sudan and in an urban area of Khartoum, the capital. In order to differentiate the effects of drug selection from neutral influences on population structure, parasites were also genotyped for 3 putatively neutral microsatellite loci (polyalpha, TA81 and pfg377), and for 2 antigenic loci that are either under balancing selection or neutral, merozoite surface protein 1 and 2, (MSP-1 and MSP-2). Cross-sectional surveys were carried out during the peak transmission (wet) season and in the ensuing dry season. No significant variation in frequencies of MSP-1 and MSP-2 alleles was seen among villages in the eastern region and between the villages and Khartoum, nor between the wet and dry season. However, the drug resistance genes, pfmdr-1, pfcrt and dhfr and to a lesser extent the microsatellite loci showed high FST values when comparing villages with Khartoum, indicating strong geographical differentiation at these loci. Moreover, variation in frequencies of the drug resistance genes, pfmdr-1, pfcrt and dhfr, was observed between the wet and dry season. These differences most probably reflect the variation in drug pressure between each region, and in drug usage between the wet and dry season in a given region.