Insights into the genetic architecture of morphological traits in two passerine bird species.

Knowledge about the underlying genetic architecture of phenotypic traits is needed to understand and predict evolutionary dynamics. The number of causal loci, magnitude of the effects and location in the genome are, however, still largely unknown. Here, we use genome-wide single-nucleotide polymorphism (SNP) data from two large-scale data sets on house sparrows and collared flycatchers to examine the genetic architecture of different morphological traits (tarsus length, wing length, body mass, bill depth, bill length, total and visible badge size and white wing patches). Genomic heritabilities were estimated using relatedness calculated from SNPs. The proportion of variance captured by the SNPs (SNP-based heritability) was lower in house sparrows compared with collared flycatchers, as expected given marker density (6348 SNPs in house sparrows versus 38 689 SNPs in collared flycatchers). Indeed, after downsampling to similar SNP density and sample size, this estimate was no longer markedly different between species. Chromosome-partitioning analyses demonstrated that the proportion of variance explained by each chromosome was significantly positively related to the chromosome size for some traits and, generally, that larger chromosomes tended to explain proportionally more variation than smaller chromosomes. Finally, we found two genome-wide significant associations with very small-effect sizes. One SNP on chromosome 20 was associated with bill length in house sparrows and explained 1.2% of phenotypic variation (VP), and one SNP on chromosome 4 was associated with tarsus length in collared flycatchers (3% of VP). Although we cannot exclude the possibility of undetected large-effect loci, our results indicate a polygenic basis for morphological traits.

Rapid and unpredictable changes of the G-matrix in a natural bird population over 25 years.

Knowledge of the genetic variances and covariances of traits (the G-matrix) is fundamental for the understanding of evolutionary dynamics of populations. Despite its essential importance in evolutionary studies, empirical tests of the temporal stability of the G-matrix in natural populations are few. We used a 25-year-long individual-based field study on almost 7000 breeding attempts of the collared flycatcher (Ficedula albicollis) to estimate the stability of the G-matrix over time. Using animal models to estimate G for several time periods, we show that the structure of the time-specific G-matrices changed significantly over time. The temporal changes in the G-matrix were unpredictable, and the structure at one time period was not indicative of the structure at the next time period. Moreover, we show that the changes in the time-specific G-matrices were not related to changes in mean trait values or due to genetic drift. Selection, differences in acquisition/allocation patterns or environment-dependent allelic effects are therefore likely explanations for the patterns observed, probably in combination. Our result cautions against assuming constancy of the G-matrix and indicates that even short-term evolutionary predictions in natural populations can be very challenging.

Studies on the effect of chronic consumption of moderate amounts of ethanol on male rat hepatic microsomal drug-metabolizing activity.

Weanling, male Sprague-Dawley rats given 10% ethanol in the drinking water and food ad lib. for up to 8 weeks consumed 17% of their calories as ethanol. The alanine aminotransferase (ALT), aspartate aminotransferase (AST), and liver histology by light microscopy were unaffected by this treatment. Similarly, hepatic microsomal NADPH-cytochrome c reductase, ethylmorphine N-demethylase and benzphetamine N-demethylase activities were also not affected by ethanol consumption. On the other hand, cytochrome P-450 content, aniline hydroxylase activity and acetaminophen metabolism as measured by both the cysteine conjugate and the [3H]acetaminophen covalently-bound to microsomal protein were increased significantly by ethanol consumption. The maximal effect was seen by 6 weeks. The 2- to 3-fold increase in aniline and acetaminophen metabolism, the absence of liver damage, and the similarity in weight gains and caloric intakes for controls and treated animals suggest that the rat on 10% ethanol in the drinking water is a reasonable model for studies of the effect of moderate alcohol consumption on specific biochemical pathways.

Effects of chronic ethanol consumption on male Syrian hamster hepatic, microsomal mixed-function oxidases.

Chronic alcohol consumption significantly increases the risk of drug interactions. We have described its effects on hamster microsomal monooxygenases. Male Syrian hamsters (85 g) were given 10% ethanol in water and food ad lib for up to 6 weeks. Microsomal electron transport components and metabolism of ethylmorphine, benzphetamine, aniline, and acetaminophen were measured. At 4 weeks, SDS-PAGE of ethanol microsomes showed an induced band with an Mr of 53,900 daltons and there was a 2-3 fold stimulation of aniline and acetaminophen metabolism. Cytochrome P-450 increase was not significant. For the six week period, Caloric intake (3 weeks, p less than 0.001), liquid consumption (3 weeks, p less than 0.05) and body weights (6 weeks, p less than 0.05) of ethanol animals were significantly greater than controls; kidney weights were significantly less (p less than 0.05). Ethanol consumption increased from 20% of the daily caloric intake (week 1) to 31% (week 6). Induction of specific substrate metabolism without apparent deleterious physiological changes establishes hamsters fed 10% ethanol in drinking water as a biochemical model for the study of chronic alcohol consumption and specific drug interactions.