Segregating hybrids often exhibit phenotypes that are extreme or novel relative to the parental lines. This phenomenon is referred to as transgressive segregation, and it provides a mechanism by which hybridization might contribute to adaptive evolution. Genetic studies indicate that transgressive segregation typically results from recombination between parental taxa that possess quantitative trait loci (QTLs) with antagonistic effects (i.e. QTLs with effects that are in the opposite direction to parental differences for those traits). To assess whether this genetic architecture is common, we tabulated the direction of allelic effects for 3252 QTLs from 749 traits and 96 studies. Most traits (63.6%) had at least one antagonistic QTL, indicating that the genetic substrate for transgressive segregation is common. Plants had significantly more antagonistic QTLs than animals, which agrees with previous reports that transgressive segregation is more common in plants than in animals. Likewise, antagonistic QTLs were more frequent in intrathan in interspecific crosses and in morphological than in physiological traits. These results indicate that transgressive segregation provides a general mechanism for the production of extreme phenotypes at both above and below the species level and testify to the possible creative part of hybridization in adaptive evolution and speciation.

Selection is widely accepted as the principal force shaping phenotypic variation within populations. Its importance in speciation and macroevolution has been questioned, however, because phenotypic differences between species or higher taxa sometimes appear to be nonadaptive. Here, we use the quantitative trait locus (QTL) sign test to evaluate the importance of directional selection in phenotypic divergence. If a trait has a history of directional selection, QTL effects should be mostly in the same direction; otherwise QTLs with antagonistic effects should be common. Analysis of QTL effects for 572 traits from 86 studies revealed significantly fewer antagonistic QTLs than expected under neutrality, a result that validates Darwin's claim that phenotypic diversification is caused mainly by selection. Moreover, interspecific trait differences were more strongly or consistently selected than intraspecific differences, strengthening a growing consensus among students of speciation that directional selection is the primary cause of speciation. Contrary to studies of selection in contemporary populations, life history traits appear to be selected more strongly than morphological traits, but traits related to the timing of development are weakly selected relative to most other traits. It is often lamented that studies of present-day populations provide only the briefest snapshot of evolution and tell us little about the evolutionary forces that have shaped a particular trait or organism in the past (1). Although ancestral phenotypes can be reconstructed with phylogenetic methods (2) or directly determined from fossils (3), neither approach reveals the evolutionary processes that created these phenotypes. Even if these historical data could help, there is considerable uncertainty associated with the reconstruction of ancestral character states (4), and a fossil record is missing for most taxa and incomplete for others. As a result, a direct link between the action of microevolutionary forces detected in studies of contemporary populations and patterns of speciation and macroevolution has been difficult to make (1), yet this is a central problem in evolutionary biology.A possible method for reconstructing the selective history of complex traits has, however, recently been proposed (5). The method is based on the direction of effects of quantitative trait loci (QTLs) that contribute to phenotypic differences. If a trait has had a continuous history of directional selection, then QTL effects should be in the same direction within a line. In contrast, if a trait has diverged under neutrality, QTLs with opposing or antagonistic effects should be common. This approach has been formalized as the QTL sign test (5), which compares the proportion of antagonistic QTLs in a given line with those predicted under neutral conditions.In this article, we review the QTL literature to estimate the distribution of plus and minus QTL alleles for different kinds of organisms and for different kinds of traits. Three comparisons were of partic...

Evaluating the genetic architecture of sexual dimorphism can aid our understanding of the extent to which shared genetic control of trait variation versus sex-specific control impacts the evolutionary dynamics of phenotypic change within each sex. We performed a QTL analysis on Silene latifolia to evaluate the contribution of sex-specific QTL to phenotypic variation in 46 traits, whether traits involved in trade-offs had colocalized QTL, and whether the distribution of sex-specific loci can explain differences between the sexes in their variance/covariance matrices. We used a backcross generation derived from two artificial-selection lines. We found that sex-specific QTL explained a significantly greater percent of the variation in sexually dimorphic traits than loci expressed in both sexes. Genetically correlated traits often had colocalized QTL, whose signs were in the expected direction. Lastly, traits with different genetic correlations within the sexes displayed a disproportionately high number of sex-specific QTL, and more QTL co-occurred in males than females, suggesting greater trait integration. These results show that sex differences in QTL patterns are congruent with theory on the resolution of sexual conflict and differences based on G-matrix results. They also suggest that trade-offs and trait integration are likely to affect males more than females. K E Y W O R D S :Artificial selection, genetic correlations, linkage map, sex-specific expression, sexual conflict.

Sexual dimorphism is one of the most widespread and recognizable patterns of phenotypic variation in the biotic world. Sexual dimorphism in floral display is striking in the dioecious plant Silene latifolia, with males making many, small flowers compared to females. We investigated this dimorphism via artificial selection on two populations to determine whether genetic variation exists within populations for flower size and the extent of the between-sex correlation, whether a flower size and number trade-off exists within each sex, and whether pollen and ovule production vary with flower size. We selected for decreased flower size (calyx width) in females and increased flower size in males and measured the response to selection in size and correlated responses in flower dry mass, flower number, and pollen or ovule number per flower. Four bouts of selection in each of two selection programs were performed, for a total of three selection lines to decrease size, three to increase it, and two control lines. Flower size always significantly responded to selection and we always found a significant correlated response in the sex not under selection. Selection decreased but did not eliminate the sexual dimorphism in flower dry mass and number. A negative relationship between flower size and number within each sex was revealed. Whereas ovule number showed a significant correlated response to selection on flower size, pollen number did not. Our results indicate that although substantial additive genetic variation for flower size exists, the high between-sex genetic correlation would likely constrain flower size from becoming more sexually dimorphic. Furthermore, floral display within each sex is constrained by a flower size and number trade-off. Given this trade-off and lack of variation in pollen production with flower size, we suggest that sexual dimorphism evolved via sexual selection to increase flower number in males but not females.

A recurring theme in defense allocation theories is that defenses are costly. Most studies that attempt to quantify a cost of defense seek to establish a trade-off between a component of plant fitness and the level of a constitutive defense. Such estimates are ambiguous because they cannot discount the cost of traits that are correlated with defense but are not themselves defensive. We examined the effects of damage-induced synthesis of furanocoumarins, known defense compounds, on the growth of wild parsnip. Plants that had 2% of their leaf area removed accumulated 8.6% less total biomass and 14% less root biomass than intact plants over a 4-week period. We also found that this small amount of leaf damage significantly reduced net photosynthetic rates 0.5 h after damage; the effect was temporary, as photosynthetic rates were no longer significantly different after 48 h. Lastly, we found that increases in respiration rates associated with damage coincided spatially and temporally with increases in furanocoumarin production, and that respiration increases were phenotypically correlated with furanocoumarin production. When damage-induced changes in furanocoumarin content and respiration rates were expressed in glucose equivalents and compared, the energetic cost of furanocoumarin production (12.6 μg glucose cm) accounted for all of the increase in respiration (12.0 μg glucose cm). A comparison of other secondary compounds in damaged and intact leaflets revealed that myristicin, a furanocoumarin synergist, is the only other compound aside from furanocoumarins that is inducible. The inducible defense system of wild parsnip thus appears to involve a small subset of secondary compounds. Synthesis of these compounds is tightly linked to damage-induced rates of respiration. Because the negative impact that damage had on the rate of net photosynthesis was short-lived, the impact of damage on growth observed in this study was likely due to the cost of furanocoumarin synthesis elicited by damage rather than the loss of photosynthetic tissue caused by damage.