Book reviews

Environmental Biology of Fishes -     

THE EVOLUTION OF GENETIC CORRELATIONS: AN ANALYSIS OF PATTERNS

The genetic correlation is a central parameter of quantitative genetics, providing a measure of the rate at which traits respond to indirect selection (i.e., selection that does not act upon the traits under study, but some other trait with which they have genes in common). In this paper, I review the pattern of variation among four combinations of traits: life history × life history (L × L), morphological × morphological (M × M), life history × morphological (L × M), and behavioral × behavioral (B × B). A few other combinations were investigated, but insufficient data were obtained for separate analysis. A total of 1798 correlations, distributed over 51 different animal and plant species, were analyzed. The analysis was conducted at two levels: first by dividing the data set solely by trait combination, and second by blocking the data by trait combination and species. Because selection will tend to fix alleles that show positive correlations with fitness traits faster than those that are negative and because the latter are expected to arise more frequently by mutation, correlations between life-history traits are predicted to be more often negative than those between morphological traits. This prediction was supported, with the ranking in decreasing proportion of negative correlations being: L × L > L × M > B × B > M × M. The mean magnitude of the genetic correlation shows little variation among morphological and life-history combinations, and the distribution of values is remarkably flat. However, the estimated standard errors and the coefficient of variation (SE/r_G) are large, making it difficult to separate biological factors influencing the pattern of dispersion from experimental error. Analysis of the phenotypic and genetic correlations suggest that for the combinations M × M and L × M, but not L × L or B × B, the phenotypic correlation is an adequate estimate of the genetic correlation.     

Are we underestimating the genetic variances of dimorphic traits?

Populations often contain discrete classes or morphs (e.g., sexual dimorphisms, wing dimorphisms, trophic dimorphisms) characterized by distinct patterns of trait expression. In quantitative genetic analyses, the different morphs can be considered as different environments within which traits are expressed. Genetic variances and covariances can then be estimated independently for each morph or in a combined analysis. In the latter case, morphs can be considered as separate environments in a bivariate analysis or entered as fixed effects in a univariate analysis. Although a common approach, we demonstrate that the latter produces downwardly biased estimates of additive genetic variance and heritability unless the quantitative genetic architecture of the traits concerned is perfectly correlated between the morphs. This result is derived for four widely used quantitative genetic variance partitioning methods. Given that theory predicts the evolution of genotype‐by‐environment (morph) interactions as a consequence of selection favoring different trait combinations in each morph, we argue that perfect correlations between the genetic architectures of the different morphs are unlikely. A sampling of the recent literature indicates that the majority of researchers studying traits expressed in different morphs recognize this and do estimate morph‐specific quantitative genetic architecture. However, ca. 16% of the studies in our sample utilized only univariate, fixed‐effects models. We caution against this approach and recommend that it be used only if supported by evidence that the genetic architectures of the different morphs do not differ.     

Intra‐ and trans‐generational effects of larval diet on susceptibility to an entomopathogenic fungus,Beauveria bassiana,in the greater wax moth,Galleria mellonella

In addition to nutritional conditions experienced by individuals themselves, those experienced by their parents can affect their immune function. Here, we studied the intra‐ and trans‐generational effects of larval diet on susceptibility to an entomopathogenic fungus, Beauveria bassiana, in the greater wax moth, Galleria mellonella. In the first part of the study, a split‐brood design was used to compare the susceptibility of full sibs raised either on low‐ or on high‐nutrition larval diet. In the second part of the study, a similar experimental design was employed to investigate the effects of maternal and paternal diet as well as their interaction on offspring's susceptibility. In the first part of the study, we found that individuals fed with high‐nutrition diet had higher mortality from infection than individuals fed with low‐nutrition diet. However, diet did not affect post‐infection survival time. Conversely, in the second part of the study, maternal diet was found to have no significant effect on final mortality rate of offspring, but it affected survival time: larvae with high‐nutrition maternal diet survived fewer days after infection than larvae with low‐nutrition maternal diet. Paternal diet had no significant effect on offspring's susceptibility to the fungus, indicating that paternal effects are not as important as maternal effects in influencing immune function in this species. Our findings provide further indication that maternal nutrition affects immune function in insects, and suggest that the direct effects of nutrition on immunity may be different, yet parallel, to those caused by parental nutrition.     

Interferon-Gamma Promotes Infection of Astrocytes by Trypanosoma cruzi

The inflammatory cytokine interferon-gamma (IFNγ) is crucial for immunity against intracellular pathogens such as the protozoan parasite Trypanosoma cruzi, the causative agent of Chagas disease (CD). IFNγ is a pleiotropic cytokine which regulates activation of immune and non-immune cells; however, the effect of IFNγ in the central nervous system (CNS) and astrocytes during CD is unknown. Here we show that parasite persists in the CNS of C3H/He mice chronically infected with the Colombian T. cruzi strain despite the increased expression of IFNγ mRNA. Furthermore, most of the T. cruzi-bearing cells were astrocytes located near IFNγ⁺ cells. Surprisingly, in vitro experiments revealed that pretreatment with IFNγ promoted the infection of astrocytes by T. cruzi increasing uptake and proliferation of intracellular forms, despite inducing increased production of nitric oxide (NO). Importantly, the effect of IFNγ on T. cruzi uptake and growth is completely blocked by the anti-tumor necrosis factor (TNF) antibody Infliximab and partially blocked by the inhibitor of nitric oxide synthesis L-NAME. These data support that IFNγ fuels astrocyte infection by T. cruzi and critically implicate IFNγ-stimulated T. cruzi-infected astrocytes as sources of TNF and NO, which may contribute to parasite persistence and CNS pathology in CD.     

The evolution of phenotypes and genetic parameters under preferential mating

This article extends and adds more realism to Lande's analytical model for evolution under mate choice by using individual‐based simulations in which females sample a finite number of males and the genetic architecture of the preference and preferred trait evolves. The simulations show that the equilibrium heritabilities of the preference and preferred trait and the genetic correlation between them (r_G), depend critically on aspects of the mating system (the preference function, mode of mate choice, choosiness, and number of potential mates sampled), the presence or absence of natural selection on the preferred trait, and the initial genetic parameters. Under some parameter combinations, preferential mating increased the heritability of the preferred trait, providing a possible resolution for the lek paradox. The Kirkpatrick–Barton approximation for r_G proved to be biased downward, but the realized genetic correlations were also low, generally <0.2. Such low values of r_G indicate that coevolution of the preference and preferred trait is likely to be very slow and subject to significant stochastic variation. Lande's model accurately predicted the incidence of runaway selection in the simulations, except where preferences were relative and the preferred trait was subject to natural selection. In these cases, runaways were over‐ or underestimated, depending on the number of males sampled. We conclude that rapid coevolution of preferences and preferred traits is unlikely in natural populations, but that the parameter combinations most conducive to it are most likely to occur in lekking species.