Can evolution of sexual dimorphism be triggered by developmental temperatures?

Genetic prerequisites for the evolution of sexual dimorphism, sex-specific heritabilities and low or negative genetic correlations between homologous traits in males and females are rarely found. However, sexual dimorphism is evolving rapidly following environmental change, suggesting that sexual dimorphism and its genetic background could be environmentally sensitive. Yet few studies have explored the sensitivity of the genetic background of sexual dimorphism on environmental variation. In this study, on Drosophila melanogaster, we used a large nested full-sib-half-sib breeding design where families were split into four different developmental temperatures: two constant temperature treatments of 25 and 30 °C and two cycling temperatures with means of 25 and 30 °C, respectively. After emergence, we tested heat shock tolerance of adult flies. We found that sexual dimorphism was strongly affected by temperature during development. Moreover, we found that female heritability was significantly lower in flies developing at hot temperature and more so under hot and cycling temperatures. Interestingly, most of the genetic variation for heat shock tolerance was orthogonal (i.e. noncorrelated) between sexes, allowing independent evolution of heat shock tolerance in males and females. These findings give support to the hypothesis that the evolution of sexual dimorphism can be influenced by the environments experienced during development.     

Pupal Melanization in Heliconius erato phyllis (Lepidoptera; Nymphalidae): Genetic and Environmental Effects

This paper deals with estimates of heritability and the effect of two different kinds of environment on the melanization of pupae in the butterfly Heliconius erato phyllis. The results for heritability showed greater differences when the offspring were regressed on male or female values for pupal colour. Pupal colour followed a system of discrete scores, from 2 for the light pupae to 5 for the darkest one. Estimate of the heritability (h²) was 0.44 when the average score of the siblings were regressed on the mid-parental value. When regressed on the male parent, h² was larger (0.54), being very low when regressed on the female parent (0.09). Estimate by the analysis of variance was also 0.44 when both male and female sibs were included in the analysis (for male sibs, h²=0.43 and for female sibs, 0.47). To test for the effect of the environment, each brood was divided in three, one being the control, the second subjected to a black environment when reaching the fifth instar and the third to a white environment. Those in the black environment originated dark pupae that scored 5 or 4; for those in the white environment, there was no difference with the controls. Caterpillars when entering the prepupal stage were also subjected to the black treatment (early and late prepupal stage, respectively, for treatments called black A and black B). A significant effect was observed only when early prepupal stage was subjected to the black environment.     

Haploinsufficiency in the PPARalpha and LDL receptor genes leads to gender- and age-specific obesity and hyperinsulinemia

When preparing peroxisome proliferator-activated receptor (PPAR)alpha:low-density lipoprotein receptor (LDLR) (-/-) double knockout mice, we unexpectedly found a unique gender- and age-specific obesity in the F1 generation, PPARalpha (+/-):LDLR (+/-), even in mice fed standard chow. Body weights of the male heterozygous mice increased up to about 60 g at 75 weeks of age, then decreased by about 30 g at 100 weeks of age. More than 95% of the heterozygous mice between 35- and 75-week-olds were overweight. Of interest, the obese heterozygous mice also exhibited hyperinsulinemia correlating with moderate insulin resistance. Hepatic gene expression of LDLR was lower than expected in the heterozygous mice, particularly at 50 and 75 weeks of age. In contrast, the hepatic expression of PPARalpha was higher than expected in obese heterozygous mice, but decreased in non-obese older heterozygous mice. Modulated expression of these genes may be partially associated with the onset of the hyperinsulinemia.     

EASY AND FLEXIBLE BAYESIAN INFERENCE OF QUANTITATIVE GENETIC PARAMETERS

There has been a tremendous advancement of Bayesian methodology in quantitative genetics and evolutionary biology. Still, there are relatively few publications that apply this methodology, probably because the availability of multipurpose and user-friendly software is somewhat limited. It is here described how only a few rows of code of the well-developed and very flexible Bayesian software WinBUGS ( Lunn et al. 2000 ) can be used for inference of the additive polygenic variance and heritabilty in pedigrees of general design. The presented code is illustrated by application to an earlier published dataset of Scots pine.     

Quantitative genetic estimates of growth-related traits in the common carp (Cyprinus carpio L.): A review

The common carp (Cyrpinus carpio L.) is the oldest cultured and the most domesticated fish species, as well as one of the most important freshwater fishes in the world. However, scientific studies on evaluating the growth-related quantitative traits in this fish are limited. Heritability, the most important parameter in selective breeding programs, was extensively studied for the growth-related traits. The values varied widely among the experiments and methods used because of the existence of common environmental, dominance and maternal effects. However, correlations in phenotypic and genetic levels first evaluated several years ago were limited. On the other hand, heterosis was widely reported and easily obtained for growth-related traits in the common carp. Meanwhile, genotype environment interaction and prediction of breeding values have been studied recently, and are very important in conducting selective breeding programs. The developmental quantitative genetics of growth-related traits was first analyzed in the common carp for reasonable selection during ontogeny. It is expected that genetic improvement will be achieved by carrying out direct selective breeding in the common carp.     

Testing the heritability and parent-of-origin hypotheses for ages at onset of psoriatic arthritis under biased sampling

The heritability and parent-of-origin effect hypotheses for chronic diseases can be evaluated by estimating and conducting inference about the parameters that measure the within-family dependences in disease onset times. We model the within-family associations in these times using a Gaussian copula whose correlation matrix accommodates the different pairwise family relationships. We derive score-type statistics to test the heritability and parent-of-origin effect hypotheses when the families selection protocol induces a sampling bias. We illustrate the use of the developed methods through an application to a motivating family study in Psoriatic arthritis and provide strong evidence of excessive paternal transmission of risk.     

SNP-based heritability and genetic architecture of cranial cruciate ligament rupture in Labrador Retrievers

Cranial cruciate ligament rupture (CCLR) is one of the leading causes of pelvic limb lameness in dogs. About 6% of Labrador Retrievers suffer from this orthopedic problem. The aim of this study was to determine the heritability of CCLR in this breed using SNP array genotyping data. DNA samples were collected from CCLR-affected dogs (n = 190) and unaffected dogs over the age of 8 years (n = 143). All 333 dogs were genotyped directly or imputed up to approximately 710k SNPs on the Affymetrix Axiom CanineHD SNP array. Heritability of CCLR was calculated using multiple methodologies, including linear mixed models, Bayesian models and a model that incorporates LD. The covariates of sex and sterilization status were added to each analysis to assess their impact. Across the algorithms of these models, heritability ranged from 0.550 to 0.886, depending on covariate inclusion. The relatively high heritability for this disease indicates that a substantial genetic component contributes to CCLR in the Labrador Retriever.     

Germline epigenetic inheritance: Challenges and opportunities for linking human paternal experience with offspring biology and health

Recently, novel experimental approaches and molecular techniques have demonstrated that a male's experiences can be transmitted through his germline via epigenetic processes. These findings suggest that paternal exposures influence phenotypic variation in unexposed progeny–a proposal that runs counter to canonical ideas about inheritance developed during the 20th century. Nevertheless, support for paternal germline epigenetic inheritance (GEI) in nonhuman mammals continues to grow and the mechanisms underlying this phenomenon are becoming clearer. To what extent do similar processes operate in humans, and if so, what are their implications for understanding human phenotypic variation, health, and evolution? Here, we review evidence for GEI in human and nonhuman mammals and evaluate these findings in relation to historical conceptions of heredity. Drawing on epidemiological data, reproductive biology, and molecular embryology, we outline developments and opportunities for the study of GEI in human populations, emphasizing the challenges that researchers in this area still face.