Elevated oxidative stress in pied flycatcher nestlings of eumelanic foster fathers under low rearing temperatures.

Striking variation in melanin coloration within natural populations is likely due to the different fitness outcomes of alternative phenotypes in varying environmental conditions. There are two types of melanin: eumelanins yield blackish hues, whereas pheomelanins yield reddish hues. The production of eumelanins requires low levels of glutathione (GSH), which is the most important intracellular antioxidant, whereas the production of pheomelanins requires high levels of GSH. We investigated the oxidative status of male pied flycatchers (Ficedula hypoleuca) with different degrees of melanin coloration under different temperatures during the nestling period. Moreover, we assessed the oxidative status of offspring in relation to their biological or foster father's melanin coloration and ambient temperature. To separate offspring genotype effects and paternal effects in different temperatures, we used a partial cross-foster design. The temperature differently affected the oxidative status of differently colored male pied flycatchers and their foster offspring. When the weather was relatively cold, black males had higher glutathione S-transferase levels compared with brown males, indicating enhanced stress in black males. Foster offspring of black males had a lower ratio between reduced and oxidized GSH followed by higher total amount of GSH than foster offspring of brown males. Thus, foster offspring of black males seem to suffer from oxidative stress under relatively cold weather compared with those of brown males, and vice versa under relatively warm weather. Although differently colored males experienced changes in their oxidative status under different temperatures, the link between paternal melanin coloration and offspring oxidative stress appears to be environmentally induced.

Major histocompatibility complex heterozygosity enhances reproductive success.

We investigated how heterozygosity at the major histocompatibility complex (MHC) affects fitness in wild-derived (F2) house mice (Mus musculus musculus). To compare and control for potential confounding effects from close inbreeding and genome-wide heterozygosity, we used mice that were systematically outbred. We assessed how heterozygosity at MHC and background loci (using 15 microsatellite markers on 11 different chromosomes) affects individual survival and reproductive success (RS) in large, semi-natural population enclosures. We found that overall heterozygosity significantly increased RS, and this correlation was entirely explained by heterozygosity at two MHC loci. Moreover, we found that the effects of MHC heterozygosity depend on the level of background heterozygosity, and the benefits of maximal MHC heterozygosity show a curvilinear effect with increasing background heterozygosity. The enhanced RS from MHC heterozygosity was not because of increased survival, and although MHC heterozygosity was correlated with body mass, body mass did not correlate with RS when heterozygosity is controlled. Breeders were more MHC heterozygous than nonbreeders for both sexes, indicating that MHC heterozygosity enhanced fecundity, mating success or both. Our results show that (i) MHC heterozygosity enhances fitness among wild, outbred as well as congenic laboratory mice; (ii) heterozygosity-fitness correlations can potentially be explained by a few loci, such as MHC; (iii) MHC heterozygosity can increase fitness, even without affecting survival, by increasing mating and RS; and (iv) MHC effects depend on background genes, and maximal MHC heterozygosity is most beneficial at intermediate or optimal levels of background heterozygosity.

Experimental infection magnifies inbreeding depression in house mice.

It is often assumed that inbreeding reduces resistance to pathogens, yet there are few experimental tests of this idea in vertebrates, and no tests for the effects of moderate levels of inbreeding more commonly found in nature. We mated wild-derived mice with siblings or first cousins and compared the resistance of their offspring to Salmonella infection with outbred controls under laboratory and seminatural conditions. In the laboratory, full-sib inbreeding reduced resistance to Salmonella and survivorship, whereas first-cousin inbreeding had no detectable effects. In competitive population enclosures, we found that first-cousin inbreeding reduced male fitness by 57% in infected vs. only 34% in noninfected control populations. Our study provides experimental evidence that inbreeding reduces resistance and ability to survive pathogenic infection, and moreover, it shows that even moderate inbreeding can cause significant fitness declines under naturalistic conditions of social stress, and especially with exposure to infectious agents.

Experimentally activated immune defence in female pied flycatchers results in reduced breeding success.

Traditional explanations for the negative fitness consequences of parasitism have focused on the direct pathogenic effects of infectious agents. However, because of the high selection pressure by the parasites, immune defences are likely to be costly and trade off with other fitness-related traits, such as reproductive effort. In a field experiment, we immunized breeding female flycatchers with non-pathogenic antigens (diphtheria-tetanus vaccine), which excluded the direct negative effects of parasites, in order to test the consequences of activated immune defence on hosts' investment in reproduction and self-maintenance. Immunized females decreased their feeding effort and investment in self-maintenance (rectrix regrowth) and had lower reproductive output (fledgling quality and number) than control females injected with saline. Our results reveal the phenotypic cost of immune defence by showing that an activated immune system per se can lower the host's breeding success. This may be caused by an energetic or nutritional trade-off between immune function and physical workload when feeding young or be an adaptive response to 'infection' to avoid physiological disorders such as oxidative stress and immunopathology.