Colour polymorphism in vertebrates is usually under genetic control and may be associated with variation in physiological traits. The melanocortin 1 receptor (Mc1r) has been involved repeatedly in melanin-based pigmentation but it was thought to have few other physiological effects. However, recent pharmacological studies suggest that MC1R could regulate the aspects of immunity. We investigated whether variation at Mc1r underpins plumage colouration in the Eleonora’s falcon. We also examined whether nestlings of the different morphs differed in their inflammatory response induced by phytohemagglutinin (PHA). Variation in colouration was due to a deletion of four amino acids at the Mc1r gene. Cellular immune response was morph specific. In males, but not in females, dark nestling mounted a lower PHA response than pale ones. Although correlative, our results raise the neglected possibility that MC1R has pleiotropic effects, suggesting a potential role of immune capacity and pathogen pressure on the maintenance of colour polymorphism in this species.
In long-lived species, the age-, stage- and/or sex-dependent patterns of survival and reproduction determine the evolution of life history strategies, the shape of the reproductive value, and ultimately population dynamics. We evaluate the combined effects of age and sex in recruitment, breeder survival and breeding success of the globally endangered Egyptian vulture (Neophron percnopterus), using 31-years of exhaustive data on marked individuals in Spain. Mean age of first reproduction was 7-yrs for both sexes, but females showed an earlier median and a larger variance than males. We found an age-related improvement in breeding success at the population level responding to the selective appearance and disappearance of phenotypes of different quality but unrelated to within-individual aging effects. Old males (≥8 yrs) showed a higher survival than both young males (≤7 yrs) and females, these later in turn not showing aging effects. Evolutionary trade-offs between age of recruitment and fitness (probably related to costs of territory acquisition and defense) as well as human-related mortality may explain these findings. Sex- and age-related differences in foraging strategies and susceptibility to toxics could be behind the relatively low survival of females and young males, adding a new concern for the conservation of this endangered species.
The major histocompatibility complex (MHC), which harbours the most polymorphic vertebrate genes, plays a critical role in the host–pathogen coevolutionary arms race. However, the extent to which MHC diversity determines disease susceptibility and long‐term persistence of populations is currently under debate, as recent studies have demonstrated that low MHC variability does not necessarily hamper population viability. However, these studies typically assayed small and decimated populations in species with restricted distribution, thereby making inferences about the evolutionary potential of these populations difficult. Here, we show that MHC impoverishment has not constrained the ecological radiation and flourishing of falcons (Aves: Falconidae) worldwide. We found two remarkably different patterns of MHC variation within the genus Falco. Whereas MHC variation in kestrels (the basal group within the genus) is very high, falcons exhibit ancestrally low intra‐ and interspecific MHC variability. This pattern is not due to the inadvertent survey of paralogous genes or pseudogenes. Further, patterns of variation in mitochondrial or other nuclear genes do not indicate a generalized low level of genome‐wide variability among falcons. Although a relative contribution of genetic drift cannot be completely ruled out, we propose the falcons went through an evolutionary transition, driven and maintained by natural selection, from primarily highly variable towards low polymorphic and slow‐evolving MHC genes with a very specific immune function. This study highlights that the importance of MHC diversity cannot be generalized among vertebrates, and hints at the evolution of compensatory immune mechanisms in falcons to cope with emerging and continuously evolving pathogens.
Colour polymorphism results from the expression of multiallelic genes generating phenotypes with very distinctive colourations. Most colour polymorphisms are due to differences in the type or amount of melanins present in each morph, which also differ in several behavioural, morphometric and physiological attributes. Melanin-based colour morphs could also differ in the levels of glutathione (GSH), a key intracellular antioxidant, because of the role of this molecule in melanogenesis. As GSH inhibits the synthesis of eumelanin (i.e. the darkest melanin form), individuals of darker morphs are expected to have lower GSH levels than those of lighter morphs. We tested this prediction in nestlings of two polymorphic raptors, the booted eagle Hieraaetus pennatus and the Eleonora's falcon Falco eleonorae, both of which occur in two morphs differing in the extent of eumelanic plumage. As expected, melanic booted eagle nestlings had lower blood GSH levels than light morph eagle nestlings. In the Eleonora's falcon, however, melanic nestlings only had lower GSH levels after controlling for the levels of other antioxidants. We also found that melanic female eagle nestlings had higher levels of antioxidants other than GSH and were in better body condition than light female eagle nestlings. These findings suggest an adaptive response of melanic nestlings to compensate for reduced GSH levels. Nevertheless, these associations were not found in falcons, indicating species-specific particularities in antioxidant machinery. Our results are consistent with previous work revealing the importance of GSH on the expression of melanic characters that show continuous variation, and suggest that this pathway also applies to discrete colour morphs. We suggest that the need to maintain low GSH levels for eumelanogenesis in dark morph individuals may represent a physiological constraint that helps regulate the evolution and maintenance of polymorphisms.