Background The trade-off between current and residual reproductive values is central to life history theory, although the possible mechanisms underlying this trade-off are largely unknown. The ‘molt constraint’ hypothesis suggests that molt and plumage functionality are compromised by the preceding breeding event, yet this candidate mechanism remains insufficiently explored. Methodology/Principal Findings The seasonal change in photoperiod was manipulated to accelerate the molt rate. This treatment simulates the case of naturally late-breeding birds. House sparrows Passer domesticus experiencing accelerated molt developed shorter flight feathers with more fault bars and body feathers with supposedly lower insulation capacity (i.e. shorter, smaller, with a higher barbule density and fewer plumulaceous barbs). However, the wing, tail and primary feather lengths were shorter in fast-molting birds if they had an inferior body condition, which has been largely overlooked in previous studies. The rachis width of flight feathers was not affected by the treatment, but it was still condition-dependent. Conclusions/Significance This study shows that sedentary birds might face evolutionary costs because of the molt rate–feather quality conflict. This is the first study to experimentally demonstrate that (1) molt rate affects several aspects of body feathers as well as flight feathers and (2) the costly effects of rapid molt are condition-specific. We conclude that molt rate and its association with feather quality might be a major mediator of life history trade-offs. Our findings also suggest a novel advantage of early breeding, i.e. the facilitation of slower molt and the condition-dependent regulation of feather growth.

Summary 1.The functional significance of intra-and interspecific structural variations in the flight feathers of birds is poorly understood. Here, a phylogenetic comparative analysis of four structural features (rachis width, barb and barbule density and porosity) of proximal and distal primary feathers of 137 European bird species was conducted. 2. Flight type (flapping and soaring, flapping and gliding, continuous flapping or passerine type), habitat (terrestrial, riparian or aquatic), wing characteristics (wing area, S and aspect ratio, AR) and moult strategy were all found to affect feather structure to some extent. Species characterized by low wing-beat frequency flight (soaring and gliding) have broader feather rachises (shafts) and feather vanes with lower barb density than birds associated with more active flapping modes of flight. However, the effect of flying mode on rachis width disappeared after controlling for S and AR, suggesting that rachis width is primarily determined by wing morphology. 3. Rachis width and feather vane density are likely related to differences in force distribution across the wingspan during different flight modes. An increase in shaft diameter, barb density and porosity from the proximal to distal wing feathers was found and was highest in species with flapping flight indicating that aerodynamic forces are more biased towards the distal feathers in flapping flyers than in soarers and gliders. 4. Habitat affected barb and barbule density, which was greatest in aquatic species, and within this group, barb density was greater in divers than non-divers, suggesting that the need for water repellency and resistance to water penetration may influence feather structure. However, we found little support for the importance of porosity in water repellency and water penetration, because porosity was similar in aquatic, riparian and terrestrial species and among the aquatic birds (divers and non-divers). We also found that barb density was affected by moult pattern. 5. Our results have broad implications for the understanding of the selection pressures driving flight feather functional morphology. Specifically, the large sample size relative to any previous studies has emphasized that the morphology of flight feathers is the result of a suite of selection pressures. As well as routine flight needs, constraints during moulting, habitat (particularly aquatic) and migratory requirements also affect flight feather morphology. Identifying the exact nature of these trade-offs will perhaps inform the reconstruction of the flying modes of extinct birds.

Parasites usurp indispensable resources for birds during a moult, and this is particularly relevant for those parasites residing in host intestines. This might compromise the nutritionally demanding moult and, thus, feather functionality. Although lower feather quality has profound and multifaceted adverse effects on residual fitness, surprisingly, little is known about parasites' effect on feather traits, especially over the longer term. We conducted an aviary experiment by medicating half of a group of naturally infested house sparrows Passer domesticus against intestinal coccidians for 15 months, spanning two consecutive postnuptial moults, whereas the other half was kept infested (i.e. without medication). Coccidian infestation significantly and negatively affected the size of the uropygial gland during the second moulting period compared to the medicated group. Furthermore, wing length was significantly shorter after the second moulting in the non-medicated compared to the medicated female birds, which indicates that the negative effects of coccidians emerge only after a prolonged exposure to parasite infestation. Non-medicated birds grew poorer quality flight feathers detected in a large number of feather traits both after the first and second moults. In the case of non-medicated birds, the primaries were lighter and shorter, and had a smaller vane area, thinner rachis and decreased stiffness, although a higher barb and barbule density, which may have various consequences for fitness through reducing flight performance. Our findings demonstrate that, besides the well-known immediate consequences for host breeding success, parasites might also have serious, long-lasting effects through influencing feather quality and, ultimately, fitness of the host.

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Large brains (relative to body size) might confer fitness benefits to animals. Although the putative costs of well-developed brains can constrain the majority of species to modest brain sizes, these costs are still poorly understood. Given that the neural tissue is energetically expensive and demands antioxidants, one potential cost of developing and maintaining large brains is increased oxidative stress ('oxidation exposure' hypothesis). Alternatively, because large-brained species exhibit slow-paced life histories, they are expected to invest more into self-maintenance such as an efficacious antioxidative defence machinery ('oxidation avoidance' hypothesis). We predict decreased antioxidant levels and/or increased oxidative damage in large-brained species in case of oxidation exposure, and the contrary in case of oxidation avoidance. We address these contrasting hypotheses for the first time by means of a phylogenetic comparative approach based on an unprecedented data set of four redox state markers from 85 European bird species. Large-brained birds suffered less oxidative damage to lipids (measured as malondialdehyde levels) and exhibited higher total nonenzymatic antioxidant capacity than small-brained birds, whereas uric acid and glutathione levels were independent of brain size. These results were not altered by potentially confounding variables and did not depend on how relative brain size was quantified. Our findings partially support the 'oxidation avoidance' hypothesis and provide a physiological explanation for the linkage of large brains with slow-paced life histories: reduced oxidative stress of large-brained birds can secure brain functionality and healthy life span, which are integral to their lifetime fitness and slow-paced life history.

Energy charge controls intermediary metabolism and cellular regulation. Here we show that inhibition of energy conservation at the level of glucose uptake, glycolysis, citric acid cycle, and oxidative phosphorylation induces cell death, leading to fragmentation of DNA into an oligonucleosomal ladder and morphological changes typical for apoptosis. Bcl-2, the prototype of oncogenes that suppress cell death, efficiently inhibits apoptosis induced by metabolic inhibitors. Bcl-2 does not antagonize the inhibitory potential of mitochondrial inhibitors, and cannot prevent or delay the decrease of the cellular ATP level subsequent to metabolic inhibition. Thus, we propose that Bcl-2 blocks apoptosis at a point downstream of the collapse of the cellular-energy homeostasis.Keywords : apoptosis ; ATP; energy conservation ; Bcl-2 ; metabolic regulation.Apoptosis, a common form of cell death, can be induced by mic reticulum (ER) membranes [15]. The mechanism of action of Bcl-2 is largely unknown. It has been shown that Bcl-2 a wide array of physiological and pathological stimuli [1,2]. This form of cell death is characterized by morphological retards diminution of the mitochondrial membrane potential (∆ψ) and reactive oxygen species (ROS) generation in T-cell changes of cellular structures, such as cell shrinkage, chromatin condensation, and membrane blebbing [1]. Molecular-biological hybridomas in response to dexamethasone and ceramide [10], protects against lipid peroxidation in IL-3Ϫdependent lymphoid studies on cell death have identified a number of genetic factors implicated in induction or suppression of apoptosis [2].progenitor cells [16] and regulates intracellular calcium repartitioning [17,18]. The biochemical mechanism of apoptosis remains elusive. The common theme emerging from most of the studies is mitoIn the present study we report that inhibition of energy conservation at the level of glycolysis, citric acid cycle or oxidachondrial dysfunction [3]. It has been shown that alterations in mitochondrial structure and function are early events in tive phosphorylation results in cell death showing oligonucleosomal DNA degradation, chromosomal condensation and apoptosis induced by tumor-necrosis factor [4,5], dexamethasone [6], oxygen radicals [7], nitric oxide [8] and activation of fragmentation, characteristics of apoptosis. Bcl-2 inhibited cell death induced by blockage of energy metabolism. However, exp53 [9]. The first signs of mitochondrial instability, reduced transmembrane potential and generation of reactive oxygen radi-pression of Bcl-2 neither blocks the activity of electron-transport-chain inhibitors, nor does it rescue cellular ATP levels. Apcals, both precede oligonucleosomal DNA fragmentation [10], a characteristic feature of apoptosis. Extensive DNA damage by parently, Bcl-2 orchestrates a protective response to depletion of cellular ATP. oxygen radicals induces activation of poly-(ADP-ribose) polymerase, leading to depletion of its substrate, NAD ϩ , and subsequently the cellular ATP pool [11]. An...

It is well known that avian brood parasites lay their eggs in the nests of other bird species, called hosts. It remains less clear, however, just how parasites are able to recognize their hosts and identify the exact location of the appropriate nests to lay their eggs in. While previous studies attributed high importance to visual signals in finding the hosts’ nests (e.g. nest building activity or the distance and direct sight of the nest from vantage points used by the brood parasites), the role of host acoustic signals during the nest searching stage has been largely neglected. We present experimental evidence that both female and male common cuckoos Cuculus canorus pay attention to their host’s, the great reed warbler’s Acrocephalus arundinaceus alarm calls, relative to the calls of an unparasitized species used as controls. Parallel to this, we found no difference between the visibility of parasitized and unparasitized nests during drone flights, but great reed warblers that alarmed more frequently experienced higher rates of parasitism. We conclude that alarm calls might be advantageous for the hosts when used against enemies or for alerting conspecifics, but can act in a detrimental manner by providing important nest location cues for eavesdropping brood parasites. Our results suggest that host alarm calls may constitute a suitable trait on which cuckoo nestlings can imprint on to recognize their primary host species later in life. Our study contributes to the growing body of knowledge regarding the context-dependency of animal signals, by providing a novel example of a beneficial acoustic trait intercepted by a heterospecific and used against the emitter.

To avoid mobbing attacks by their hosts during egg laying, some avian brood parasites have evolved traits to visually and/or acoustically resemble predator(s) of their hosts. Prior work established that reed warblers (Acrocephalus scirpaceus), a small host species of the brood parasitic common cuckoo (Cuculus canorus), delayed returning to the nest when confronted by either the calls of the female cuckoo or that of the predatory sparrowhawk (Accipiter nisus). It remains less clear, however, whether female cuckoo calls also suppress the nest defences of larger and more aggressive hosts. Such hosts typically attack vigorously, and can even hurt the brood parasitic intruders, instead of fleeing in the face of danger. Here, we tested whether the female cuckoo calls dampen mobbing intensity in a much larger Acrocephalus host of the common cuckoo, the great reed warbler (A. arundinaceus). We presented great reed warbler pairs with female common cuckoo models at their nests without and then with playing back the female‐specific bubbling calls of the cuckoo. As controls, we tested the hosts’ responses to harmless collared dove (Streptopelia decaocto) models, also without and then with the playbacks of dove calls. We found that the playback of female brood parasite calls reduced the aggression of hosts towards the cuckoo models as compared to model presentations without female calls, but we detected no such effect of the control calls with dove models. Our results revealed that female cuckoo calls effectively suppress the antiparasitic responses of great reed warbler hosts, which could aid parasites to approach the nest undiscovered and to evade the costly attacks of this large host. Therefore, the female call can be regarded as a general part of the cuckoo's trickery repertoire for successful parasitism.