寄生虫与宿主的相互作用

介绍了寄生虫对宿主的影响:降低宿主的适应性和繁殖能力;改变宿主的行为;影响宿主基因表达。同时还阐述了宿主对寄生虫的一系列抵抗行为包括:驱逐行为,梳理行为,逃避行为等。从而说明了寄生虫和宿主这对矛盾体间的相互作用关系。     

Interactions between monogenean parasites and their fish hosts

Parasite factors associated with recognition and selection of the host and the mechanisms in the host responsible for acceptance or rejection of the invading organism were evaluated. Sensory structures in parasites are able to detect differences between different fish species and this ability to discern between fishes may be based on both chemical and mechanical stimuli on the host surface. Complex glycoproteins, proteins, carbohydrates and simple molecules attract parasites or modify their behaviour. Furthermore, attachment of the monogenean parasite to a host is dependent on both mechanical structures and chemical factors in the parasite. These systems comprise anterior pads, posterior haptors, gland secretions, and muscular elements. The parasite needs access to appropriate nutrients which can be absorbed and used for reproduction and in this context signals from the host are needed for an optimal physiological response of the parasite. The innate and adaptive immune systems of the host are important elements in this question. Investigations have indicated that innate host factors (complement, lectins, acute phase reactants, macrophages) can bind to monogeneans and elicit severe damage to the parasites. The targets for these hostile products are not only the monogenean tegument, but may involve the gastrodermis and glands. However, the parasite's ability to avoid and even exploit the wide array of immunological elements of the host may be an important player in the dynamic interactions between host and monogenean determining host specificity. Even fish hosts susceptible to a certain parasite show an ability to mount a protective response at post-infection periods. Elevation of the host's production of adaptive and non-adaptive factors following monogenean infections of a certain duration may explain the acquired response.     

Population structure and the co-evolution between social parasites and their hosts

Co-evolutionary trajectories of host-parasite interactions are strongly affected by the antagonists' evolutionary potential, which in turn depends on population sizes as well as levels of recombination, mutation, and gene flow. Under similar selection pressures, the opponent with the higher evolutionary rate is expected to lead the co-evolutionary arms race and to develop local adaptations. Here, we use mitochondrial DNA sequence data and microsatellite markers to assess the amount of genetic variability and levels of gene flow in two host-parasite systems, each consisting of an ant social parasite--the European slavemaker Harpagoxenus sublaevis and the North American slavemaker Protomognathus americanus--and its two main host species. Our population genetic analyses revealed limited gene flow between individual populations of both host and parasite species, allowing for a geographic mosaic of co-evolution. In a between-system comparison, we found less genetic variability and more pronounced structure in Europe, where previous behavioural studies demonstrated strong local adaptation. Within the European host-parasite system, the larger host species Leptothorax acervorum exhibited higher levels of both genetic variability and gene flow, and previous field data showed that it is less affected by the social parasite H. sublaevis than the smaller host Leptothorax muscorum, which has genetically depleted and isolated populations. In North America, the parasite P. americanus showed higher levels of gene flow between sites, but overall less genetic diversity than its hyper-variable main host species, Temnothorax longispinosus. Interestingly, recent ecological and chemical studies demonstrated adaptation of P. americanus to local host populations, indicating the importance of migration in co-evolutionary interactions.     

Interactions between malaria parasites and their mosquito hosts in the midgut

This review examines what is presently known of the molecular interactions between Plasmodium and Anopheles that take place in the latter's midgut upon ingestion of the parasites with an infectious blood meal. In order to become 'established' in the gut and to transform into a sporozoite-producing oocyst, the malaria parasite needs to undergo different developmental steps that are often characterized by the use of selected resources provided by the mosquito vector. Moreover, some of these resources may be used by the parasite in order to overcome the insect host's defence mechanisms. The molecular partners of this interplay are now in the process of being defined and analyzed for both Plasmodium and mosquito and, thus, understood; these will be presented here in some detail.     

The interrelations between apple aphids and their parasites and hyperparasites

Zusammenfassung Es wird eine übersicht gegeben von den wichtigsten Parasiten und Hyperparasiten von drei wichtigen Blattlaus-Arten vom Apfel in Holland. (Tafel 1). Die prim?ren Parasiten wurden nur im Anfang des Frühjahrs in betr?chtlichen Zahlen gezüchtet; sp?ter wurde ihre Wirkung durch die Hyperparasiten stark reduziert oder sogar fast eliminiert (Tafel 2 und 3).      

An investigation of the relationship between innovation and cultural diversity

In this paper we apply reaction-diffusion models to explore the relationship between the rate of behavioural innovation and the level of cultural diversity. We investigate how both independent invention and the modification and refinement of established innovations impact on cultural dynamics and diversity. Further, we analyse these relationships in the presence of biases in cultural learning and find that the introduction of new variants typically increases cultural diversity substantially in the short term, but may decrease long-term diversity. Independent invention generally supports higher levels of cultural diversity than refinement. Repeated patterns of innovation through refinement generate characteristic oscillating trends in diversity, with increasing trends towards greater average diversity observed for medium but not low innovation rates. Conformity weakens the relationship between innovation and diversity. The level of cultural diversity, and pattern of temporal dynamics, potentially provide clues as to the underlying process, which can be used to interpret empirical data.     

A test of the relationship between seasonal rainfall and saguaro cacti branching patterns

Reproductive output, as well as photosynthetically active radiation interception and CO₂ uptake, increase as saguaro cacti Carnegiea gigantea (Engelm.) Britt. and Rose branch, and branching increases with increasing moisture. The Sonoran Desert experiences distinct summer and winter precipitation regimes that vary in both geography and scale. Many aspects of saguaro ecology are known to depend on the summer rains, which has resulted in an emphasis on summer rains in the literature. Similarly, branching studies have been limited geographically to areas that receive relatively high amounts of summer rainfall. These studies, therefore, attribute branching patterns to the summer (or possibly annual) rains, and conclusions reflect the summer precipitation bias.
Environmental variability in space was explored in the present study to investigate saguaro branching patterns. I collected height and branching data in thirty saguaro populations across their American range. Stepwise regression was used to determine which climate, vegetation and soil variables best predict branching. Contrary to the literature, this study found that winter precipitation, particularly from January to April, was the best predictor of branching, not summer or annual rain. Surprisingly, the relationship between the summer monsoons (July and August precipitation) and branching was negative. This is likely due to the fact that summer and winter rainfall patterns are geographically distinct. Winter precipitation appears to play a key role in branching, and thus in seed production. This suggests that saguaros benefit from moisture during the winter, possibly utilizing cold-season rains for increasing their reproductive output through branching, and challenging the view that the summer rains dominate virtually every aspect of the saguaro life-cycle, and creating a more balanced view of saguaro ecology.     

Aminergic neurons in the brain of blowflies and Drosophila: dopamine- and tyrosine hydroxylase-immunoreactive neurons and their relationship with putative histaminergic neurons

Summary The distribution and morphology of neurons reacting with antisera against dopamine (DA), tyrosine hydroxylase (TH) and histamine (HA) were analyzed in the blowflies Calliphora erythrocephala and Phormia terraenovae. TH-immunoreactive (THIR) and HA-immunoreactive (HAIR) neurons were also mapped in the fruitfly Drosophila melanogaster. The antisera against DA and TH specifically labeled the same neurons in the blowflies. About 300 neurons displayed DA immunoreactivity (DAIR) and THIR in the brain and subesophageal ganglion of the blowflies. Most of these neurons were located in bilateral clusters; some were distributed as bilateral pairs, and two ventral unpaired median (VUM) neurons were seen in the subesophageal ganglion. Immunoreactive processes were found in all compartments of the mushroom bodies except the calyces, in all divisions of the central body complex, in the medulla, lobula and lobula plate of the optic lobe, and in non-glomerular neuropil of protocerebrum, tritocerebrum and the subesophageal ganglion. No DA or TH immunoreactivity was seen in the antennal lobes. In Drosophila, neurons homologous to the blowfly neurons were detected with the TH antiserum. In Phormia and Drosophila, 18 HA-immunoreactive neurons were located in the protocerebrum and 2 in the subesophageal ganglion. The HAIR neurons arborized extensively, but except for processes in the lobula, all HAIR processes were seen in non-glomerular neuropil. The deuto- and tritocerebrum was devoid of HAIR processes. Double labeling experiments demonstrated that TH and HA immunoreactivity was not colocalized in any neuron. In some regions there wasm however, substantial superposition between the two systems. The morphology of the extensively arborizing aminergic neurons described suggests that they have modulatory functions in the brain and subesophageal ganglion.     

Exploring the relationship between incidence and the average age of infection during seasonal epidemics

The inverse relationship between the incidence and the average age of first infection for immunizing agents has become a basic tenet in the theory underlying the mathematical modeling of infectious diseases. However, this relationship assumes that the infection has reached an endemic equilibrium. In reality, most infectious diseases exhibit seasonal and/or long-term oscillations in incidence. We use a seasonally forced age-structured SIR model to explore the relationship between the number of cases and the average age of first infection over a single epidemic cycle. Contrary to the relationship for the equilibrium dynamics, we find that the average age of first infection is greatest at or near the peak of the epidemic when mixing is homogeneous. We explore the sensitivity of our findings to assumptions about the natural history of infection, population mixing behavior, the mechanism of seasonality, and of the timing of case reporting in relation to the infectious period. We conclude that seasonal variation in the average age of first infection tends to be greatest for acute infections, and the relationship between the number of cases and the average age of first infection can vary depending on the nature of population mixing and the natural history of infection.     

An evolving picture of the interactions between malaria parasites and their host erythrocytes

In patients with malaria, Plasmodium falciparum parasites multiply to enormous numbers in the bloodstream, initiating processes of erythrocyte destruction, endothelial activation and microvascular inflammation that cause devastating pathological effects on host tissues and organs. Recent research casts new light on a mechanism by which hemoglobin mutations may protect against these effects, and on a critical receptor-ligand interaction that provides fresh opportunities for the development of vaccines against blood-stage infection.The symptoms of malaria occur in the period of the Plasmodium life cycle when erythrocytes are infested by parasites. This period commences when parasites emerge from the liver after replicating from the sporozoites introduced by a mosquito bite. The new blood-stage parasites multiply quickly as haploid, asexual forms in one-, two- or three-day cycles (depending on the Plasmodium species) and increase their numbers enormously, often infecting 1% or more of the trillions of erythrocytes in the bloodstream. These populations of asexual forms are required for the production of sexual gametocyte forms that enter feeding mosquitoes, in which the parasites mate and produce new sporozoites for transmission to other human hosts. While large numbers of erythrocytes support the propagation and survival of malaria parasites, the inflammatory and erythrocyte-destroying effects of the parasite biomass cause devastating pathological effects on host tissues and organs.These pathological effects and the deaths that they cause have exerted powerful selection pressure on the human genome over thousands of generations. Outcomes of this pressure include the sickle cell hemoglobin (HbS) mutation, which protects young children against the life-threatening complications of Plasmodium falciparum malaria, and various blood group antigens, which affect the ligand-receptor interactions utilized by different Plasmodium parasites for erythrocyte invasion. Two recent papers in Science and Nature offer fresh and interesting discoveries from research in these areas: (i) a molecular mechanism by which mutation of hemoglobin may protect against malaria ¹, and (ii) a newly discovered ligand-receptor interaction that may be critical for P. falciparum invasion of human erythrocytes ².HbS represents a classic example of a balanced polymorphism: the heterozygous sickle cell trait (HbAS, from the inheritance of one normal HbA and one sickle HbS β-globin-coding gene) protects against severe life-threatening malaria, while the homozygous HbAA condition offers no protection from malaria and the homozygous HbSS condition produces frequent fatalities from sickle cell anemia ³. Although early studies implicated poor growth of P. falciparum in HbAS erythrocytes as a mechanism of protection that keeps parasitemias low, other work found that laboratory-adapted parasite clones grew normally in HbAS erythrocytes even under reduced oxygen conditions ^{4, 5}. Further, it was clear that substantial parasitemias and frequent episodes of uncomplicated malaria occurred in HbAS as well as HbAA children, despite marked differences in the incidence of severe malaria between these groups ⁶. Differential protection against severe malaria is also provided by hemoglobin C (HbC) in West Africa ⁷. These field observations suggest a mechanism of protection that, instead of merely reducing the numbers of parasitized erythrocytes in the circulation, works to ameliorate the inflammation that arises at the host-parasite interface from the interactions of infected erythrocytes with the endothelium and other blood elements. Indeed, parasitized HbAC and HbAS erythrocytes show significant impairment of cytoadherence in association with perturbed display of the P. falciparum major cytoadherence protein (PfEMP1) on abnormal knob protrusions ^{5, 8}.Using cryo-electron tomography, Cryklaff et al. ¹ show that P. falciparum hijacks and remodels erythrocyte actin into a network that may support the trafficking of PfEMP1 and other virulence proteins to the host cell membrane, where these proteins form the knobs involved in sequestration-related events and inflammation (Figure 1). Branching patterns of actin were found in association with Maurer''s clefts, membranous compartments that have an important role in exporting proteins from the parasite to the periphery of the host cell cytoplasm ⁹. Further, Cryklaff et al. ¹ observed significantly reduced actin remodeling and aberrant Maurer''s clefts in HbCC and HbSC erythrocytes, suggesting that these mutant hemoglobin states may interfere with the installation of actin scaffolds that help to tether Maurer''s clefts and support vesicle and protein trafficking to the erythrocyte membrane.Open in a separate windowFigure 1Junctures of pathogenesis in P. falciparum malaria: cytoadherence of parasitized erythrocytes to microvascular endothelium and parasite invasion of erythrocytes. P. falciparum parasites display knobs at the surface of their host erythrocytes as they mature from ring to trophozoite and schizont forms. PfEMP1 cytoadherence proteins are concentrated on knobs, where they bind receptors (e.g., CD36 and ICAM-1), activate endothelial cells, and recruit blood elements including platelets and white blood cells. By adhering in microvessels, the mature parasites avoid being carried by the bloodstream to the spleen where they are destroyed. Sequestration-related events lead to upregulation of tissue factor, resulting in thrombin and complement activation, platelet activation, cytokine production, endothelial dysfunction and inflammation ¹⁴. To support the transport of PfEMP1 and other proteins including the knob-associated histidine-rich protein (KAHRP) to the erythrocyte membrane, P. falciparum parasites tether membranous Maurer''s clefts beneath the cytoskeleton ⁹. In knobs, PfEMP1 associates with KAHRP anchored to spectrin-actin-protein 4.1 complexes, to spectrin-actin junctions, and to the band 3-binding domain of ankyrin ^{15, 16}. Cryklaff et al. ¹ report that P. falciparum remodels host actin into a network of filaments associated with Maurer''s clefts and the erythrocyte membrane; this network may support protein and vesicle trafficking to the knobs. Hemoglobin variants HbS and HbC interfere with proper knob formation and PfEMP1 display, weaken the binding of parasitized erythrocytes to endothelium and may thereby reduce sequestration-related pathology ^{5, 8}. Aberrant Maurer''s clefts and compromised remodeling of the actin network occur in HbSC and HbCC erythrocytes ¹; these abnormalities remain to be demonstrated in HbAS and HbAC erythrocytes. Inset (left) is adapted from ref ¹⁷. Merozoites released from mature schizonts invade erythrocytes by steps of initial contact, reorientation with attachment, junction formation, and entry and membrane resealing. Most members of the PfEBL and PfRH protein families have overlapping and individually dispensable functions that support a diversity of invasion pathways by attachment to different blood group antigens. These events are followed by binding of P. falciparum AMA1 and RON proteins at the attachment interface, triggering junction formation (not shown) ¹⁸. The interaction of the PfRH5-PfRipr complex ¹² with basigin ² appears to be essential for invasion and may have a critical function beyond the roles of binding and attachment that characterize other members of the PfEBL and PfRH families. Inset (right) is adapted from ref ¹⁸.Are there also significant differences between the actin networks and/or Maurer''s clefts of HbAS, HbAC and HbAA erythrocytes? HbAS and HbAC are, after all, the prevalent malaria-protective states of HbS and HbC. On this question the report of Cryklaff et al. ¹ is unfortunately silent; actin remodeling and Maurer''s clefts in HbAS and HbAC erythrocytes still need to be investigated, as do the effects of HbAS and HbAC erythrocyte extracts on actin polymerization in vitro. Mechanisms apart from disturbed actin remodeling may still account for abnormal PfEMP1 display and knob formation on parasitized HbAC and HbAS erythrocytes. For example, hemichromes generated more readily from oxidation of HbC or HbS may physically hinder the docking of virulence proteins and thus interrupt the formation of regular knob arrays in the erythrocyte cytoskeleton (where hemichromes are known to bind). Another possibility is that HbC and HbS elevate the levels of oxidative stress in parasitized erythrocytes, damaging membranes and biochemically hampering the functions of Maurer''s clefts and their associated vesicles in the transport of knob-forming proteins. The challenge for the research field in the coming years will be to sort out these possible mechanisms and their contributions to malaria protection by the heterozygous HbAS and HbAC conditions.P. falciparum invades erythrocytes by various pathways involving different ligand-receptor interactions ¹⁰. Partner ligands in these interactions include members of two molecular families known as the EBA (erythrocyte binding antigen) and RBL (reticulocyte binding-like) proteins. In P. falciparum, members of these families are termed PfEBL (P. falciparum erythrocyte binding-like) and PfRH (P. falciparum reticulocyte binding-like homolog) proteins. Evidence suggests that the roles of many of these proteins are overlapping: P. falciparum lines can often invade erythrocytes that lack receptors for specific PfEBL or PfRH proteins (because of inherent mutations or enzyme treatment) and, conversely, knockout parasites that do not express individual PfEBL or PfRH proteins have been found to efficiently invade erythrocytes. It thus came as a surprise that focused efforts to knock out the gene encoding an atypical, foreshortened member of the PfRH family, PfRH5, did not succeed in two laboratories ^{10, 11}. While polymorphisms in PfRH5 could be linked to receptor preferences and an ability of a P. falciparum line to also invade Aotus monkey erythrocytes ¹¹, the function of PfRH5 as a parasite ligand and the erythrocyte receptor(s) that it uses for invasion remained unknown.Crosnier et al. ² have now identified the PfRH5 receptor by applying an avidity-based extracellular interaction screen (AVEXIS) to the expressed proteins of an erythrocyte ectodomain library. Results show that PfRH5 binds an isoform of basigin on erythrocytes (BSG-S, the Ok blood group antigen, CD147) and that P. falciparum appears to generally require this interaction to efficiently invade human erythrocytes. In contrast to the effects of glycan removal (by neuraminidase) from Aotus erythrocytes on PfRH5 binding and parasite invasion by particular P. falciparum lines ¹¹, removal of all glycans from human basigin does not alter PfRH5 binding ². Further, in experiments with multiple P. falciparum clones, Crosnier et al. show that the invasion of human erythrocytes is potently inhibited by a soluble pentamerized form of basigin, by anti-basigin monoclonal antibodies, and by reduction of basigin levels on the erythrocyte surface ².Two of five single amino acid polymorphisms (E92K, L90P) in basigin affected PfRH5 binding to or invasion of human erythrocytes. While one of these polymorphisms (E92K) is associated with a relatively rare Ok^a- blood group in Japan, there are no data to suggest that L90P (or perhaps another undiscovered basigin polymorphism) was naturally selected to high prevalence in malaria-endemic areas. Although the native function of basigin on human erythrocytes is unknown, its high level of conservation suggests that P. falciparum may have evolved to depend on basigin to a much greater extent than on other, more polymorphic receptors. Interestingly, PfRH5 is also unlike other members of the PfEBL and PfRH families in that it lacks a transmembrane domain; recent evidence indicates that it forms a complex with a processed EGF-like PfRH5-interacting protein (PfRipr) and that this complex, in turn, associates tightly with another partner on the merozoite membrane ¹² (Figure 1). Attempts to disrupt the PfRipr gene also have been unsuccessful ¹².These findings suggest a critical role for the PfRH5-PfRipr complex that goes beyond an additional contribution of mechanical attachment within the binding repertoire of PfEBL and PfRH proteins. Possibilities for essential function might include PfRH5-PfRipr participation in a signaling pathway required for invasion, or an essential partnership in the junction during merozoite entry (Figure 1). Recent results also show promise for the use of PfRH5 and PfRipr as targets for intervention: rabbit IgG antibodies against virally-vectored, full-length PfRH5 outperformed antibodies that were generated by the same strategy against nine other erythrocytic-stage vaccine candidates, including four other PfEBL and PfRH proteins ¹³; rabbit antibodies against PfRipr likewise inhibited merozoite attachment and parasite growth in culture ¹². Although variations in the susceptibility of different P. falciparum lines were observed in these studies (likely due to different utilization patterns of ligand-receptor interactions), striking neutralization was nevertheless achieved in all cases. These results support PfRH5 and other components of its binding complex as new targets for therapeutic intervention and give an important boost to vaccine efforts against the asexual blood stages of P. falciparum.     

Inverse relationship between testicular proliferation and apoptosis in mammalian seasonal breeders

Seasonal cycles of testicular activity occur in many mammals and can include transitions between total arrest and recrudescence of spermatogenesis. We hypothesize that involution and reactivation of testis result from two antagonistic processes, proliferation and programmed cell death (apoptosis), which are activated at different times. To test this hypothesis, quantitative measurements of both proliferation-specific marker and apoptotic produced nucleosomes have been compared with sperm and testosterone production in testes from adult roe deer during breeding and non-breeding seasons (May to September). Testes of brown hare were included from periods of testes regression (June to August) and recrudescence (November to December). The highest testicular weights in roe deer were found in the rutting period from late July to early August (27.25 +/- 8.56 g), corresponding with the highest number of testicular sperm/g parenchyma. The peak of sperm production coincided with a peak in testosterone concentration (1.19 +/- 0.53 microg/g testis). The maximum level of proliferation-specific marker was also found during the breeding season (98.6 +/- 58.2 U/g testis in comparison to 20.1 +/- 22.0 U/g in the prerutting period). In contrast, the most significant apoptosis was observed in the nonbreeding season than the breeding period (71.11 +/- 5.79 U/mg testis and 18.88 +/- 6.79 U/mg, respectively). Testicular proliferation was low in the brown hare (0.061 +/- 0.062 U/g) during involution of the testes. It was newly activated in November and December (0.85 +/- 0.33 U/g), preceding the increase in testicular volume. Testosterone production increased in conjunction with testicular proliferation. At this time, testicular apoptosis was significantly lower (14.16 +/- 2.12 U/mg testis) than during the period of pronounced testicular regression (30.16 +/- 19.95 U/g). These results suggest that regulation of seasonal testicular activity is characterized by an inverse relationship of proliferation and apoptosis.     

The relationship between specialization and local abundance: the case of helminth parasites of birds

Positive relationships are commonly observed between the abundance of a species in a locality and the frequency of its occurrence among localities on a larger scale. This pattern may not hold for parasitic organisms when the average abundance of a parasite among its hosts is related to the number of host species in which it occurs, because of the additive investment in specific adaptations to counter host immune responses required for each host species in a parasites repertoire. For a rigorous test of the hypothesis that there is a trade-off between the number of host species that can be successfully exploited and the average abundance of parasites in those hosts, one needs to take into account the phylogenetic (or taxonomic) distances among the host species used by a parasite. Differences in immune responses are likely to increase with increasing phylogenetic distances. The trade-off hypothesis was tested in a comparative analysis of 393 species of trematodes, cestodes and nematodes parasitic in birds surveyed from the same geographical area, using an index of host specificity that measures the average taxonomic distances between a parasites known host species. After correcting for the influences of parasite phylogeny and other potential confounding variables, mean abundance was negatively correlated with the average taxonomic distance among host species for nematodes, and with the variance in taxonomic distances among hosts for cestodes. In the case of trematodes, these variables covaried positively. The trade-off between average infection success and how taxonomically distant a parasites host species are from each other was only found in two of the three groups of helminths investigated, possibly because of compensating features in trematodes, such as their ability to multiply asexually in intermediate hosts. These results provide empirical evidence consistent with the hypothesis that specialization allows greater local adaptation and therefore greater local population abundance, supporting key predictions regarding the evolution of ecological specialization.Electronic Supplementary Material Supplementary material is available for this article at     

Co-evolutionary arms race between brood parasites and their hosts at the nestling stage

Traditionally it was thought that the arms race between brood parasites and their hosts was confined to the egg stage of the breeding cycle because many host species are able to reject mimetic parasitic eggs but they are unable to reject strongly different parasitic chicks. However, recently, new cases of chick rejection, discrimination, or mimicry, have been published confirming the possibility that an equivalent arms race to that found at the egg stage could ever be played out at the chick stage. Here, I review the evidence for the existence of a co-evolutionary arms race at the nestling stage. Recent findings include new deceiving strategies used by brood parasitic chicks, defensive strategies used by foster parents and adaptive strategies of host nestlings. This review shows that both chick discrimination and relationships between brood parasites and their hosts at the nestling stage are much more complicated than previously believed. At least in some brood parasite-host systems, an arms race at the nestling stage is working.     

Physiology of the seasonal relationship between the photochemical reflectance index and photosynthetic light use efficiency

The photochemical reflectance index (PRI) is regarded as a promising proxy to track the dynamics of photosynthetic light use efficiency (LUE) via remote sensing. The implementation of this approach requires the relationship between PRI and LUE to scale not only in space but also in time. The short-term relationship between PRI and LUE is well known and is based on the regulative process of non-photochemical quenching (NPQ), but at the seasonal timescale the mechanisms behind the relationship remain unclear. We examined to what extent sustained forms of NPQ, photoinhibition of reaction centres, seasonal changes in leaf pigment concentrations, or adjustments in the capacity of alternative energy sinks affect the seasonal relationship between PRI and LUE during the year in needles of boreal Scots pine. PRI and NPQ were highly correlated during most of the year but decoupled in early spring when the foliage was deeply downregulated. This phenomenon was attributed to differences in the physiological mechanisms controlling the seasonal dynamics of PRI and NPQ. Seasonal adjustments in the pool size of the xanthophyll cycle pigments, on a chlorophyll basis, controlled the dynamics of PRI, whereas the xanthophyll de-epoxidation status and other xanthophyll-independent mechanisms controlled the dynamics of NPQ at the seasonal timescale. We conclude that the PRI leads to an underestimation of NPQ, and consequently overestimation of LUE, under conditions of severe stress in overwintering Scots pine, and most likely also in species experiencing severe drought. This severe stress-induced decoupling may challenge the implementation of the PRI approach.