Ksp1 is an autophagic receptor protein for the Snx4-assisted autophagy of Ssn2/Med13.

Ksp1 is a casein II-like kinase whose activity prevents aberrant macroautophagy/autophagy induction in nutrient-rich conditions in yeast. Here, we describe a kinase-independent role of Ksp1 as a novel autophagic receptor protein for Ssn2/Med13, a known cargo of Snx4-assisted autophagy of transcription factors. In this pathway, a subset of conserved transcriptional regulators, Ssn2/Med13, Rim15, and Msn2, are selectively targeted for vacuolar proteolysis following nitrogen starvation, assisted by the sorting nexin heterodimer Snx4-Atg20. Here we show that phagophores also engulf Ksp1 alongside its cargo for vacuolar proteolysis. Ksp1 directly associates with Atg8 following nitrogen starvation at the interface of an Atg8-family interacting motif (AIM)/LC3-interacting region (LIR) in Ksp1 and the LIR/AIM docking site (LDS) in Atg8. Mutating the LDS site prevents the autophagic degradation of Ksp1. However, deletion of the C terminal canonical AIM still permitted Ssn2/Med13 proteolysis, suggesting that additional non-canonical AIMs may mediate the Ksp1-Atg8 interaction. Ksp1 is recruited to the perivacuolar phagophore assembly site by Atg29, a member of the trimeric scaffold complex. This interaction is independent of Atg8 and Snx4, suggesting that Ksp1 is recruited early to phagophores, with Snx4 delivering Ssn2/Med13 thereafter. Finally, normal cell survival following prolonged nitrogen starvation requires Ksp1. Together, these studies define a kinase-independent role for Ksp1 as an autophagic receptor protein mediating Ssn2/Med13 degradation. They also suggest that phagophores built by the trimeric scaffold complex are capable of receptor-mediated autophagy. These results demonstrate the dual functionality of Ksp1, whose kinase activity prevents autophagy while it plays a scaffolding role supporting autophagic degradation.Abbreviations: 3-AT: 3-aminotriazole; 17C: Atg17-Atg31-Atg29 trimeric scaffold complex; AIM: Atg8-family interacting motif; ATG: autophagy related; CKM: CDK8 kinase module; Cvt: cytoplasm-to-vacuole targeting; IDR: intrinsically disordered region; LIR: LC3-interacting region; LDS: LIR/AIM docking site; MoRF: molecular recognition feature; NPC: nuclear pore complex; PAS: phagophore assembly site; PKA: protein kinase A; RBP: RNA-binding protein; UPS: ubiquitin-proteasome system. SAA-TF: Snx4-assisted autophagy of transcription factors; Y2H: yeast two-hybrid.

Ecological barriers mediate spatiotemporal shifts of bird communities at a continental scale.

Species' range shifts and local extinctions caused by climate change lead to community composition changes. At large spatial scales, ecological barriers, such as biome boundaries, coastlines, and elevation, can influence a community's ability to shift in response to climate change. Yet, ecological barriers are rarely considered in climate change studies, potentially hindering predictions of biodiversity shifts. We used data from two consecutive European breeding bird atlases to calculate the geographic distance and direction between communities in the 1980s and their compositional best match in the 2010s and modeled their response to barriers. The ecological barriers affected both the distance and direction of bird community composition shifts, with coastlines and elevation having the strongest influence. Our results underscore the relevance of combining ecological barriers and community shift projections for identifying the forces hindering community adjustments under global change. Notably, due to (macro)ecological barriers, communities are not able to track their climatic niches, which may lead to drastic changes, and potential losses, in community compositions in the future.

Drivers of the changing abundance of European birds at two spatial scales.

Detecting biodiversity change and identifying its causes is challenging because biodiversity is multifaceted and temporal data often contain bias. Here, we model temporal change in species' abundance and biomass by using extensive data describing the population sizes and trends of native breeding birds in the United Kingdom (UK) and the European Union (EU). In addition, we explore how species' population trends vary with species' traits. We demonstrate significant change in the bird assemblages of the UK and EU, with substantial reductions in overall bird abundance and losses concentrated in a relatively small number of abundant and smaller sized species. By contrast, rarer and larger birds had generally fared better. Simultaneously, overall avian biomass had increased very slightly in the UK and was stable in the EU, indicating a change in community structure. Abundance trends across species were positively correlated with species' body mass and with trends in climate suitability, and varied with species' abundance, migration strategy and niche associations linked to diet. Our work highlights how changes in biodiversity cannot be captured easily by a single number; care is required when measuring and interpreting biodiversity change given that different metrics can provide very different insights. This article is part of the theme issue 'Detecting and attributing the causes of biodiversity change: needs, gaps and solutions'.

Projected climate change impacts on the phylogenetic diversity of the world's terrestrial birds: more than species numbers.

Ongoing climate change is a major threat to biodiversity. As abiotic tolerances and dispersal abilities vary, species-specific responses have the potential to further amplify or ameliorate the ensuing impacts on species assemblages. Here, we investigate the effects of climate change on species distributions across non-marine birds, quantifying its projected impact on species richness (SR) as well as on different aspects of phylogenetic diversity globally. Going beyond previous work, we disentangle the potential impacts of species gains versus losses on assemblage-level phylogenetic diversity under climate change and compare the projected impacts to randomized assemblage changes. We show that beyond its effects on SR, climate change could have profound impacts on assemblage-level phylogenetic diversity and composition, which differ significantly from random changes and among regions. Though marked species losses are most frequent in tropical and subtropical areas in our projections, phylogenetic restructuring of species communities is likely to occur all across the globe. Furthermore, our results indicate that the most severe changes to the phylogenetic diversity of local assemblages are likely to be caused by species range shifts and local species gains rather than range reductions and extinctions. Our findings highlight the importance of considering diverse measures in climate impact assessments.

Cyclin C-Cdk8 Kinase Phosphorylation of Rim15 Prevents the Aberrant Activation of Stress Response Genes.

Cells facing adverse environmental cues respond by inducing signal transduction pathways resulting in transcriptional reprograming. In the budding yeast Saccharomyces cerevisiae, nutrient deprivation stimulates stress response gene (SRG) transcription critical for entry into either quiescence or gametogenesis depending on the cell type. The induction of a subset of SRGs require nuclear translocation of the conserved serine-threonine kinase Rim15. However, Rim15 is also present in unstressed nuclei suggesting that additional activities are required to constrain its activity in the absence of stress. Here we show that Rim15 is directly phosphorylated by cyclin C-Cdk8, the conserved kinase module of the Mediator complex. Several results indicate that Cdk8-dependent phosphorylation prevents Rim15 activation in unstressed cells. First, Cdk8 does not control Rim15 subcellular localization and rim15∆ is epistatic to cdk8∆ with respect to SRG transcription and the execution of starvation programs required for viability. Next, Cdk8 phosphorylates a residue in the conserved PAS domain in vitro. This modification appears important as introducing a phosphomimetic at Cdk8 target residues reduces Rim15 activity. Moreover, the Rim15 phosphomimetic only compromises cell viability in stresses that induce cyclin C destruction as well as entrance into meiosis. Taken together, these findings suggest a model in which Cdk8 phosphorylation contributes to Rim15 repression whilst it cycles through the nucleus. Cyclin C destruction in response to stress inactivates Cdk8 which in turn stimulates Rim15 to maximize SRG transcription and cell survival.

Global impacts of climate change on avian functional diversity.

Climate change is predicted to drive geographical range shifts, leading to fluctuations in species richness (SR) worldwide. However, the effect of these changes on functional diversity (FD) remains unclear, in part because comprehensive species-level trait data are generally lacking at global scales. Here, we use morphometric and ecological traits for 8268 bird species to estimate the impact of climate change on avian FD. We show that future bird assemblages are likely to undergo substantial shifts in trait structure, with a magnitude of change greater than predicted from SR alone, and a direction of change varying according to geographical location and trophic guild. For example, our models predict that FD of insect predators will increase at higher latitudes with concurrent losses at mid-latitudes, whereas FD of seed dispersing birds will fluctuate across the tropics. Our findings highlight the potential for climate change to drive continental-scale shifts in avian FD with implications for ecosystem function and resilience.

Phenological trends in the pre- and post-breeding migration of long-distance migratory birds.

Phenological mismatch is often cited as a putative driver of population declines in long-distance migratory birds. The mechanisms and cues utilized to advance breeding ground arrival will impact the adaptability of species to further warming. Furthermore, timing of post-breeding migration potentially faces diverging selective pressures, with earlier onset of tropical dry seasons favouring migration advancement, while longer growing seasons in temperate areas could facilitate delayed departures. Despite this, few studies exist of migration phenology on the non-breeding grounds or on post-breeding passage. Here, we use first arrival and last departure dates of 20 species of trans-Saharan migratory birds from tropical non-breeding grounds (The Gambia), between 1964 and 2019. Additionally, we use first arrival and last departure dates, as well as median arrival and departure dates, at an entry/departure site to/from Europe (Gibraltar), between 1991 and 2018. We assess phenological trends in pre- and post-breeding migration, as well as individual species' durations of stay in breeding and non-breeding areas. Furthermore, we assess the extent to which inter-annual variation in these timings may be explained by meteorological and ecological variables. We find significant advances in pre-breeding migration at both locations, while post-breeding migration is delayed. At Gibraltar, these trends do not differ between first/last and median dates of migration. The combination of these trends suggests substantial changes in the temporal usage of the two continents by migratory birds. Duration of stay (of species, not individuals) within Europe increased by 16 days, on average, over the 27-year monitoring period. By contrast, duration of species' stays on the non-breeding range declined by 63 days, on average, over the 56-year monitoring period. Taken together these changes suggest substantial, previously unreported alterations to annual routines in Afro-Palaearctic migrants.

Snx4-assisted vacuolar targeting of transcription factors defines a new autophagy pathway for controlling ATG expression.

Autophagy, in part, is controlled by the repression and activation of autophagy-related (ATG) genes. Here, we describe a new selective autophagy pathway that targets functional transcriptional regulators to control their activity. This pathway is activated in response to nitrogen starvation and recycles transcriptional activators (Msn2 and Rim15) and a repressor (Ssn2/Med13) of ATG expression. Further analysis of Ssn2/Med13 vacuolar proteolysis revealed that this pathway utilizes the core autophagic machinery. However, it is independent of known nucleophagy mechanisms, receptor proteins, and the scaffold protein Atg11. Instead, Ssn2/Med13 exits the nucleus through the nuclear pore complex (NPC) and associates with the cytoplasmic nucleoporin Gle1, a member of the RNA remodeling complex. Dbp5 and Nup159, that act in concert with Gle1, are also required for Ssn2/Med13 clearance. Ssn2/Med13 is retrieved from the nuclear periphery and degraded by Atg17-initiated phagophores anchored to the vacuole. Efficient transfer to phagophores depends on the sorting nexin heterodimer Snx4/Atg24-Atg20, which binds to Atg17, and relocates to the perinucleus following nitrogen starvation. To conclude, this pathway defines a previously undescribed autophagy mechanism that targets select transcriptional regulators for rapid vacuolar proteolysis, utilizing the RNA remodeling complex, the sorting nexin heterodimer Snx4-Atg20, Atg17, and the core autophagic machinery. It is physiologically relevant as this Snx4-assisted vacuolar targeting pathway permits cells to fine-tune the autophagic response by controlling the turnover of both positive and negative regulators of ATG transcription.Abbreviations: AIM: Atg8 interacting motif; ATG: autophagy-related; CKM: CDK8 kinase module; IDR: intrinsically disordered region; IP6: phosphoinositide inositol hexaphosphate; NPC: nuclear pore complex; PAS: phagophore assembly site; UPS: ubiquitin-proteasomal system.

Global inequities and political borders challenge nature conservation under climate change.

Underlying sociopolitical factors have emerged as important determinants of wildlife population trends and the effectiveness of conservation action. Despite mounting research into the impacts of climate change on nature, there has been little consideration of the human context in which these impacts occur, particularly at the global scale. We investigate this in two ways. First, by modeling the climatic niches of terrestrial mammals and birds globally, we show that projected species loss under climate change is greatest in countries with weaker governance and lower Gross Domestic Product, with loss of mammal species projected to be greater in countries with lower CO2 emissions. Therefore, climate change impacts on species may be disproportionately significant in countries with lower capacity for effective conservation and lower greenhouse gas emissions, raising important questions of international justice. Second, we consider the redistribution of species in the context of political boundaries since the global importance of transboundary conservation under climate change is poorly understood. Under a high-emissions scenario, we find that 35% of mammals and 29% of birds are projected to have over half of their 2070 climatic niche in countries in which they are not currently found. We map these transboundary range shifts globally, identifying borders across which international coordination might most benefit conservation and where physical border barriers, such as walls and fences, may be an overlooked obstacle to climate adaptation. Our work highlights the importance of sociopolitical context and the utility of a supranational perspective for 21st century nature conservation.

Long-acting GLP-1 receptor agonists: Findings and implications of cardiovascular outcomes trials.

Cardiovascular disease (CVD) is a common and serious comorbidity of type 2 diabetes mellitus (T2DM), and cardiovascular (CV) risk assessment has become an important aspect of evaluating new therapies for T2DM before approval by the FDA. Since 2008, in order to establish safety, new therapies for T2DM have been required to demonstrate that they will not result in an unacceptable increase in CV risk. Studies performed for this purpose are termed CV outcome trials, or CVOTs. This article reviews CVOTs completed to date for the class of long-acting glucagon-like peptide-1 receptor agonists (GLP-1RAs; liraglutide, exenatide extended-release, albiglutide, dulaglutide, semaglutide injectable, semaglutide oral) and implications for clinical management of T2DM. All CVOTs have confirmed long-acting GLP-1RAs to be noninferior to (not worse than) placebo with regard to first occurrence of a primary outcome of three-point major adverse cardiovascular events (MACE; composite outcome of cardiovascular death, nonfatal myocardial infarction, nonfatal stroke). Further, a number of the studies demonstrated a statistically significant reduction in primary outcomes of three-point MACE with GLP-1RA treatment compared with placebo. As a result, the product labeling for liraglutide, semaglutide injectable, and dulaglutide has been updated with an indication for reducing the risk of MACE in adults with T2DM and established CVD (all) or multiple CV risk factors (dulaglutide only). These findings have brought about an exciting paradigm shift from concern about not inflicting CV harm to the exciting prospect of reducing risks of CV outcomes. Major diabetes care guidelines now encourage early consideration of GLP-1RA use in patients with atherosclerotic CVD.

Long-acting GLP-1 receptor agonists: Findings and implications of cardiovascular outcomes trials.

Cardiovascular disease (CVD) is a common and serious comorbidity of type 2 diabetes mellitus (T2DM), and cardiovascular (CV) risk assessment has become an important aspect of evaluating new therapies for T2DM before approval by the FDA. Since 2008, in order to establish safety, new therapies for T2DM have been required to demonstrate that they will not result in an unacceptable increase in CV risk. Studies performed for this purpose are termed CV outcome trials, or CVOTs. This article reviews CVOTs completed to date for the class of long-acting glucagon-like peptide-1 receptor agonists (GLP-1RAs; liraglutide, exenatide extended-release, albiglutide, dulaglutide, semaglutide injectable, semaglutide oral) and implications for clinical management of T2DM. All CVOTs have confirmed long-acting GLP-1RAs to be noninferior to (not worse than) placebo with regard to first occurrence of a primary outcome of three-point major adverse cardiovascular events (MACE; composite outcome of cardiovascular death, nonfatal myocardial infarction, nonfatal stroke). Further, a number of the studies demonstrated a statistically significant reduction in primary outcomes of three-point MACE with GLP-1RA treatment compared with placebo. As a result, the product labeling for liraglutide, semaglutide injectable, and dulaglutide has been updated with an indication for reducing the risk of MACE in adults with T2DM and established CVD (all) or multiple CV risk factors (dulaglutide only). These findings have brought about an exciting paradigm shift from concern about not inflicting CV harm to the exciting prospect of reducing risks of CV outcomes. Major diabetes care guidelines now encourage early consideration of GLP-1RA use in patients with atherosclerotic CVD.

Ubiquitin-proteasome-mediated cyclin C degradation promotes cell survival following nitrogen starvation.

Environmental stress elicits well-orchestrated programs that either restore cellular homeostasis or induce cell death depending on the insult. Nutrient starvation triggers the autophagic pathway that requires the induction of several Autophagy (ATG) genes. Cyclin C-cyclin-dependent kinase (Cdk8) is a component of the RNA polymerase II Mediator complex that predominantly represses the transcription of stress-responsive genes in yeast. To relieve this repression following oxidative stress, cyclin C translocates to the mitochondria where it induces organelle fragmentation and promotes cell death prior to its destruction by the ubiquitin-proteasome system (UPS). Here we report that cyclin C-Cdk8, together with the Ume6-Rpd3 histone deacetylase complex, represses the essential autophagy gene ATG8. Similar to oxidative stress, cyclin C is destroyed by the UPS following nitrogen starvation. Removing this repression is important as deleting CNC1 allows enhanced cell growth under mild starvation. However, unlike oxidative stress, cyclin C is destroyed prior to its cytoplasmic translocation. This is important as targeting cyclin C to the mitochondria induces both mitochondrial fragmentation and cell death following nitrogen starvation. These results indicate that cyclin C destruction pathways are fine tuned depending on the stress and that its terminal subcellular address influences the decision between initiating cell death or cell survival pathways.

Burning savanna for avian species richness and functional diversity.

Prescribed fire is used throughout fire-prone landscapes to conserve biodiversity. Current best practice in managing savanna systems advocates methods based on the assumption that increased fire-mediated landscape heterogeneity (pyrodiversity) will promote biodiversity. However, considerable knowledge gaps remain in our understanding of how savanna wildlife responds to the composition and configuration of pyrodiverse landscapes. The effects of pyrodiversity on functional diversity have rarely been quantified and assessing this relationship at a landscape scale that is commensurate with fire management is important for understanding mechanisms underlying ecosystem resilience. Here, we assess the impact of spatiotemporal variation in a long-term fire regime on avian diversity in North West Province, South Africa. We examined the relationship between (1) species richness, (2) three indices of functional diversity (i.e., functional richness, functional evenness, and functional dispersion) and four measures of pyrodiversity, the spatial extents of fire age classes, and habitat type at the landscape scale. We then used null models to assess differences between observed and expected functional diversity. We found that the proportion of newly burned (<1-yr post-fire), old, unburned (≥10 yr post-fire), and woodland habitat on the landscape predicted species and functional richness. Species richness also increased with the degree of edge contrast between patches of varying fire age, while functional dispersion increased with the degree of patch shape complexity. Lower than expected levels of functional richness suggest that habitat filtering is occurring, resulting in functional redundancy across our study sites. We demonstrate that evaluating functional diversity and redundancy is an important component of conservation planning as they may contribute to previously reported fire resilience. Our findings suggest that it is the type and configuration, rather than the diversity, of fire patches on the landscape that promote avian diversity and conserve ecological functions. A management approach is needed that includes significant coverage of adjacent newly burned and older, unburned savanna habitat; the latter, in particular, is inadequately represented under current burning practices.

The influence of different aspects of grouse moorland management on nontarget bird assemblages.

Conflict between stakeholders with opposing interests can hamper biodiversity conservation. When conflicts become entrenched, evidence from applied ecology can reveal new ways forward for their management. In particular, where disagreement exists over the efficacy or ethics of management actions, research clarifying the uncertain impacts of management on wildlife can move debates forwards to conciliation.Here, we explore a case-study of entrenched conflict where uncertainty exists over the impacts of multiple management actions: namely, moorlands managed for the shooting of red grouse (willow ptarmigan) Lagopus lagopus in the United Kingdom (UK). Debate over how UK moorlands should be managed is increasingly polarized. We evaluate, for the first time at a regional scale, the relative impacts of two major moorland management practices-predator control and heather burning-on nontarget bird species of conservation concern.Birds were surveyed on 18 estates across Northern England and Southeast Scotland. Sites ranged from intensively managed grouse moors to moorland sites with no management for grouse shooting. We hypothesised that both targeted predator control and burning regimes would enhance ground-nesting wader numbers and, as a consequence of this, and of increased grouse numbers, nontarget avian predators should also be more abundant on heavily managed sites.There were positive associations between predator control and the abundance of the three most widespread species of ground-nesting wader: strong effects for European golden plover Pluvialis apricaria and Eurasian curlew Numenius arquata and, less strongly, for common snipe Gallinago gallinago. These effects saturated at low levels of predator control. Evidence for effects of burning was much weaker. We found no evidence of enhanced numbers of nontarget predators on heavily managed sites.

The limits to population density in birds and mammals.

We address two fundamental ecological questions: what are the limits to animal population density and what determines those limits? We develop simple alternative models to predict population limits in relation to body mass. A model assuming that within-species area use increases with the square of daily travel distance broadly predicts the scaling of empirical extremes of minimum density across birds and mammals. Consistent with model predictions, the estimated density range for a given mass, 'population scope', is greater for birds than for mammals. However, unlike mammals and carnivorous birds, expected broad relationships between body mass and density extremes are not supported by data on herbivorous and omnivorous birds. Our results suggest that simple constraints on mobility and energy use/supply are major determinants of the scaling of density limits, but further understanding of interactions between dietary constraints and density limits are needed to predict future wildlife population responses to anthropogenic threats.

Cyclin C directly stimulates Drp1 GTP affinity to mediate stress-induced mitochondrial hyperfission.

Mitochondria exist in an equilibrium between fragmented and fused states that shifts heavily toward fission in response to cellular damage. Nuclear-to-cytoplasmic cyclin C relocalization is essential for dynamin-related protein 1 (Drp1)-dependent mitochondrial fission in response to oxidative stress. This study finds that cyclin C directly interacts with the Drp1 GTPase domain, increases its affinity to GTP, and stimulates GTPase activity in vitro. In addition, the cyclin C domain that binds Drp1 is contained within the non-Cdk binding second cyclin box domain common to all cyclin family members. This interaction is important, as this domain is sufficient to induce mitochondrial fission when expressed in mouse embryonic fibroblasts in the absence of additional stress signals. Using gel filtration chromatography and negative stain electron microscopy, we found that cyclin C interaction changes the geometry of Drp1 oligomers in vitro. High-molecular weight low-GTPase activity oligomers in the form of short filaments and rings were diminished, while dimers and elongated filaments were observed. Our results support a model in which cyclin C binding stimulates the reduction of low-GTPase activity Drp1 oligomers into dimers capable of producing high-GTPase activity filaments.

Bioenergy cropland expansion may offset positive effects of climate change mitigation for global vertebrate diversity.

Climate and land-use change interactively affect biodiversity. Large-scale expansions of bioenergy have been suggested as an important component for climate change mitigation. Here we use harmonized climate and land-use projections to investigate their potential combined impacts on global vertebrate diversity under a low- and a high-level emission scenario. We combine climate-based species distribution models for the world's amphibians, birds, and mammals with land-use change simulations and identify areas threatened by both climate and land-use change in the future. The combined projected effects of climate and land-use change on vertebrate diversity are similar under the two scenarios, with land-use change effects being stronger under the low- and climate change effects under the high-emission scenario. Under the low-emission scenario, increases in bioenergy cropland may cause severe impacts in biodiversity that are not compensated by lower climate change impacts. Under this low-emission scenario, larger proportions of species distributions and a higher number of small-range species may become impacted by the combination of land-use and climate change than under the high-emission scenario, largely a result of bioenergy cropland expansion. Our findings highlight the need to carefully consider both climate and land-use change when projecting biodiversity impacts. We show that biodiversity is likely to suffer severely if bioenergy cropland expansion remains a major component of climate change mitigation strategies. Our study calls for an immediate and significant reduction in energy consumption for the benefit of both biodiversity and to achieve the goals of the Paris Agreement.

Snf1 cooperates with the CWI MAPK pathway to mediate the degradation of Med13 following oxidative stress.

Eukaryotic cells, when faced with unfavorable environmental conditions, mount either pro-survival or pro-death programs. The conserved cyclin C-Cdk8 kinase plays a key role in this decision. Both are members of the Cdk8 kinase module that, along with Med12 and Med13, associate with the core Mediator complex of RNA polymerase II. In Saccharomyces cerevisiae, oxidative stress triggers Med13 destruction, which releases cyclin C into the cytoplasm to promote mitochondrial fission and programmed cell death. The SCFGrr1 ubiquitin ligase mediates Med13 degradation dependent on the cell wall integrity pathway, MAPK Slt2. Here we show that the AMP kinase Snf1 activates a second SCFGrr1 responsive degron in Med13. Deletion of Snf1 resulted in nuclear retention of cyclin C and failure to induce mitochondrial fragmentation. This degron was able to confer oxidative-stress-induced destruction when fused to a heterologous protein in a Snf1 dependent manner. Although snf1∆ mutants failed to destroy Med13, deleting the degron did not prevent destruction. These results indicate that the control of Med13 degradation following H2O2 stress is complex, being controlled simultaneously by CWI and MAPK pathways.

Tritrophic phenological match-mismatch in space and time.

Increasing temperatures associated with climate change may generate phenological mismatches that disrupt previously synchronous trophic interactions. Most work on mismatch has focused on temporal trends, whereas spatial variation in the degree of trophic synchrony has largely been neglected, even though the degree to which mismatch varies in space has implications for meso-scale population dynamics and evolution. Here we quantify latitudinal trends in phenological mismatch, using phenological data on an oak-caterpillar-bird system from across the UK. Increasing latitude delays phenology of all species, but more so for oak, resulting in a shorter interval between leaf emergence and peak caterpillar biomass at northern locations. Asynchrony found between peak caterpillar biomass and peak nestling demand of blue tits, great tits and pied flycatchers increases in earlier (warm) springs. There is no evidence of spatial variation in the timing of peak nestling demand relative to peak caterpillar biomass for any species. Phenological mismatch alone is thus unlikely to explain spatial variation in population trends. Given projections of continued spring warming, we predict that temperate forest birds will become increasingly mismatched with peak caterpillar timing. Latitudinal invariance in the direction of mismatch may act as a double-edged sword that presents no opportunities for spatial buffering from the effects of mismatch on population size, but generates spatially consistent directional selection on timing, which could facilitate rapid evolutionary change.

Flight range, fuel load and the impact of climate change on the journeys of migrant birds.

Climate change is predicted to increase migration distances for many migratory species, but the physiological and temporal implications of longer migratory journeys have not been explored. Here, we combine information about species' flight range potential and migratory refuelling requirements to simulate the number of stopovers required and the duration of current migratory journeys for 77 bird species breeding in Europe. Using tracking data, we show that our estimates accord with recorded journey times and stopovers for most species. We then combine projections of altered migratory distances under climate change with models of avian flight to predict future migratory journeys. We find that 37% of migratory journeys undertaken by long-distance migrants will necessitate an additional stopover in future. These greater distances and the increased number of stops will substantially increase overall journey durations of many long-distance migratory species, a factor not currently considered in climate impact studies.