New Directions for Understanding the Spatial Resilience of Social–Ecological Systems

The concept of spatial resilience has brought a new focus on the influence of multi-scale processes on the dynamics of ecosystems. Initial ideas about spatial resilience focused on coral reefs and emphasized escalating anthropogenic disturbances across the broader seascape. This perspective resonated with a new awareness of global drivers of change, such as growth in international trade and shifts in climate, and the need to respond by scaling up governance and management. We review recent trends and emerging ideas in spatial resilience, using coral reefs and dependent communities as exemplars of multi-scale social–ecological systems. Despite recent advances, management and governance of ecosystems remain spatially fragmented and constrained to small scales. Temporally, many interventions still miss or ignore warning signals and struggle to cope with history, politics, long-term cumulative pressures, feedbacks, and sudden surprises. Significant recent progress has been made in understanding the relevance of spatial and temporal scale, heterogeneity, networks, the importance of place, and multi-scale governance. Emerging themes include better integration of ecology and conservation with social and economic science, and incorporating temporal dynamics in spatial analyses. A better understanding of the multi-scale spatial and temporal processes that drive the resilience of linked social-ecosystems will help address the widespread mismatch between the scales of ongoing ecological change and effective long-term governance of land- and seascapes.     

The copper chaperone CCS facilitates copper binding to MEK1/2 to promote kinase activation

Normal physiology relies on the precise coordination of intracellular signaling pathways that respond to nutrient availability to balance cell growth and cell death. The canonical mitogen-activated protein kinase pathway consists of the RAF-MEK-ERK signaling cascade and represents one of the most well-defined axes within eukaryotic cells to promote cell proliferation, which underscores its frequent mutational activation in human cancers. Our recent studies illuminated a function for the redox-active micronutrient copper (Cu) as an intracellular mediator of signaling by connecting Cu to the amplitude of mitogen-activated protein kinase signaling via a direct interaction between Cu and the kinases MEK1 and MEK2. Given the large quantities of molecules such as glutathione and metallothionein that limit cellular toxicity from free Cu ions, evolutionarily conserved Cu chaperones facilitate efficient delivery of Cu to cuproenzymes. Thus, a dedicated cellular delivery mechanism of Cu to MEK1/2 likely exists. Using surface plasmon resonance and proximity-dependent biotin ligase studies, we report here that the Cu chaperone for superoxide dismutase (CCS) selectively bound to and facilitated Cu transfer to MEK1. Mutants of CCS that disrupt Cu(I) acquisition and exchange or a CCS small-molecule inhibitor were used and resulted in reduced Cu-stimulated MEK1 kinase activity. Our findings indicate that the Cu chaperone CCS provides fidelity within a complex biological system to achieve appropriate installation of Cu within the MEK1 kinase active site that in turn modulates kinase activity and supports the development of novel MEK1/2 inhibitors that target the Cu structural interface or blunt dedicated Cu delivery mechanisms via CCS.     

Killer whale (Orcinus orca) population dynamics in response to a period of rapid ecosystem change in the eastern North Atlantic

This study investigates survival and abundance of killer whales (Orcinus orca) in Norway in 1988–2019 using capture–recapture models of photo‐identification data. We merged two datasets collected in a restricted fjord system in 1988–2008 (Period 1) with a third, collected after their preferred herring prey shifted its wintering grounds to more exposed coastal waters in 2012–2019 (Period 2), and investigated any differences between these two periods. The resulting dataset, spanning 32 years, comprised 3284 captures of 1236 whales, including 148 individuals seen in both periods. The best‐supported models of survival included the effects of sex and time period, and the presence of transients (whales seen only once). Period 2 had a much larger percentage of transients compared to Period 1 (mean = 30% vs. 5%) and the identification of two groups of whales with different residency patterns revealed heterogeneity in recapture probabilities. This caused estimates of survival rates to be biased downward (females: 0.955 ± 0.027 SE, males: 0.864 ± 0.038 SE) compared to Period 1 (females: 0.998 ± 0.002 SE, males: 0.985 ± 0.009 SE). Accounting for this heterogeneity resulted in estimates of apparent survival close to unity for regularly seen whales in Period 2. A robust design model for Period 2 further supported random temporary emigration at an estimated annual probability of 0.148 (± 0.095 SE). This same model estimated a peak in annual abundance in 2015 at 1061 individuals (95% CI 999–1127), compared to a maximum of 731 (95% CI 505–1059) previously estimated in Period 1, and dropped to 513 (95% CI 488–540) in 2018. Our results indicate variations in the proportion of killer whales present of an undefined population (or populations) in a larger geographical region. Killer whales have adjusted their distribution to shifts in key prey resources, indicating potential to adapt to rapidly changing marine ecosystems.     

Forest complexity drives dung beetle assemblages along an edge-interior gradient in the southwest Amazon rainforest

1. The habitat heterogeneity hypothesis predicts that heterogeneous habitats may provide more niches and diverse ways of exploiting environmental resources, thereby allowing more species to coexist, persist and diversify. 2. We aimed to investigate how an edge-interior gradient related to forest complexity influences species composition, abundance and richness of dung beetles in the western Amazon rainforest. We expected dung beetle abundance and richness to increase along the forest edge-interior gradient, in accordance with the habitat heterogeneity hypothesis. We also expected strong changes in species composition driven by species turnover in the forest interior and nestedness along the forest edges. We sampled dung beetles using baited pitfall traps across an edge-interior gradient. We also assessed the variation in forest features along the edge-interior gradient to identify changes in forest complexity. 3. Both species richness and abundance of dung beetles increased along the forest edge-interior, following the gradient of forest complexity. The Sorensen dissimilarity of dung beetle assemblages was higher among sampling units placed near the forest edge, although neither turnover, nor nestedness was different between the extremes of the forest edge-interior gradient. There was a clear compositional change along the edge-interior gradient mostly driven by species turnover. Individual indicator value analysis revealed that species were strongly associated with the forest interior conditions. 4. The simplification of the Amazon rainforest near clearings causes compositional changes in dung beetle assemblages. These changes are characterised by species-poor and low-abundance assemblages and may impair dung beetle ecological functions and therefore forest recovery.     

Identification of biochemically neutral positions in liver pyruvate kinase

Understanding how each residue position contributes to protein function has been a long-standing goal in protein science. Substitution studies have historically focused on conserved protein positions. However, substitutions of nonconserved positions can also modify function. Indeed, we recently identified nonconserved positions that have large substitution effects in human liver pyruvate kinase (hLPYK), including altered allosteric coupling. To facilitate a comparison of which characteristics determine when a nonconserved position does vs does not contribute to function, the goal of the current work was to identify neutral positions in hLPYK. However, existing hLPYK data showed that three features commonly associated with neutral positions—high sequence entropy, high surface exposure, and alanine scanning—lacked the sensitivity needed to guide experimental studies. We used multiple evolutionary patterns identified in a sequence alignment of the PYK family to identify which positions were least patterned, reasoning that these were most likely to be neutral. Nine positions were tested with a total of 117 amino acid substitutions. Although exploring all potential functions is not feasible for any protein, five parameters associated with substrate/effector affinities and allosteric coupling were measured for hLPYK variants. For each position, the aggregate functional outcomes of all variants were used to quantify a “neutrality” score. Three positions showed perfect neutral scores for all five parameters. Furthermore, the nine positions showed larger neutral scores than 17 positions located near allosteric binding sites. Thus, our strategy successfully enriched the dataset for positions with neutral and modest substitutions.     

Genetic Ablation of CD38 Protects against Western Diet-Induced Exercise Intolerance and Metabolic Inflexibility

Nicotinamide adenine dinucleotide (NAD⁺) is a key cofactor required for essential metabolic oxidation-reduction reactions. It also regulates various cellular activities, including gene expression, signaling, DNA repair and calcium homeostasis. Intracellular NAD⁺ levels are tightly regulated and often respond rapidly to nutritional and environmental changes. Numerous studies indicate that elevating NAD⁺ may be therapeutically beneficial in the context of numerous diseases. However, the role of NAD⁺ on skeletal muscle exercise performance is poorly understood. CD38, a multi-functional membrane receptor and enzyme, consumes NAD⁺ to generate products such as cyclic-ADP-ribose. CD38 knockout mice show elevated tissue and blood NAD⁺ level. Chronic feeding of high-fat, high-sucrose diet to wild type mice leads to exercise intolerance and reduced metabolic flexibility. Loss of CD38 by genetic mutation protects mice from diet-induced metabolic deficit. These animal model results suggest that elevation of tissue NAD⁺ through genetic ablation of CD38 can profoundly alter energy homeostasis in animals that are maintained on a calorically-excessive Western diet.