Operationalizing resilience for adaptive coral reef management under global environmental change

Cumulative pressures from global climate and ocean change combined with multiple regional and local‐scale stressors pose fundamental challenges to coral reef managers worldwide. Understanding how cumulative stressors affect coral reef vulnerability is critical for successful reef conservation now and in the future. In this review, we present the case that strategically managing for increased ecological resilience (capacity for stress resistance and recovery) can reduce coral reef vulnerability (risk of net decline) up to a point. Specifically, we propose an operational framework for identifying effective management levers to enhance resilience and support management decisions that reduce reef vulnerability. Building on a system understanding of biological and ecological processes that drive resilience of coral reefs in different environmental and socio‐economic settings, we present an Adaptive Resilience‐Based management (ARBM) framework and suggest a set of guidelines for how and where resilience can be enhanced via management interventions. We argue that press‐type stressors (pollution, sedimentation, overfishing, ocean warming and acidification) are key threats to coral reef resilience by affecting processes underpinning resistance and recovery, while pulse‐type (acute) stressors (e.g. storms, bleaching events, crown‐of‐thorns starfish outbreaks) increase the demand for resilience. We apply the framework to a set of example problems for Caribbean and Indo‐Pacific reefs. A combined strategy of active risk reduction and resilience support is needed, informed by key management objectives, knowledge of reef ecosystem processes and consideration of environmental and social drivers. As climate change and ocean acidification erode the resilience and increase the vulnerability of coral reefs globally, successful adaptive management of coral reefs will become increasingly difficult. Given limited resources, on‐the‐ground solutions are likely to focus increasingly on actions that support resilience at finer spatial scales, and that are tightly linked to ecosystem goods and services.     

Increased expression of the anti-apoptotic protein Bcl-xL in the brain is associated with resilience to stress-induced depression-like behavior

Clinical observations and the results of animal studies have implicated changes in neuronal survival and plasticity in both the etiology of mood disorders, especially stress-induced depression, and anti-depressant drug action. Stress may predispose individuals toward depression through down-regulation of neurogenesis and an increase in apoptosis in the brain. Substantial individual differences in vulnerability to stress are evident in humans and were found in experimental animals. Recent studies revealed an association between the brain anti-apoptotic protein B cell lymphoma like X, long variant (Bcl-xL) expression and individual differences in behavioral vulnerability to stress. The ability to increase Bcl-xL gene expression in the hippocampus in response to stress may be an important factor for determining the resistance to the development of stress-induced depression. Treatment with anti-depressant drugs may change Bcl-xL response properties. In the rat brainstem, expression of this anti-apoptotic gene becomes sensitive to swim stress during the long-term fluoxetine treatment, an effect that appeared concomitantly with the anti-depressant-like action of the drug in the forced swim test, suggesting that Bcl-xL may be a new target for depression therapy. The processes and pathways linking stress stimuli to behavior via intracellular anti-apoptotic protein are discussed here in the context of Bcl-xL functions in the mechanisms of individual differences in behavioral resilience to stress and anti-depressant-induced effects on the behavioral despair.     

国外韧性城市形态研究述评

面对突发的自然和人为灾害,城市表现出极大的脆弱性。韧性城市形态被认为是化解城市脆弱性的关键得到关注,梳理国外研究成果对应对我国快速城市化进程中的不确定灾害风险具有重要意义。以韧性城市形态为主题,从概念与特征、形态要素韧性表现、评估及韧性设计等方面追踪国外研究进展。研究结果表明:国外文献重点探讨了形态与自然灾害的关联;韧性城市形态的概念尚未达成一致意见;从宏观、中观、微观空间层次视角探讨城市形态要素韧性表现成果较多;形态要素韧性评估集中于道路网络要素的韧性表现;形态要素韧性设计关键在于空间异质性。基于分析结果可知,我国未来研究重点应集中在全方位构建韧性城市形态研究框架、丰富并拓展形态要素韧性评估方法与技术、重视形态要素空间异质性等方面。     

The balance between stress resilience and vulnerability is regulated by corticotropin‐releasing hormone during the critical postnatal period for sensory development

Determining whether a stressful event will lead to stress‐resilience or vulnerability depends probably on an adjustable stress response set point, which is most likely effective during postnatal sensory development and involves the regulation of corticotrophin‐releasing hormone (CRH) expression. During the critical period of thermal‐control establishment in 3‐day‐old chicks, heat stress was found to render resilient or sensitized response, depending on the ambient temperature. These two different responses were correlated with the amount of activation of the hypothalamic–pituitary–adrenal (HPA) axis. The expression of CRH mRNA in the hypothalamic paraventricular nucleus was augmented during heat challenge a week after heat conditioning in chicks which were trained to be vulnerable to heat, while it declined in chicks that were trained to be resilient. To study the role of CRH in HPA‐axis plasticity, CRH or Crh‐antisense were intracranially injected into the third ventricle. CRH caused an elevation of both body temperature and plasma corticosterone level, while Crh‐antisense caused an opposite response. Moreover, these effects had long term implications by reversing a week later, heat resilience into vulnerability and vice versa. Chicks that had been injected with CRH followed by exposure to mild heat stress, normally inducing resilience, demonstrated, a week later, an elevation in body temperature, and Crh mRNA level similar to heat vulnerability, while Crh‐antisense injected chicks, which were exposed to harsh temperature, responded in heat resilience. These results demonstrate a potential role for CRH in determining the stress resilience/vulnerability balance. © 2014 Wiley Periodicals, Inc. Develop Neurobiol 75: 842–853, 2015     

A role for repressive histone methylation in cocaine-induced vulnerability to stress

Substance abuse increases an individual's vulnerability to stress-related illnesses, which is presumably mediated by drug-induced neural adaptations that alter subsequent responses to stress. Here, we identify repressive histone methylation in nucleus accumbens (NAc), an important brain reward region, as a key mechanism linking cocaine exposure to increased stress vulnerability. Repeated cocaine administration prior to subchronic social defeat stress potentiated depressive-like behaviors in mice through decreased levels of histone H3 lysine 9 dimethylation in NAc. Cre-mediated reduction of the histone methyltransferase, G9a, in NAc promoted increased susceptibility to social stress, similar to that observed with repeated cocaine. Conversely, G9a overexpression in NAc after repeated cocaine protected mice from the consequences of subsequent stress. This resilience was mediated, in part, through repression of BDNF-TrkB-CREB signaling, which was induced after repeated cocaine or stress. Identifying such common regulatory mechanisms may aid in the development of new therapies for addiction and depression.     

Molecular adaptations underlying susceptibility and resistance to social defeat in brain reward regions

While stressful life events are an important cause of psychopathology, most individuals exposed to adversity maintain normal psychological functioning. The molecular mechanisms underlying such resilience are poorly understood. Here, we demonstrate that an inbred population of mice subjected to social defeat can be separated into susceptible and unsusceptible subpopulations that differ along several behavioral and physiological domains. By a combination of molecular and electrophysiological techniques, we identify signature adaptations within the mesolimbic dopamine circuit that are uniquely associated with vulnerability or insusceptibility. We show that molecular recapitulations of three prototypical adaptations associated with the unsusceptible phenotype are each sufficient to promote resistant behavior. Our results validate a multidisciplinary approach to examine the neurobiological mechanisms of variations in stress resistance, and illustrate the importance of plasticity within the brain's reward circuits in actively maintaining an emotional homeostasis.     

The plant cytoskeleton takes center stage in abiotic stress responses and resilience

Stress resilience behaviours in plants are defensive mechanisms that develop under adverse environmental conditions to promote growth, development and yield. Over the past decades, improving stress resilience, especially in crop species, has been a focus of intense research for global food security and economic growth. Plants have evolved specific mechanisms to sense external stress and transmit information to the cell interior and generate appropriate responses. Plant cytoskeleton, comprising microtubules and actin filaments, takes a center stage in stress-induced signalling pathways, either as a direct target or as a signal transducer. In the past few years, it has become apparent that the function of the plant cytoskeleton and other associated proteins are not merely limited to elementary processes of cell growth and proliferation, but they also function in stress response and resilience. This review summarizes recent advances in the role of plant cytoskeleton and associated proteins in abiotic stress management. We provide a thorough overview of the mechanisms that plant cells employ to withstand different abiotic stimuli such as hypersalinity, dehydration, high temperature and cold, among others. We also discuss the crucial role of the plant cytoskeleton in organellar positioning under the influence of high light intensity.     

Management under uncertainty: guide-lines for incorporating connectivity into the protection of coral reefs

The global decline in coral reefs demands urgent management strategies to protect resilience. Protecting ecological connectivity, within and among reefs, and between reefs and other ecosystems is critical to resilience. However, connectivity science is not yet able to clearly identify the specific measures for effective protection of connectivity. This article aims to provide a set of principles or practical guidelines that can be applied currently to protect connectivity. These ‘rules of thumb’ are based on current knowledge and expert opinion, and on the philosophy that, given the urgency, it is better to act with incomplete knowledge than to wait for detailed understanding that may come too late. The principles, many of which are not unique to connectivity, include: (1) allow margins of error in extent and nature of protection, as insurance against unforeseen or incompletely understood threats or critical processes; (2) spread risks among areas; (3) aim for networks of protected areas which are: (a) comprehensive and spread—protect all biotypes, habitats and processes, etc., to capture as many possible connections, known and unknown; (b) adequate—maximise extent of protection for each habitat type, and for the entire region; (c) representative—maximise likelihood of protecting the full range of processes and spatial requirements; (d) replicated—multiple examples of biotypes or processes enhances risk spreading; (4) protect entire biological units where possible (e.g. whole reefs), including buffers around core areas. Otherwise, choose bigger rather than smaller areas; (5) provide for connectivity at a wide range of dispersal distances (within and between patches), emphasising distances <20–30 km; and (6) use a portfolio of approaches, including but not limited to MPAs. Three case studies illustrating the application of these principles to coral reef management in the Bohol Sea (Philippines), the Great Barrier Reef (Australia) and Kimbe Bay (Papua New Guinea) are described.     

Metabolomic identification of molecular changes associated with stress resilience in the chronic mild stress rat model of depression

Chronic stressful events are key risk factors for major depressive disorder (MDD), yet some individuals exposed to stressful events do not develop MDD. This disparity suggests the significance of resilience to deleterious stress effects. However, the underlying molecular mechanisms of stress resilience are poorly understood. In the present study, the chronic mild stress (CMS) rat model of depression was used to reveal the individual differences in stress response. Employing a gas chromatography/mass spectrometry metabolomic approach, the molecular changes associated with stress resilience in rat cerebellum were characterized by comparing anhedonic, CMS resilient and control groups. The results showed that four cerebellar metabolites—proline, lysine, glutamine, and dihydroxyacetone phosphate—were identified as the key differential metabolites associated with stress resilience. These metabolites may play a potential role in rendering individuals less vulnerable to CMS exposure. These findings provide insight into the molecular mechanisms underlying stress resilience and shed light on novel therapeutic opportunities to augment stress resiliency.     

Allostasis,Allostatic Load,and the Aging Nervous System: Role of Excitatory Amino Acids and Excitotoxicity

The adaptive responses of the body to challenges, often known as "stressors", consists of active responses that maintain homeostasis. This process of adaptation is known as "allostasis", meaning "achieving stability through change". Many systems of the body show allostasis, including the autonomic nervous system and hypothalamo-pituitary-adrenal (HPA) axis and they help to re-establish or maintain homeostasis through adaptation. The brain also shows allostasis, involving the activation of nerve cell activity and the release of neurotransmitters. When the individual is challenged repeatedly or when the allostatic systems remain turned on when no longer needed, the mediators of allostasis can produce a wear and tear on the body that has been termed "allostatic load". Examples of allostatic load include the accumulation of abdominal fat, the loss of bone minerals and the atrophy of nerve cells in the hippocampus. Circulating stress hormones play a key role, and, in the hippocampus, excitatory amino acids and NMDA receptors are important mediators of neuronal atrophy. The aging brain seems to be more vulnerable to such effects, although there are considerable individual differences in vulnerability that can be developmentally determined. Yet, at the same time, excitatory amino acids and NMDA receptors mediate important types of plasticity in the hippocampus. Moreover, the brain retains considerable resilience in the face of stress, and estrogens appear to play a role in this resilience. This review discusses the current status of work on underlying mechanisms for these effects.     

The exposure,sensitivity and vulnerability of natural vegetation in China to climate thermal variability (1901–2013): An indicator-based approach

Vulnerability assessments can be helpful in assessing the impact of climate change on natural ecosystems and are expected to support adaptation and/or mitigation strategies in the 21st century. A challenge when conducting such assessments is the integration of the multi-level properties and processes of ecosystems into an assessment framework. Focusing on the primary stresses of climate thermal variability (at both upper and lower extremes), this study proposes a quantitative indicator system—following the IPCC framework of vulnerability assessment—that assesses the impact of historical climate change, during 1901–2013, on the natural terrestrial vegetation types in China. The final output of the vulnerability assessment was expressed as a composite index, composed of ecosystem exposure, sensitivity and resilience to climate thermal change, and including biological, ecological and spatial traits of vegetation types in the assessment. The exposure to temperature variability was generally higher in January than in July, and higher in non-arborous vegetation types than forests. In contrast, sensitivity was higher for forests, wetlands and alpine tundra regions, especially for small areas and areas with scattered patterns. Original forests—especially those distributed in the north—had lower resilience than other vegetation types. The vulnerability of natural vegetation types in China to the temperature variability of the past century was very low to moderate, with a few exceptions, including tropical mangroves and the semi-arid to arid vegetation types in northwestern China, which had high vulnerability. Vulnerability was stronger in winter than in summer. Our results are generally in accord with the scenario-based projections on the geographical pattern of vegetation vulnerability to climate change, and revealed the difference caused by not considering moisture. The risks for these fragmented and narrow-range ecosystems are highlighted, and the importance of natural resilience is stressed for the assessment of vegetation vulnerability to climate change. Given the inadequate coverage of the natural reserve network in China (after the large investment in recent decades) found in the high-vulnerability vegetation types (with a few exceptions), the assessment of natural resilience of ecosystems could be critical for the optimal design of socio-economic strategies in response to the impacts of future climate change.     

Predicting regional neurodegeneration from the healthy brain functional connectome

Neurodegenerative diseases target large-scale neural networks. Four competing mechanistic hypotheses have been proposed to explain network-based disease patterning: nodal stress, transneuronal spread, trophic failure, and shared vulnerability. Here, we used task-free fMRI to derive the healthy intrinsic connectivity patterns seeded by brain regions vulnerable to any of five distinct neurodegenerative diseases. These data enabled us to investigate how intrinsic connectivity in health predicts region-by-region vulnerability to disease. For each illness, specific regions emerged as critical network "epicenters" whose normal connectivity profiles most resembled the disease-associated atrophy pattern. Graph theoretical analyses in healthy subjects revealed that regions with higher total connectional flow and, more consistently, shorter functional paths to the epicenters, showed greater disease-related vulnerability. These findings best fit a transneuronal spread model of network-based vulnerability. Molecular pathological approaches may help clarify what makes each epicenter vulnerable to its targeting disease and how toxic protein species travel between networked brain structures.     

Climate change, connectivity and conservation decision making: back to basics

1.  The challenge of climate change forces us to re-examine the assumptions underlying conservation planning.
2.  Increasing 'connectivity' has emerged as the most favoured option for conservation in the face of climate change.
3.  We argue that the importance of connectivity is being overemphasized: quantifying the benefits of connectivity per se is plagued with uncertainty, and connectivity can be co-incidentally improved by targeting more concrete metrics: habitat area and habitat quality.
4.   Synthesis and applications . Before investing in connectivity projects, conservation practitioners should analyse the benefits expected to arise from increasing connectivity and compare them with alternative investments, to ensure as much biodiversity conservation and resilience to climate change as possible within their budget. Strategies that we expect to remain robust in the face of climate change include maintaining and increasing the area of high quality habitats, prioritizing areas that have high environmental heterogeneity and controlling other anthropogenic threatening processes.     

Processes Contributing to Resilience of Coastal Wetlands to Sea-Level Rise

The objectives of this study were to identify processes that contribute to resilience of coastal wetlands subject to rising sea levels and to determine whether the relative contribution of these processes varies across different wetland community types. We assessed the resilience of wetlands to sea-level rise along a transitional gradient from tidal freshwater forested wetland (TFFW) to marsh by measuring processes controlling wetland elevation. We found that, over 5 years of measurement, TFFWs were resilient, although some marginally, and oligohaline marshes exhibited robust resilience to sea-level rise. We identified fundamental differences in how resilience is maintained across wetland community types, which have important implications for management activities that aim to restore or conserve resilient systems. We showed that the relative importance of surface and subsurface processes in controlling wetland surface elevation change differed between TFFWs and oligohaline marshes. The marshes had significantly higher rates of surface accretion than the TFFWs, and in the marshes, surface accretion was the primary contributor to elevation change. In contrast, elevation change in TFFWs was more heavily influenced by subsurface processes, such as root zone expansion or compaction, which played an important role in determining resilience of TFFWs to rising sea level. When root zone contributions were removed statistically from comparisons between relative sea-level rise and surface elevation change, sites that previously had elevation rate deficits showed a surplus. Therefore, assessments of wetland resilience that do not include subsurface processes will likely misjudge vulnerability to sea-level rise.     

Can some microbes promote host stress and benefit evolutionarily from this strategy?

Microbes can influence host physiology and behavior in many ways. Here we review evidence suggesting that some microbes can contribute to host stress (and other microbes can contribute to increased resilience to stress). We explain how certain microbes, which we call “stress microbes,” can potentially benefit evolutionarily from inducing stress in a host, gaining access to host resources that can help fuel rapid microbial replication by increasing glucose levels in the blood, increasing intestinal permeability, and suppressing the immune system. Other microbes, which we term “resilience microbes,” can potentially benefit from making hosts more resilient to stress. We hypothesize that “stress microbes” use a fast life history strategy involving greater host exploitation while “resilience microbes” use a slow life history strategy characterized by more aligned evolutionary interests with the host. In this paper, we review the evidence that microbes affect host stress and explain the evolutionary pressures that could lead microbes to manipulate host stress, discuss the physiological mechanisms that are known to be involved in both stress and microbial activity, and provide some testable predictions that follow from this hypothesis.     

Capturing the cornerstones of coral reef resilience: linking theory to practice

Coral reefs can undergo unexpected and dramatic changes in community composition, so called phase shifts. This can have profound consequences for ecosystem services upon which human welfare depends. Understanding of this behavior is in many aspects still in its infancy. Resilience has been argued to provide insurance against unforeseen ecosystem responses in the face of environmental change, and has become a prime goal for the management of coral reefs. However, diverse definitions of resilience can be found in the literature, making its meaning ambiguous. Several studies have used the term as a theoretical framework and concern regarding its practical applicability has been raised. Consequently, operationalizing theory to make resilience observable is an important task, particularly for policy makers and managers dealing with pressing environmental problems. Ultimately this requires some type of empirical assessments, something that has proven difficult due to the multidimensional nature of the concept. Biodiversity, spatial heterogeneity, and connectivity have been proposed as cornerstones of resilience as they may provide insurance against ecological uncertainty. The aim of this article is to provide an overview of the divergent uses of the concept and to propose empirical indicators of the cornerstones of coral reef resilience. These indicators include functional group approaches, the ratios of “good” and “bad” colonizers of space, measurements of spatial heterogeneity, and estimates of potential space availability against grazing capacity. The essence of these operational indicators of resilience is to use them as predictive tools to recognize vulnerability before disturbance occurs that may lead to abrupt phase shifts. Moving toward operationalizing resilience theory is imperative to the successful management of coral reefs in an increasingly disturbed and human-dominated environment. Communicating by Ecology Editor Professor Peter Mumby Order of authors 2–3 is alphabetic     

Vulnerability of European freshwater catchments to climate change

Climate change is expected to exacerbate the current threats to freshwater ecosystems, yet multifaceted studies on the potential impacts of climate change on freshwater biodiversity at scales that inform management planning are lacking. The aim of this study was to fill this void through the development of a novel framework for assessing climate change vulnerability tailored to freshwater ecosystems. The three dimensions of climate change vulnerability are as follows: (i) exposure to climate change, (ii) sensitivity to altered environmental conditions and (iii) resilience potential. Our vulnerability framework includes 1685 freshwater species of plants, fishes, molluscs, odonates, amphibians, crayfish and turtles alongside key features within and between catchments, such as topography and connectivity. Several methodologies were used to combine these dimensions across a variety of future climate change models and scenarios. The resulting indices were overlaid to assess the vulnerability of European freshwater ecosystems at the catchment scale (18 783 catchments). The Balkan Lakes Ohrid and Prespa and Mediterranean islands emerge as most vulnerable to climate change. For the 2030s, we showed a consensus among the applied methods whereby up to 573 lake and river catchments are highly vulnerable to climate change. The anthropogenic disruption of hydrological habitat connectivity by dams is the major factor reducing climate change resilience. A gap analysis demonstrated that the current European protected area network covers <25% of the most vulnerable catchments. Practical steps need to be taken to ensure the persistence of freshwater biodiversity under climate change. Priority should be placed on enhancing stakeholder cooperation at the major basin scale towards preventing further degradation of freshwater ecosystems and maintaining connectivity among catchments. The catchments identified as most vulnerable to climate change provide preliminary targets for development of climate change conservation management and mitigation strategies.     

Resilience in reef‐building corals: The ecological and evolutionary importance of the host response to thermal stress

Coral reefs are under extreme threat due to a number of stressors, but temperature increases due to changing climate are the most severe. Rising ocean temperatures coupled with local extremes lead to extensive bleaching, where the coral‐algal symbiosis breaks down and corals may die, compromising the structure and function of reefs. Although the symbiotic nature of the coral colony has historically been a focus of research on coral resilience, the host itself is a foundational component in the response to thermal stress. Fixed effects in the coral host set trait baselines through evolutionary processes, acting on many loci of small effect to create mosaics of thermal tolerance across latitudes and individual coral reefs. These genomic differences can be strongly heritable, producing wide variation among clones of different genotypes or families of a specific larval cross. Phenotypic plasticity is overlaid on these baselines and a growing body of knowledge demonstrates the potential for acclimatization of reef‐building corals through a variety of mechanisms that promote resilience and stress tolerance. The long‐term persistence of coral reefs will require many of these mechanisms to adjust to warmer temperatures within a generation, bridging the gap to reproductive events that allow recombination of standing diversity and adaptive change. Business‐as‐usual climate scenarios will probably lead to the loss of some coral populations or species in the future, so the interaction between intragenerational effects and evolutionary pressure is critical for the survival of reefs.     

Experience-dependent neuroplasticity of the developing hypothalamus: integrative epigenomic approaches

Augmented maternal care during the first postnatal week promotes life-long stress resilience and improved memory compared with the outcome of routine rearing conditions. Recent evidence suggests that this programming commences with altered synaptic connectivity of stress sensitive hypothalamic neurons. However, the epigenomic basis of the long-lived consequences is not well understood. Here, we employed whole-genome bisulfite sequencing (WGBS), RNA-sequencing (RNA-seq), and a multiplex microRNA (miRNA) assay to examine the effects of augmented maternal care on DNA cytosine methylation, gene expression, and miRNA expression. A total of 9,439 differentially methylated regions (DMRs) associated with augmented maternal care were identified in male offspring hypothalamus, as well as a modest but significant decrease in global DNA methylation. Differentially methylated and expressed genes were enriched for functions in neurotransmission, neurodevelopment, protein synthesis, and oxidative phosphorylation, as well as known stress response genes. Twenty prioritized genes were identified as highly relevant to the stress resiliency phenotype. This combined unbiased approach enabled the discovery of novel genes and gene pathways that advance our understanding of the epigenomic mechanisms underlying the effects of maternal care on the developing brain.