Incorporating adaptive responses into future projections of coral bleaching

Climate warming threatens to increase mass coral bleaching events, and several studies have projected the demise of tropical coral reefs this century. However, recent evidence indicates corals may be able to respond to thermal stress though adaptive processes (e.g., genetic adaptation, acclimatization, and symbiont shuffling). How these mechanisms might influence warming‐induced bleaching remains largely unknown. This study compared how different adaptive processes could affect coral bleaching projections. We used the latest bias‐corrected global sea surface temperature (SST) output from the NOAA/GFDL Earth System Model 2 (ESM2M) for the preindustrial period through 2100 to project coral bleaching trajectories. Initial results showed that, in the absence of adaptive processes, application of a preindustrial climatology to the NOAA Coral Reef Watch bleaching prediction method overpredicts the present‐day bleaching frequency. This suggests that corals may have already responded adaptively to some warming over the industrial period. We then modified the prediction method so that the bleaching threshold either permanently increased in response to thermal history (e.g., simulating directional genetic selection) or temporarily increased for 2–10 years in response to a bleaching event (e.g., simulating symbiont shuffling). A bleaching threshold that changes relative to the preceding 60 years of thermal history reduced the frequency of mass bleaching events by 20–80% compared with the ‘no adaptive response’ prediction model by 2100, depending on the emissions scenario. When both types of adaptive responses were applied, up to 14% more reef cells avoided high‐frequency bleaching by 2100. However, temporary increases in bleaching thresholds alone only delayed the occurrence of high‐frequency bleaching by ca. 10 years in all but the lowest emissions scenario. Future research should test the rate and limit of different adaptive responses for coral species across latitudes and ocean basins to determine if and how much corals can respond to increasing thermal stress.     

Improving marine disease surveillance through sea temperature monitoring,outlooks and projections

To forecast marine disease outbreaks as oceans warm requires new environmental surveillance tools. We describe an iterative process for developing these tools that combines research, development and deployment for suitable systems. The first step is to identify candidate host–pathogen systems. The 24 candidate systems we identified include sponges, corals, oysters, crustaceans, sea stars, fishes and sea grasses (among others). To illustrate the other steps, we present a case study of epizootic shell disease (ESD) in the American lobster. Increasing prevalence of ESD is a contributing factor to lobster fishery collapse in southern New England (SNE), raising concerns that disease prevalence will increase in the northern Gulf of Maine under climate change. The lowest maximum bottom temperature associated with ESD prevalence in SNE is 12°C. Our seasonal outlook for 2015 and long-term projections show bottom temperatures greater than or equal to 12°C may occur in this and coming years in the coastal bays of Maine. The tools presented will allow managers to target efforts to monitor the effects of ESD on fishery sustainability and will be iteratively refined. The approach and case example highlight that temperature-based surveillance tools can inform research, monitoring and management of emerging and continuing marine disease threats.     

Trypanosoma (Schizotrypanum) cruzi: repetitive DNA sequence evolution in three geographically distinct isolates

1. Middle-repetitive DNA sequences were analyzed by molecular hybridization to determine both the extent of complementarity and time of evolutionary divergence between isolates of Trypanosoma cruzi from Argentina, Mexico, or Venezuela. 2. Although molecular hybridizations showed no significant difference between the middle-repetitive DNAs of the Mexican and Venezuelan isolates, there was a 2.7% base pair mismatch in hybrid molecules formed by association of strands from both the Mexican and Argentine isolates. 3. Using the rates for divergence of middle-repetitive DNA in sea urchins, the Mexican and Argentine isolates were estimated to have diverged approximately 20-25 million years ago. 4. Analysis of the kinetics for the DNA hybridizations indicates that only minor amplifications of specific gene sequences or changes in the complexity of the genomes could have occurred during the divergence of the three isolates studied.     

Fine structure of the cerebral ocelli of a sipunculid,Phascolosoma agassizii

Summary The brain ofPhascolosoma agassizii, a sipunculid worm, contains a pair of ocelli. Each ocellus lies at the inner end of the ocular tube, an invagination that connects the concavity of the ocellus with the anterior surface of the head. The cuticle which covers the epidermis of the worm extends into and lines the ocular tube. The cells of the neck of the tube are columnar and contain longitudinally oriented tonofilaments extending into microvilli that project into the cuticle in the tube. Cilia also project from the apices of these cells. Toward the base of the ocular tube are two kinds of columnar cells: supportive and photoreceptive. The supportive cells contain varying concentrations of melanin-like granules forming the pigmented component of the ocellus. Numerous longitudinally oriented tonofilaments in these cells extend into microvilli projecting into the cuticular layer. The photoreceptor cells, containing many microtubules, lie between the supportive cells and spread out at their tips giving off an irregular array of miorovilli, the presumed photoreceptors, and cilia. These photoreceptors are regarded as belonging to the rhabdomeric type, albeit cilia are present.This investigation was financed by grant number GM 10292 from the National Institute of General Medical Science.     

Ternary complex structure of human HGPRTase, PRPP, Mg2+, and the inhibitor HPP reveals the involvement of the flexible loop in substrate binding.

Site-directed mutagenesis was used to replace Lys68 of the human hypoxanthine phosphoribosyltransferase (HGPRTase) with alanine to exploit this less reactive form of the enzyme to gain additional insights into the structure activity relationship of HGPRTase. Although this substitution resulted in only a minimal (one- to threefold) increase in the Km values for binding pyrophosphate or phosphoribosylpyrophosphate, the catalytic efficiencies (k(cat)/Km) of the forward and reverse reactions were more severely reduced (6- to 30-fold), and the mutant enzyme showed positive cooperativity in binding of alpha-D-5-phosphoribosyl-1-pyrophosphate (PRPP) and nucleotide. The K68A form of the human HGPRTase was cocrystallized with 7-hydroxy [4,3-d] pyrazolo pyrimidine (HPP) and Mg PRPP, and the refined structure reported. The PRPP molecule built into the [(Fo - Fc)phi(calc)] electron density shows atomic interactions between the Mg PRPP and enzyme residues in the pyrophosphate binding domain as well as in a long flexible loop (residues Leu101 to Gly111) that closes over the active site. Loop closure reveals the functional roles for the conserved SY dipeptide of the loop as well as the molecular basis for one form of gouty arthritis (S103R). In addition, the closed loop conformation provides structural information relevant to the mechanism of catalysis in human HGPRTase.     

Selective inhibition of human Molt-4 leukemia type II inosine 5'-monophosphate dehydrogenase by the 1,5-diazabicyclo[3.1.0]hexane-2,4-diones

Inosine 5'-monophosphate dehydrogenase (IMPDH) is the rate-limiting enzyme in de novo purine biosynthesis. IMPDH activity results from expression of two isoforms. Type I is constitutively expressed and predominates in normal resting cells, while Type II is selectively up-regulated in neoplastic and replicating cells. Inhibitors of IMPDH activity selectively targeting the Type II isoform have great potential as cancer chemotherapeutic agents. For this study, an expression system was developed which yields 35-50 mg of soluble, purified recombinant Type I and II protein from 1 L of bacteria. In addition, three 1,5-diazabicyclo[3.1.0]hexane-2,4-diones were synthesized and shown to act as specific inhibitors of human recombinant Type II IMPDH. The agents are competitive inhibitors with respect to the endogenous substrate IMP and K(i) values range from 5 to 44 microM but were inactive as inhibitors of the Type I isoform at concentrations ranging from 0.5 to 500 microM. IC(50) values for recombinant Type II inhibition were determined and compared to IC(50) values obtained from Molt-4 cell extracts of IMPDH. Cytotoxicity assays revealed that the compounds inhibited Molt-4 leukemia growth with ED(50) values of 3.2-7.6 microM. Computational docking studies predict that the compounds bind to IMPDH in the IMP-binding site, although interactions with residues differ from those previously determined to interact with bound IMP. While all residues predicted to interact directly with the bound compounds are conserved in the Type I and Type II isoforms, sequence divergence within a helix adjacent to the active site may contribute to the observed selectivity for the human Type II isoform. These compounds represent the first class of selective IMPDH Type II inhibitors which may serve as lead compounds for the development of isoform-selective cancer chemotherapy.     

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.     

Refugia under threat: Mass bleaching of coral assemblages in high‐latitude eastern Australia

Environmental anomalies that trigger adverse physiological responses and mortality are occurring with increasing frequency due to climate change. At species' range peripheries, environmental anomalies are particularly concerning because species often exist at their environmental tolerance limits and may not be able to migrate to escape unfavourable conditions. Here, we investigated the bleaching response and mortality of 14 coral genera across high‐latitude eastern Australia during a global heat stress event in 2016. We evaluated whether the severity of assemblage‐scale and genus‐level bleaching responses was associated with cumulative heat stress and/or local environmental history, including long‐term mean temperatures during the hottest month of each year (SST_LTMAX), and annual fluctuations in water temperature (SST_VAR) and solar irradiance (PARZ_VAR). The most severely‐bleached genera included species that were either endemic to the region (Pocillopora aliciae) or rare in the tropics (e.g. Porites heronensis). Pocillopora spp., in particular, showed high rates of immediate mortality. Bleaching severity of Pocillopora was high where SST_LTMAX was low or PARZ_VAR was high, whereas bleaching severity of Porites was directly associated with cumulative heat stress. While many tropical Acropora species are extremely vulnerable to bleaching, the Acropora species common at high latitudes, such as A. glauca and A. solitaryensis, showed little incidence of bleaching and immediate mortality. Two other regionally‐abundant genera, Goniastrea and Turbinaria, were also largely unaffected by the thermal anomaly. The severity of assemblage‐scale bleaching responses was poorly explained by the environmental parameters we examined. Instead, the severity of assemblage‐scale bleaching was associated with local differences in species abundance and taxon‐specific bleaching responses. The marked taxonomic disparity in bleaching severity, coupled with high mortality of high‐latitude endemics, point to climate‐driven simplification of assemblage structures and progressive homogenisation of reef functions at these high‐latitude locations.