A roadmap to integrating resilience into the practice of coral reef restoration.

Recent warm temperatures driven by climate change have caused mass coral bleaching and mortality across the world, prompting managers, policymakers, and conservation practitioners to embrace restoration as a strategy to sustain coral reefs. Despite a proliferation of new coral reef restoration efforts globally and increasing scientific recognition and research on interventions aimed at supporting reef resilience to climate impacts, few restoration programs are currently incorporating climate change and resilience in project design. As climate change will continue to degrade coral reefs for decades to come, guidance is needed to support managers and restoration practitioners to conduct restoration that promotes resilience through enhanced coral reef recovery, resistance, and adaptation. Here, we address this critical implementation gap by providing recommendations that integrate resilience principles into restoration design and practice, including for project planning and design, coral selection, site selection, and broader ecosystem context. We also discuss future opportunities to improve restoration methods to support enhanced outcomes for coral reefs in response to climate change. As coral reefs are one of the most vulnerable ecosystems to climate change, interventions that enhance reef resilience will help to ensure restoration efforts have a greater chance of success in a warming world. They are also more likely to provide essential contributions to global targets to protect natural biodiversity and the human communities that rely on reefs.

Turning a lost reef ecosystem into a national restoration program.

Achieving a sustainable socioecological future now requires large-scale environmental repair across legislative borders. Yet, enabling large-scale conservation is complicated by policy-making processes that are disconnected from socioeconomic interests, multiple sources of knowledge, and differing applications of policy. We considered how a multidisciplinary approach to marine habitat restoration generated the scientific evidence base, community support, and funding needed to begin the restoration of a forgotten, functionally extinct shellfish reef ecosystem. The key actors came together as a multidisciplinary community of researchers, conservation practitioners, recreational fisher communities, and government bodies that collaborated across sectors to rediscover Australia's lost shellfish reefs and communicate the value of its restoration. Actions undertaken to build a case for large-scale marine restoration included synthesizing current knowledge on Australian shellfish reefs and their historical decline, using this history to tell a compelling story to spark public and political interest, integrating restoration into government policy, and rallying local support through community engagement. Clearly articulating the social, economic, and environmental business case for restoration led to state and national funding for reef restoration to meet diverse sustainability goals (e.g., enhanced biodiversity and fisheries productivity) and socioeconomic goals (e.g., job creation and recreational opportunities). A key lesson learned was the importance of aligning project goals with public and industry interests so that projects could address multiple political obligations. This process culminated in Australia's largest marine restoration initiative and shows that solutions for large-scale ecosystem repair can rapidly occur when socially valued science acts on political opportunities.

Transformación de un Ecosistema Arrecifal Perdido en un Programa Nacional de Restauración Resumen Actualmente se requiere una reparación ambiental a gran escala que atraviese fronteras legislativas para lograr un futuro socio-ecológico sustentable. Aun así, habilitar la conservación a gran escala es complicado debido a los procesos de elaboración de políticas que están desconectadas de los intereses socio-económicos, las múltiples fuentes de conocimiento y las diferentes aplicaciones de las políticas. Consideramos cómo una estrategia multidisciplinaria para la restauración de hábitats marinos generó una base de evidencia científica, apoyo comunitario y el financiamiento necesario para así iniciar la restauración de un ecosistema arrecifal de conchas funcionalmente extinto. Los actores clave formaron una comunidad multidisciplinaria de investigadores, practicantes de la conservación, comunidades de pescadores recreativos y órganos gubernamentales que colaboró con varios sectores para redescubrir los arrecifes perdidos de Australia y comunicó el valor de su restauración. Las acciones realizadas para armar el caso para la restauración marina a gran escala incluyeron la síntesis del conocimiento actual sobre los arrecifes de conchas en Australia y su declinación histórica, el uso de esta historia para contar una narración convincente que active el interés público y político, la integración de la restauración a la política gubernamental y la movilización del apoyo local por medio de la participación comunitaria. Claramente, la articulación del caso del negocio social, económico y ambiental para la restauración llevó al financiamiento estatal y nacional para la restauración arrecifal a cumplir diversos objetivos socio-económicos (p. ej.: creación de empleos, oportunidades recreativas) y de restauración (p. ej.: una productividad realzada de la biodiversidad y las pesquerías). Una lección clave que aprendimos fue lo importante que es alinear los objetivos del proyecto con los intereses públicos y de la industria, de tal manera que los proyectos aborden las múltiples obligaciones políticas. Este proceso culminó con la iniciativa de restauración marina más grande en Australia y demuestra que las soluciones para la reparación de los ecosistemas a gran escala pueden ocurrir rápidamente cuando la ciencia con valor social actúa sobre las oportunidades políticas.

Dephosphorylation of F-BAR protein Cdc15 modulates its conformation and stimulates its scaffolding activity at the cell division site.

Cytokinesis in Schizosaccharomyces pombe requires the function of Cdc15, the founding member of the pombe cdc15 homology (PCH) family of proteins. As an early, abundant contractile ring component with multiple binding partners, Cdc15 plays a key role in organizing the ring. We demonstrate that Cdc15 phosphorylation at many sites generates a closed conformation, inhibits Cdc15 assembly at the division site in interphase, and precludes interaction of Cdc15 with its binding partners. Cdc15 dephosphorylation induces an open conformation, oligomerization, and scaffolding activity during mitosis. Cdc15 mutants with reduced phosphorylation precociously appear at the division site in filament-like structures and display increased association with protein partners and the membrane. Our results indicate that Cdc15 phosphoregulation impels both assembly and disassembly of the contractile apparatus and suggest a regulatory strategy that PCH family and BAR superfamily members might broadly employ to achieve temporal specificity in their roles as linkers between membrane and cytoskeleton.

Cumulative Risk on the Oxytocin Receptor Gene (OXTR) Predicts Empathic Communication by Physician Assistant Students.

In the relationship between patients and health care providers, few communicative features are as significant as the providers' ability to express empathy. A robust empirical literature describes the importance of physician communication skills-particularly those that convey empathy-yet few studies have examined empathic communication by physician assistants, who provide primary care for an increasing number of Americans. The present study examines the empathic communication of physician assistant students in interactions with standardized patients. Over a 6-month period, each student conducted three clinical interviews, each of which was evaluated for empathic communication by the patients, the students' clinical instructors, and third-party observers. Students also provided saliva samples for genotyping six single-nucleotide polymorphisms on the oxytocin receptor gene (OXTR) that are linked empirically to empathic behavior. Consistent with recent research, this study adopted a cumulative risk approach wherein students were scored for their number of risky alleles on the single-nucleotide polymorphisms. Results indicated that cumulative risk on OXTR receptor gene predicted lower patient empathy scores as rated by instructors and observers, but not by standardized patients.

The hydrolethalus syndrome protein HYLS-1 links core centriole structure to cilia formation.

Centrioles are subcellular organelles composed of a ninefold symmetric microtubule array that perform two important functions: (1) They build centrosomes that organize the microtubule cytoskeleton, and (2) they template cilia, microtubule-based projections with sensory and motile functions. We identified HYLS-1, a widely conserved protein, based on its direct interaction with the core centriolar protein SAS-4. HYLS-1 localization to centrioles requires SAS-4 and, like SAS-4, HYLS-1 is stably incorporated into the outer centriole wall. Unlike SAS-4, HYLS-1 is dispensable for centriole assembly and centrosome function in cell division. Instead, HYLS-1 plays an essential role in cilia formation that is conserved between Caenorhabditis elegans and vertebrates. A single amino acid change in human HYLS1 leads to a perinatal lethal disorder termed hydrolethalus syndrome, and we show that this mutation impairs HYLS-1 function in ciliogenesis. HYLS-1 is required for the apical targeting/anchoring of centrioles at the plasma membrane but not for the intraflagellar transport-dependent extension of the ciliary axoneme. These findings classify hydrolethalus syndrome as a severe human ciliopathy and shed light on the dual functionality of centrioles, defining the first stably incorporated centriolar protein that is not required for centriole assembly but instead confers on centrioles the capacity to initiate ciliogenesis.

Mod5 protein binds to tRNA gene complexes and affects local transcriptional silencing.

The tRNA gene-mediated (tgm) silencing of RNA polymerase II promoters is dependent on subnuclear clustering of the tRNA genes, but genetic analysis shows that the silencing requires additional mechanisms. We have identified proteins that bind tRNA gene transcription complexes and are required for tgm silencing but not required for gene clustering. One of the proteins, Mod5, is a tRNA modifying enzyme that adds an N6-isopentenyl adenosine modification at position 37 on a small number of tRNAs in the cytoplasm, although a subpopulation of Mod5 is also found in the nucleus. Recent publications have also shown that Mod5 has tumor suppressor characteristics in humans as well as confers drug resistance through prion-like misfolding in yeast. Here, we show that a subpopulation of Mod5 associates with tRNA gene complexes in the nucleolus. This association occurs and is required for tgm silencing regardless of whether the pre-tRNA transcripts are substrates for Mod5 modification. In addition, Mod5 is bound to nuclear pre-tRNA transcripts, although they are not substrates for the A37 modification. Lastly, we show that truncation of the tRNA transcript to remove the normal tRNA structure also alleviates silencing, suggesting that synthesis of intact pre-tRNAs is required for the silencing mechanism. These results are discussed in light of recent results showing that silencing near tRNA genes also requires chromatin modification.

The contribution of autophagy to lymphocyte survival and homeostasis.

Over the life span of a T lymphocyte, from thymic development to death, it is subjected to a variety of stresses and stimuli. Upon receipt of each stress or stimulus, a potentially life-changing fate decision must be made, namely, whether to commit to a form of programmed cell death or to make the necessary adaptations to effectively deal with the changing environment. In our laboratory, we have identified several stresses that a T lymphocyte will encounter during a normal life span. Our studies have focused on how T cells utilize autophagy to get a grasp on the situation, or in cases in which survival is untenable, how T cells use autophagy to hasten their demise. This review focuses on the functions of T-cell autophagy in maintaining homeostasis, eliminating excess or dangerous levels of mitochondria, trimming levels of endoplasmic reticulum, and promoting a healthy metabolic level to allow cells to perform as productive components of the immune system. In addition, the use of autophagy signaling molecules to perform autophagy-independent tasks involved in the maintenance of immune homeostasis is discussed.

Suspended sediment prolongs larval development in a coral reef fish.

Increasing sediment input into coastal environments is having a profound influence on shallow marine habitats and associated species. Coral reef ecosystems appear to be particularly sensitive, with increased sediment deposition and re-suspension being associated with declines in the abundance and diversity of coral reef fishes. While recent research has demonstrated that suspended sediment can have negative impacts on post-settlement coral reef fishes, its effect on larval development has not been investigated. In this study, we tested the effects of different levels of suspended sediment on larval growth and development time in Amphiprion percula, a coral reef damselfish. Larvae were subjected to four experimental concentrations of suspended sediment spanning the range found around coastal coral reefs (0-45 mg l(-1)). Larval duration was significantly longer in all sediment treatments (12 days) compared with the average larval duration in the control treatment (11 days). Approximately 75% of the fish in the control had settled by day 11, compared with only 40-46% among the sediment treatments. In the highest sediment treatment, some individuals had a larval duration twice that of the median duration in the control treatment. Unexpectedly, in the low sediment treatment, fish at settlement were significantly longer and heavier compared with fish in the other treatments, suggesting delayed development was independent of individual condition. A sediment-induced extension of the pelagic larval stage could significantly reduce numbers of larvae competent to settle and, in turn, have major effects on adult population dynamics.

Safety profile of sural nerve in posterolateral approach to the ankle joint: MRI study.

The posterolateral approach to ankle joint is well suited for ORIF of posterior malleolar fractures. There are no major neurovascular structures endangering this approach other than the sural nerve. The sural nerve is often used as an autologous peripheral nerve graft and provides sensation to the lateral aspect of the foot. The aim of this paper is to measure the precise distance of the sural nerve from surrounding soft tissue structures so as to enable safe placement of skin incision in posterolateral approach. This is a retrospective image review study involving 64 MRI scans. All measurements were made from Axial T1 slices. The key findings of the paper is the safety window for the sural nerve from the lateral border of tendoachilles (TA) is 7 mm, 1.3 cm and 2 cm at 3 cm above ankle joint, at the ankle joint and at the distal tip of fibula respectively. Our study demonstrates the close relationship of the nerve in relation to TA and fibula in terms of exact measurements. The safety margins established in this study should enable the surgeon in preventing endangerment of the sural nerve encountered in this approach.

The CENP-H-I complex is required for the efficient incorporation of newly synthesized CENP-A into centromeres.

In vertebrates, centromeres lack defined sequences and are thought to be propagated by epigenetic mechanisms involving the incorporation of specialized nucleosomes containing the histone H3 variant centromere protein (CENP)-A. However, the precise mechanisms that target CENP-A to centromeres remain poorly understood. Here, we isolated a multi-subunit complex, which includes the established inner kinetochore components CENP-H and CENP-I, and nine other proteins, from both human and chicken cells. Our analysis of these proteins demonstrates that the CENP-H-I complex can be divided into three functional sub-complexes, each of which is required for faithful chromosome segregation. Interestingly, newly expressed CENP-A is not efficiently incorporated into centromeres in knockout mutants of a subclass of CENP-H-I complex proteins, indicating that the CENP-H-I complex may function, in part, as a marker directing CENP-A deposition to centromeres.

The class III kinase Vps34 promotes T lymphocyte survival through regulating IL-7Rα surface expression.

IL-7Rα-mediated signals are essential for naive T lymphocyte survival. Recent studies show that IL-7Rα is internalized and either recycled to cell surface or degraded. However, how the intracellular process of IL-7Rα trafficking is regulated is unclear. In this paper, we show that Vps34, the class III PI3K, plays a critical role in proper IL-7Rα intracellular trafficking. Mice lacking Vps34 in T lymphocytes had a severely reduced T lymphocyte compartment. Vps34-deficient T lymphocytes exhibit increased death and reduced IL-7Rα surface expression, although three major forms of autophagy remain intact. Intracellular IL-7Rα in normal T lymphocytes at steady state is trafficked through either early endosome/multivesicular bodies to the late endosome-Golgi for surface expression or to the lysosome for degradation. However, Vps34-deficient T cells have mislocalized intracellular Eea1, HGF-regulated tyrosine kinase substrate, and Vps36 protein levels, the combined consequence of which is the inability to mobilize internalized IL-7Rα into the retromer pathway for surface display. Our studies reveal that Vps34, though dispensable for autophagy induction, is a critical regulator of naive T cell homeostasis, modulating IL-7Rα trafficking, signaling, and recycling.

Asymmetric CLASP-dependent nucleation of noncentrosomal microtubules at the trans-Golgi network.

Proper organization of microtubule arrays is essential for intracellular trafficking and cell motility. It is generally assumed that most if not all microtubules in vertebrate somatic cells are formed by the centrosome. Here we demonstrate that a large number of microtubules in untreated human cells originate from the Golgi apparatus in a centrosome-independent manner. Both centrosomal and Golgi-emanating microtubules need gamma-tubulin for nucleation. Additionally, formation of microtubules at the Golgi requires CLASPs, microtubule-binding proteins that selectively coat noncentrosomal microtubule seeds. We show that CLASPs are recruited to the trans-Golgi network (TGN) at the Golgi periphery by the TGN protein GCC185. In sharp contrast to radial centrosomal arrays, microtubules nucleated at the peripheral Golgi compartment are preferentially oriented toward the leading edge in motile cells. We propose that Golgi-emanating microtubules contribute to the asymmetric microtubule networks in polarized cells and support diverse processes including post-Golgi transport to the cell front.

Reporting of the estimated glomerular filtration rate was associated with increased use of angiotensin-converting enzyme inhibitors and angiotensin-II receptor blockers in CKD.

Many guidelines suggest that angiotensin-converting enzyme inhibitors and angiotensin-II receptor antagonists (collectively referred to as renin, angiotensin, aldosterone system blockers (RAAS blockers)) are the preferred treatment for hypertension in most patients with chronic kidney disease (CKD). Improving the recognition of CKD with the introduction of eGFR reporting was intended to have more patients recognized with and treated for this disease. To quantify this, we examined trends in RAAS-blocker use over an 88-month period before and after routine eGFR reporting in southwestern Ontario, Canada. An intervention analysis with seasonal time-series modeling on linked health administrative data for 45,361 ambulatory residents with CKD (eGFR stages 3-5) older than 65 years was performed with a primary outcome of RAAS-blocker usage. The reporting of eGFR was associated with a significant increase in the use of RAAS blockers, as the prescription rate was 571 per 1000 patients with CKD prior to reporting but improved to 607 per 1000 after reporting. There was a significant increase in RAAS-blocker use attributable to eGFR reporting of 19 per 1000 CKD patients. Since about 8% of the adult population has CKD, this equates to about 15,200 new patients receiving RAAS-blocker treatment by 1 year after the introduction of eGFR reporting in community laboratories. Thus, eGFR reporting contributes to improved, guideline-appropriate care of older patients with CKD.

APC16 is a conserved subunit of the anaphase-promoting complex/cyclosome.

Error-free chromosome segregation depends on timely activation of the multi-subunit E3 ubiquitin ligase APC/C. Activation of the APC/C initiates chromosome segregation and mitotic exit by targeting critical cell-cycle regulators for destruction. The APC/C is the principle target of the mitotic checkpoint, which prevents segregation while chromosomes are unattached to spindle microtubules. We now report the identification and characterization of APC16, a conserved subunit of the APC/C. APC16 was found in association with tandem-affinity-purified mitotic checkpoint complex protein complexes. APC16 is a bona fide subunit of human APC/C: it is present in APC/C complexes throughout the cell cycle, the phenotype of APC16-depleted cells copies depletion of other APC/C subunits, and APC16 is important for APC/C activity towards mitotic substrates. APC16 sequence homologues can be identified in metazoans, but not fungi, by four conserved primary sequence stretches. We provide evidence that the C. elegans gene K10D2.4 and the D. rerio gene zgc:110659 are functional equivalents of human APC16. Our findings show that APC/C is composed of previously undescribed subunits, and raise the question of why metazoan APC/C is molecularly different from unicellular APC/C.

Regulation of T-cell survival and mitochondrial homeostasis by TSC1.

The mammalian target of rapamycin (mTOR) is a key regulator of cell growth and metabolism. It associates with multiple proteins and forms two distinct signaling complexes, mTORC1 and mTORC2. Accumulating evidence has revealed critical roles for intact mTOR signaling during T-cell activation and responses to microbial infection. However, the importance of mTOR regulation in T cells has yet to be explored. The TSC1/TSC2 complex has been shown to inhibit mTORC1 signaling in cell line models. We show here that deletion of TSC1 in the murine T-cell lineage results in a dramatic reduction of the peripheral T-cell pool, correlating with increased cell death. While mTORC1 is constitutively activated, mTORC2 signaling, reflected by Akt phosphorylation and activity, is decreased in TSC1-deficient T cells. Furthermore, TSC1-deficient T cells contain elevated reactive oxygen species (ROS) and exhibit decreased mitochondrial content and membrane potential, which is correlated with the activation of the intrinsic death pathway. Overall, our results demonstrate that TSC1 differentially regulates mTORC1 and mTORC2 activity, promotes T-cell survival, and is critical for normal mitochondrial homeostasis in T cells.

Remnant oyster reefs as fish habitat within the estuarine seascape.

Interest in oyster reef conservation and restoration is growing globally, but particularly in Australia, it is unclear the extent to which oyster reefs complement (versus replicate) habitat provisioning by other structured habitats in the seascape. Remote underwater video surveys of two east Australian estuaries revealed that at high tide, oyster reefs not only supported distinct fish communities to bare sediments but also to adjacent seagrass beds and mangrove forests. Fish observations in oyster reefs were close to double that of mangroves and seagrass, with species richness, abundance, feeding and wandering behaviours similar. Several species of blenny and goby were unique to oyster reefs and oyster-containing mangroves, whilst recreationally fished species such as bream and mullet were more abundant on oyster reefs than in other habitats. Resolving the association between oyster reefs and fish species within the broader seascape will assist in developing restoration and management strategies that maximise fisheries benefit.

Coral restoration and adaptation in Australia: The first five years.

While coral reefs in Australia have historically been a showcase of conventional management informed by research, recent declines in coral cover have triggered efforts to innovate and integrate intervention and restoration actions into management frameworks. Here we outline the multi-faceted intervention approaches that have developed in Australia since 2017, from newly implemented in-water programs, research to enhance coral resilience and investigations into socio-economic perspectives on restoration goals. We describe in-water projects using coral gardening, substrate stabilisation, coral repositioning, macro-algae removal, and larval-based restoration techniques. Three areas of research focus are also presented to illustrate the breadth of Australian research on coral restoration, (1) the transdisciplinary Reef Restoration and Adaptation Program (RRAP), one of the world's largest research and development programs focused on coral reefs, (2) interventions to enhance coral performance under climate change, and (3) research into socio-cultural perspectives. Together, these projects and the recent research focus reflect an increasing urgency for action to confront the coral reef crisis, develop new and additional tools to manage coral reefs, and the consequent increase in funding opportunities and management appetite for implementation. The rapid progress in trialling and deploying coral restoration in Australia builds on decades of overseas experience, and advances in research and development are showing positive signs that coral restoration can be a valuable tool to improve resilience at local scales (i.e., high early survival rates across a variety of methods and coral species, strong community engagement with local stakeholders). RRAP is focused on creating interventions to help coral reefs at multiple scales, from micro scales (i.e., interventions targeting small areas within a specific reef site) to large scales (i.e., interventions targeting core ecosystem function and social-economic values at multiple select sites across the Great Barrier Reef) to resist, adapt to and recover from the impacts of climate change. None of these interventions aim to single-handedly restore the entirety of the Great Barrier Reef, nor do they negate the importance of urgent climate change mitigation action.

A unique sorting nexin regulates trafficking of potassium channels via a PDZ domain interaction.

G protein-gated potassium (Kir3) channels are important for controlling neuronal excitability in the brain. Using a proteomics approach, we have identified a unique rodent intracellular protein, sorting nexin 27 (SNX27), which regulates the trafficking of Kir3 channels. Like most sorting nexins, SNX27 possesses a functional PX domain that selectively binds the membrane phospholipid phosphatidylinositol-3-phosphate (PI3P) and is important for trafficking to the early endosome. SNX27, however, is the only sorting nexin to contain a PDZ domain. This PDZ domain discriminates between channels with similar class I PDZ-binding motifs, associating with the C-terminal end of Kir3.3 and Kir3.2c (-ESKV), but not with that of Kir2.1 (-ESEI) or Kv1.4 (-ETDV). SNX27 promotes the endosomal movement of Kir3 channels, leading to reduced surface expression, increased degradation and smaller Kir3 potassium currents. The regulation of endosomal trafficking via sorting nexins reveals a previously unknown mechanism for controlling potassium channel surface expression.

Class I PI3K Provide Lipid Substrate in T Cell Autophagy Through Linked Activity of Inositol Phosphatases.

Autophagy, a highly conserved intracellular process, has been identified as a novel mechanism regulating T lymphocyte homeostasis. Herein, we demonstrate that both starvation- and T cell receptor-mediated autophagy induction requires class I phosphatidylinositol-3 kinases to produce PI(3)P. In contrast, common gamma chain cytokines are suppressors of autophagy despite their ability to activate the PI3K pathway. T cells lacking the PI3KI regulatory subunits, p85 and p55, were almost completely unable to activate TCR-mediated autophagy and had concurrent defects in PI(3)P production. Additionally, T lymphocytes upregulate polyinositol phosphatases in response to autophagic stimuli, and the activity of the inositol phosphatases Inpp4 and SHIP are required for TCR-mediated autophagy induction. Addition of exogenous PI(3,4)P2 can supplement cellular PI(3)P and accelerate the outcome of activation-induced autophagy. TCR-mediated autophagy also requires internalization of the TCR complex, suggesting that this kinase/phosphatase activity is localized in internalized vesicles. Finally, HIV-induced bystander CD4+ T cell autophagy is dependent upon PI3KI. Overall, our data elucidate an important pathway linking TCR activation to autophagy, via induction of PI3KI activity and inositol phosphatase upregulation to produce PI(3)P.