Fluid-rock interaction, skarn genesis, and hydrothermal alteration within an upper crustal fault zone (Island of Elba, Italy)

The Terranera magnetite-hematite-pyrite deposit of the Island of Elba (Italy) is an historical skarn deposit hosted by a fault zone of regional importance (Zuccale Fault) and by its hanging wall rocks. We combine field observations with petrographic data, electron probe microanalyses (EPMA), XRPD data, fluid inclusion microthermometry, and element imaging by Laser Ablation-Inductively Coupled Plasma-Time of Flight Mass Spectrometry (LA-ICP-TOFMS) to define the ore-forming process at Terranera. We show that in this location the fault is made of four levels of mineralized fault rocks having distinct mineral compositions. In these levels, a mineral association made of diopside, clinozoisite, and other Mg-rich minerals is replaced by magnetite, hematite, pyrite, Mg-hornblende, clinochlore, and other Mg-rich phyllosilicates. This paragenesis is overprinted by goethite and clay minerals. Chlorite-quartz geothermometry and fluid inclusion microthermometry show that ore precipitation occurred at 350–180 °C from fluids of distinct bulk salinities, but goethite and clay mineral overprinting progressed at lower T. We propose that Terranera is a magnesian Fe skarn formed due to the interaction between distinct hydrothermal fluids and a dolomitic protolith, which was preserved within the fault zone. These fluids mixed and cooled during protolith metasomatism, causing ore precipitation due to oxidation and desulfidation. A very similar process was described in a large deposit of Elba (Rio Marina). Argillic alteration was widespread within the fault but met permanently intermediate sulfidation conditions. Trace element composition of hematite shows that Terranera has features that overlap those of skarn and epithermal deposits. In particular, elements that are typical of epithermal deposits (Sb, Ga, Ge, As) occur at mass fractions (50–200 μg/g) that are either unreported or not typical of hematite from skarn deposits. These features identify Terranera as formed in an ore environment that was transitional between that of a skarn and of an epithermal deposit. These features are shared by other historical deposits located at Elba and in the massive pyritic ore district of south Tuscany (e.g., Gavorrano, Fenice Capanne). This indicates that a similar environment might have occurred during the Neogene beyond Elba, in a much larger ore district of south Tuscany

Experimental techniques to assess coral physiology in situ under global and local stressors : current approaches and novel insights

This study was supported by the Hong Kong Branch of Southern Marine Science and Engineering Guangdong Laboratory (Guangzhou; SMSEGL20SC02); the Collaborative Research Fund (C7013-19G) of the Hong Kong Research Grants Council; the National Natural Science Foundation of China (41641047); the Internal Research Project of State Key Laboratory of Satellite Ocean Environment Dynamics, Second Institute of Oceanography, State Oceanic Administration (no. SOEDZZ1702); and the SKLMP Seed Collaborative Research Fund (SCRF/0027).Coral reefs are declining worldwide due to global changes in the marine environment. The increasing frequency of massive bleaching events in the tropics is highlighting the need to better understand the stages of coral physiological responses to extreme conditions. Moreover, like many other coastal regions, coral reef ecosystems are facing additional localized anthropogenic stressors such as nutrient loading, increased turbidity, and coastal development. Different strategies have been developed to measure the health status of a damaged reef, ranging from the resolution of individual polyps to the entire coral community, but techniques for measuring coral physiology in situ are not yet widely implemented. For instance, while there are many studies of the coral holobiont response in single or limited-number multiple stressor experiments, they provide only partial insights into metabolic performance under more complex and temporally and spatially variable natural conditions. Here, we discuss the current status of coral reefs and their global and local stressors in the context of experimental techniques that measure core processes in coral metabolism (respiration, photosynthesis, and biocalcification) in situ, and their role in indicating the health status of colonies and communities. We highlight the need to improve the capability of in situ studies in order to better understand the resilience and stress response of corals under multiple global and local scale stressors.Publisher PDFPeer reviewe

No detectable effect of ocean acidification on plankton metabolism in the NW oligotrophic Mediterranean Sea: Results from two mesocosm studies

Oligotrophic areas account for about 30% of oceanic primary production and are projected to expand in a warm, high-CO2 world. Changes in primary production in these areas could have important impacts on future global carbon cycling. To assess the response of primary production and respiration of plankton communities to increasing partial pressure of CO2 (pCO2) levels in Low Nutrient Low Chorophyll areas, two mesocosm experiments were conducted in the Bay of Calvi (Corsica, France) and in the Bay of Villefranche (France) in June–July 2012 and February–March 2013 under different trophic state, temperature and irradiance conditions. Nine mesocosms of 50 m3 were deployed for 20 and 12 days, respectively, and were subjected to seven pCO2 levels (3 control and 6 elevated levels). The metabolism of the community was studied using several methods based on in situ incubations (oxygen light–dark, 18O and 14C uptake). Increasing pCO2 had no significant effect on gross primary production, net community production, particulate and dissolved carbon production, as well as on community respiration. These two mesocosm experiments, the first performed under maintained low nutrient and low chlorophyll, suggest that in large areas of the ocean, increasing pCO2 levels may not lead to a significant change in plankton metabolic rates and sea surface biological carbon fixation

Gating at the Mouth of the Acetylcholine Receptor Channel: Energetic Consequences of Mutations in the αM2-Cap

Gating of nicotinic acetylcholine receptors from a C(losed) to an O(pen) conformation is the initial event in the postsynaptic signaling cascade at the vertebrate nerve-muscle junction. Studies of receptor structure and function show that many residues in this large, five-subunit membrane protein contribute to the energy difference between C and O. Of special interest are amino acids located at the two transmitter binding sites and in the narrow region of the channel, where C↔O gating motions generate a low↔high change in the affinity for agonists and in the ionic conductance, respectively. We have measured the energy changes and relative timing of gating movements for residues that lie between these two locations, in the C-terminus of the pore-lining M2 helix of the α subunit (‘αM2-cap’). This region contains a binding site for non-competitive inhibitors and a charged ring that influences the conductance of the open pore. αM2-cap mutations have large effects on gating but much smaller effects on agonist binding, channel conductance, channel block and desensitization. Three αM2-cap residues (αI260, αP265 and αS268) appear to move at the outset of channel-opening, about at the same time as those at the transmitter binding site. The results suggest that the αM2-cap changes its secondary structure to link gating motions in the extracellular domain with those in the channel that regulate ionic conductance

Identification and Structural Characterization of a New Three-Finger Toxin Hemachatoxin from Hemachatus haemachatus Venom

10.1371/journal.pone.0048112PLoS ONE710

Identification of a Negative Allosteric Site on Human α4β2 and α3β4 Neuronal Nicotinic Acetylcholine Receptors

Acetylcholine-based neurotransmission is regulated by cationic, ligand-gated ion channels called nicotinic acetylcholine receptors (nAChRs). These receptors have been linked to numerous neurological diseases and disorders such as Alzheimer's disease, Parkinson's disease, and nicotine addiction. Recently, a class of compounds has been discovered that antagonize nAChR function in an allosteric fashion. Models of human α4β2 and α3β4 nicotinic acetylcholine receptor (nAChR) extracellular domains have been developed to computationally explore the binding of these compounds, including the dynamics and free energy changes associated with ligand binding. Through a blind docking study to multiple receptor conformations, the models were used to determine a putative binding mode for the negative allosteric modulators. This mode, in close proximity to the agonist binding site, is presented in addition to a hypothetical mode of antagonism that involves obstruction of C loop closure. Molecular dynamics simulations and MM-PBSA free energy of binding calculations were used as computational validation of the predicted binding mode, while functional assays on wild-type and mutated receptors provided experimental support. Based on the proposed binding mode, two residues on the β2 subunit were independently mutated to the corresponding residues found on the β4 subunit. The T58K mutation resulted in an eight-fold decrease in the potency of KAB-18, a compound that exhibits preferential antagonism for human α4β2 over α3β4 nAChRs, while the F118L mutation resulted in a loss of inhibitory activity for KAB-18 at concentrations up to 100 µM. These results demonstrate the selectivity of KAB-18 for human α4β2 nAChRs and validate the methods used for identifying the nAChR modulator binding site. Exploitation of this site may lead to the development of more potent and subtype-selective nAChR antagonists which may be used in the treatment of a number of neurological diseases and disorders

A Unified Model of the GABA(A) Receptor Comprising Agonist and Benzodiazepine Binding Sites

We present a full-length α(1)β(2)γ(2) GABA receptor model optimized for agonists and benzodiazepine (BZD) allosteric modulators. We propose binding hypotheses for the agonists GABA, muscimol and THIP and for the allosteric modulator diazepam (DZP). The receptor model is primarily based on the glutamate-gated chloride channel (GluCl) from C. elegans and includes additional structural information from the prokaryotic ligand-gated ion channel ELIC in a few regions. Available mutational data of the binding sites are well explained by the model and the proposed ligand binding poses. We suggest a GABA binding mode similar to the binding mode of glutamate in the GluCl X-ray structure. Key interactions are predicted with residues α(1)R66, β(2)T202, α(1)T129, β(2)E155, β(2)Y205 and the backbone of β(2)S156. Muscimol is predicted to bind similarly, however, with minor differences rationalized with quantum mechanical energy calculations. Muscimol key interactions are predicted to be α(1)R66, β(2)T202, α(1)T129, β(2)E155, β(2)Y205 and β(2)F200. Furthermore, we argue that a water molecule could mediate further interactions between muscimol and the backbone of β(2)S156 and β(2)Y157. DZP is predicted to bind with interactions comparable to those of the agonists in the orthosteric site. The carbonyl group of DZP is predicted to interact with two threonines α(1)T206 and γ(2)T142, similar to the acidic moiety of GABA. The chlorine atom of DZP is placed near the important α(1)H101 and the N-methyl group near α(1)Y159, α(1)T206, and α(1)Y209. We present a binding mode of DZP in which the pending phenyl moiety of DZP is buried in the binding pocket and thus shielded from solvent exposure. Our full length GABA(A) receptor is made available as Model S1