Estimating global biomass and biogeochemical cycling of marine fish with and without fishing

Unidad de excelencia María de Maeztu CEX2019-000940-MThe biomass and biogeochemical roles of fish in the ocean are ecologically important but poorly known. Here, we use a data-constrained marine ecosystem model to provide a first-order estimate of the historical reduction of fish biomass due to fishing and the associated change in biogeochemical cycling rates. The pre-exploitation global biomass of exploited fish (10 g to 100 kg) was 3.3 ± 0.5 Gt, cycling roughly 2% of global primary production (9.4 ± 1.6 Gt year−1) and producing 10% of surface biological export. Particulate organic matter produced by exploited fish drove roughly 10% of the oxygen consumption and biological carbon storage at depth. By the 1990s, biomass and cycling rates had been reduced by nearly half, suggesting that the biogeochemical impact of fisheries has been comparable to that of anthropogenic climate change. Our results highlight the importance of developing a better mechanistic understanding of how fish alter ocean biogeochemistry

In Situ Formed Sn1 xInx In1 ySnyOz Core Shell Nanoparticles as Electrocatalysts for CO2 Reduction to Formate

Electrochemical reduction of CO2 CO2RR driven by renewable energy has gained increasing attention for sustainable production of chemicals and fuels. Catalyst design to overcome large overpotentials and poor product selectivity remains however challenging. Sn SnOx and In InOx composites have been reported active for CO2RR with high selectivity toward formate formation. In this work, the CO2RR activity and selectivity of metal metal oxide composite nanoparticles formed by in situ reduction of bimetallic amorphous SnInOx thin films are investigated. It is shown that during CO2RR the amorphous SnInOx pre catalyst thin films are reduced in situ into Sn1 XInX In1 YSnYOz core shell nanoparticles composed of Sn rich SnIn alloy nanocores with x lt; 0.2 surrounded by InOx rich bimetallic InSnOx shells with 0.3 lt; y lt; 0.4 and z amp; 8776; 1 . The in situ formed particles catalyze the CO2RR to formate with high faradaic efficiency 80 and outstanding formate mass activity 437 A gIn Sn amp; 8722;1 amp; 8722;1.0 V vs RHE in 0.1 m KHCO3 . While extensive structural investigation during CO2RR reveals pronounced dynamics in terms of particle size, the core shell structure is observed for the different electrolysis conditions essayed, with high surface oxide contents favoring formate over hydrogen selectivit

Vibrio coralliilyticus infection triggers a behavioural response and perturbs nutritional exchange and tissue integrity in a symbiotic coral

Under homoeostatic conditions, the relationship between the coralPocillopora damicornisandVibrio coralliilyticusiscommensal. An increase in temperature, or in the abundance ofV. coralliilyticus, can turn this association pathogenic,causing tissue lysis, expulsion of the corals’symbiotic algae (genusSymbiodinium), and eventually coral death. Using acombination of microfluidics,fluorescence microscopy, stable isotopes, electron microscopy and NanoSIMS isotopicimaging, we provide insights into the onset and progression ofV.coralliilyticusinfection in the daytime and at night, atthe tissue and (sub-)cellular level. The objective of our study was to connect the macro-scale behavioural response ofthe coral to the micro-scale nutritional interactions that occur between the host and its symbiont. In the daytime, polypsenhanced their mucus production, and actively spewed pathogens.Vibrioinfection primarily resulted in the formationof tissue lesions in the coenosarc. NanoSIMS analysis revealed infection reduced13C-assimilation inSymbiodinium, butincreased13C-assimilation in the host. In the night incubations, no mucus spewing was observed, and a mucusfilm wasformed on the coral surface.Vibrioinoculation and infection at night showed reduced13C-turnover inSymbiodinium, but didnot impact host13C-turnover. Our results show that both the nutritional interactions that occur between the two symbioticpartners and the behavioural response of the host organism play key roles in determining the progression and severity ofhost-pathogen interactions. More generally, our approach provides a new means of studying interactions (ranging frombehavioural to metabolic scales) between partners involved in complex holobiont systems, under both homoeostatic andpathogenic conditions

Sheldon Spectrum and the Plankton Paradox: Two Sides of the Same Coin : A trait-based plankton size-spectrum model

The Sheldon spectrum describes a remarkable regularity in aquatic ecosystems: the biomass density as a function of logarithmic body mass is approximately constant over many orders of magnitude. While size-spectrum models have explained this phenomenon for assemblages of multicellular organisms, this paper introduces a species-resolved size-spectrum model to explain the phenomenon in unicellular plankton. A Sheldon spectrum spanning the cell-size range of unicellular plankton necessarily consists of a large number of coexisting species covering a wide range of characteristic sizes. The coexistence of many phytoplankton species feeding on a small number of resources is known as the Paradox of the Plankton. Our model resolves the paradox by showing that coexistence is facilitated by the allometric scaling of four physiological rates. Two of the allometries have empirical support, the remaining two emerge from predator-prey interactions exactly when the abundances follow a Sheldon spectrum. Our plankton model is a scale-invariant trait-based size-spectrum model: it describes the abundance of phyto- and zooplankton cells as a function of both size and species trait (the maximal size before cell division). It incorporates growth due to resource consumption and predation on smaller cells, death due to predation, and a flexible cell division process. We give analytic solutions at steady state for both the within-species size distributions and the relative abundances across species

L-Plastin nanobodies perturb matrix degradation, podosome formation, stability and lifetime in THP-1 macrophages

Podosomes are cellular structures acting as degradation ‘hot-spots’ in monocytic cells. They appear as dot-like structures at the ventral cell surface, enriched in F-actin and actin regulators, including gelsolin and L-plastin. Gelsolin is an ubiquitous severing and capping protein, whereas L-plastin is a leukocyte-specific actin bundling protein. The presence of the capping protein CapG in podosomes has not yet been investigated. We used an innovative approach to investigate the role of these proteins in macrophage podosomes by means of nanobodies or Camelid single domain antibodies. Nanobodies directed against distinct domains of gelsolin, L-plastin or CapG were stably expressed in macrophage-like THP-1 cells. CapG was not enriched in podosomes. Gelsolin nanobodies had no effect on podosome formation or function but proved very effective in tracing distinct gelsolin populations. One gelsolin nanobody specifically targets actin-bound gelsolin and was effectively enriched in podosomes. A gelsolin nanobody that blocks gelsolin-G-actin interaction was not enriched in podosomes demonstrating that the calcium-activated and actin-bound conformation of gelsolin is a constituent of podosomes. THP-1 cells expressing inhibitory L-plastin nanobodies were hampered in their ability to form stable podosomes. Nanobodies did not perturb Ser5 phosphorylation of L-plastin although phosphorylated L-plastin was highly enriched in podosomes. Furthermore, nanobody-induced inhibition of L-plastin function gave rise to an irregular and unstable actin turnover of podosomes, resulting in diminished degradation of the underlying matrix. Altogether these results indicate that L-plastin is indispensable for podosome formation and function in macrophages

Tuberculosis is associated with expansion of a motile, permissive and immunomodulatory CD16(+) monocyte population via the IL-10/STAT3 axis

The human CD14+ monocyte compartment is composed by two subsets based on CD16 expression. We previously reported that this compartment is perturbed in tuberculosis (TB) patients, as reflected by the expansion of CD16+ monocytes along with disease severity. Whether this unbalance is beneficial or detrimental to host defense remains to be elucidated. Here in the context of active TB, we demonstrate that human monocytes are predisposed to differentiate towards an anti-inflammatory (M2-like) macrophage activation program characterized by theCD16+CD163+MerTK+pSTAT3+ phenotype and functional properties such as enhanced protease-dependent motility, pathogen permissivity and immunomodulation. This process is dependent on STAT3 activation, and loss-of-function experiments point towards a detrimental role in host defense against TB. Importantly, we provide a critical correlation between the abundance of the CD16+CD163+MerTK+pSTAT3+ cells and the progression of the disease either at the local level in a non-human primate tuberculous granuloma context, or at the systemic level through the detection of the soluble form of CD163 in human sera. Collectively, this study argues for the pathogenic role of the CD16+CD163+MerTK+pSTAT3+ monocyte-to-macrophage differentiation program and its potential as a target for TB therapy,and promotes the detection of circulating CD163 as a potential biomarker for disease progression and monitoringof treatment efficacy.Fil: Lastrucci, Claire. Centre National de la Recherche Scientifique; FranciaFil: Bénard, Alan. Centre National de la Recherche Scientifique; FranciaFil: Balboa, Luciana. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Pingris, Karine. Centre National de la Recherche Scientifique; FranciaFil: Souriant, Shanti. Centre National de la Recherche Scientifique; FranciaFil: Poincloux, Renaud. Centre National de la Recherche Scientifique; FranciaFil: Al Saati, Talal. Inserm; FranciaFil: Rasolofo, Voahangy. Pasteur Institute in Antananarivo; MadagascarFil: González Montaner, Pablo. Gobierno de la Ciudad de Buenos Aires. Hospital de Infecciosas ; ArgentinaFil: Inwentarz, Sandra. Gobierno de la Ciudad de Buenos Aires. Hospital de Infecciosas ; ArgentinaFil: Moraña, Eduardo José. Gobierno de la Ciudad de Buenos Aires. Hospital de Infecciosas ; ArgentinaFil: Kondova, Ivanela. Biomedical Primate Research Centre; Países BajosFil: Verreck, Franck A. W.. Biomedical Primate Research Centre; Países BajosFil: Sasiain, María del Carmen. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Neyrolles, Olivier. Centre National de la Recherche Scientifique; FranciaFil: Maridonneau Parini, Isabel. Centre National de la Recherche Scientifique; FranciaFil: Lugo Villarino, Geanncarlo. Centre National de la Recherche Scientifique; FranciaFil: Cougoule, Celine. Centre National de la Recherche Scientifique; Franci