BUSCADOR RECOLECTA

Cyanobacteria are prokaryotic organisms that capture energy from sunlight using oxygenic photosynthesis and transform CO2 into products of interest such as fatty acids. Synechococcus elongatus PCC 7942 is a model cyanobacterium efficiently engineered to accumulate high levels of omega-3 fatty acids. However, its exploitation as a microbial cell factory requires a better knowledge of its metabolism, which can be approached by using systems biology tools. To fulfill this objective, we worked out an updated, more comprehensive, and functional genome-scale model of this freshwater cyanobacterium, which was termed iMS837. The model includes 837 genes, 887 reactions, and 801 metabolites. When compared with previous models of S. elongatus PCC 7942, iMS837 is more complete in key physiological and biotechnologically relevant metabolic hubs, such as fatty acid biosynthesis, oxidative phosphorylation, photosynthesis, and transport, among others. iMS837 shows high accuracy when predicting growth performance and gene essentiality. The validated model was further used as a test-bed for the assessment of suitable metabolic engineering strategies, yielding superior production of non-native omega-3 fatty acids such as α-linolenic acid (ALA). As previously reported, the computational analysis demonstrated that fabF overexpression is a feasible metabolic target to increase ALA production, whereas deletion and overexpression of fabH cannot be used for this purpose. Flux scanning based on enforced objective flux, a strain-design algorithm, allowed us to identify not only previously known gene overexpression targets that improve fatty acid synthesis, such as Acetyl-CoA carboxylase and β-ketoacyl-ACP synthase I, but also novel potential targets that might lead to higher ALA yields. Systematic sampling of the metabolic space contained in iMS837 identified a set of ten additional knockout metabolic targets that resulted in higher ALA productions. In silico simulations under photomixotrophic conditions with acetate or glucose as a carbon source boosted ALA production levels, indicating that photomixotrophic nutritional regimens could be potentially exploited in vivo to improve fatty acid production in cyanobacteria. Overall, we show that iMS837 is a powerful computational platform that proposes new metabolic engineering strategies to produce biotechnologically relevant compounds, using S. elongatus PCC 7942 as non-conventional microbial cell factory., Peer reviewed

This paper describes a major update to the quasi-global, higher-frequency sea-level dataset known as GESLA (Global Extreme Sea Level Analysis). Versions 1 (released 2009) and 2 (released 2016) of the dataset have been used in many published studies, across a wide range of oceanographic and coastal engineering-related investigations concerned with evaluating tides, storm surges, extreme sea levels, and other related processes. The third version of the dataset (released 2021), presented here, contains double the number of years of data, and nearly four times the number of records, compared to Version 2. The dataset consists of records obtained from multiple sources around the world. This paper describes the assembly of the dataset, its processing, and its format, and outlines potential future improvements., We received no direct funding to assemble GESLA 3, however part of our time was funded on relevant grants, as follows: IDH time was partly funded via the NERC-funded CHANCE Project (NE/S010262/1); SAT was partly funded by the National Science Foundation (Award number 1455350 and 2013280); MM was supported by European Regional Development Fund/Ministerio de Ciencia, Innovación y Universidades – Agencia Estatal de Investigación through the MOCCA project (grant no. RTI2018-093941-B-C31); PRT was supported by the National Oceanic and Atmospheric Administration Global Ocean Monitoring and Observation Program via the University of Hawaiʻi Sea Level Center (grant no. NA11NMF4320128)., Peer reviewed

Figuras adicionales del artículo "Análisis de la producción científica internacional sobre evaluación de la efectividad de las políticas, planes, programas y proyectos en la prevención del consumo de drogas" publicado en la Revista Acta Psiquiátrica y Psicológica de América Latina 69 (3) y 69 (4)., Peer reviewed

Key message: This datapaper collects individual georeferenced tree height data from Pinus nigraArn.,P. pinasterAiton, andP. pineaL. planted in common gardens in France, Germany, Morocco, and Spain. The data can be used to assess genetic variation and phenotypic plasticity with further applications in biogeography and forest management. The three datasets are available at https://doi.org/10.5281/zenodo.3250704(Vizcaíno-Palomar et al.2018a),https://doi.org/10.5281/zenodo.3250698(Vizcaíno-Palomar et al.2018b), andhttps://doi.org/10.5281/zenodo.3250707(Vizcaíno-Palomar et al. 2018c), and the associated metadata are available at https://metadata-afs.nancy.inra.fr/geonetwork/srv/eng/catalog.search#/metadata/644682d3-78c6-4fcc-af26-b1a928be7b1b,https://metadata-afs.nancy.inra.fr/geonetwork/srv/eng/catalog.search#/metadata/535b8ad0-9315-4d78-80bd-d0f6cbb9d0ceandhttps://metadata-afs.nancy.inra.fr/geonetwork/srv/eng/catalog.search#/metadata/4cc0d2f0-00a9-42c8-aa34-fbbc647e3eb9forP. nigra, P. pinasterandP. pinea, respectively., We acknowledge the funding called Investments for the future: Programme IdEx Bordeaux (France), reference ANR-10-IDEX-03-02, thanks to that MBG coordinated this datapaper and NVP worked on it. Identically, we acknowledge funding from the French Ministry of Agriculture in charge of forests and its regional bureau in Montpellier, the ANR project AMTools (ANR-11-AGRO-0005), and the Aix-Marseille Université (as part of GG’s PhD thesis) for the French data. In the same way, we acknowledge the support from the Spanish Ministry of Agriculture, Fishery and Environment (MAPAMA) and the regional governments of Junta de Castilla y León and Generalitat Valenciana through agreements with Universidad Politécnica de Madrid (UPM). Likewise, we acknowledge funding from the Bavarian State Ministry of Food, Agriculture and Forestry (StMELF) for the German data. The creation of the network of P. pinea common gardens was made possible by the support given from FAO Silva Mediterranea (http://www.fao.org/forestry/silva-mediterranea/en/). INRA funded the creation and maintenance of the French experimental network of common gardens (GEN4X), as well as the development and implementation of the information system archiving its data, GnpIS (https://urgi.versailles.inra.fr/Tools/GnpIS). P. pinea data collected in the future will be archived on GnpIS at: https://urgi.versailles.inra.fr/ephesis/ephesis/viewer.do#dataResults). INIA funded the Spanish network by successive projects OT03-002, AT2010-007, AT2013-004, and RTA2013-00011. Finally, this publication is part of a project that has received funding from the European Union’s Horizon 2020 research and innovation programmer under grant agreement no. 676876 (GenTree)., Peer reviewed

This is a dataset of our research realized recently, which contains tested results (json files) by F-UJI tool and FAIR assesment reports of tested repositories., Peer reviewed

Fig. S1.1 Adaptive inference protocol of the Doñana long-term social-ecological research program (based on Holling and Allen 2002, Peer reviewed

Ellis van Creveld syndrome and Weyers acrofacial dysostosis are two rare genetic diseases affecting skeletal development. They are both ciliopathies, as they are due to malfunction of primary cilia, microtubule-based plasma membrane protrusions that function as cellular antennae and are required for Hedgehog signaling, a key pathway during skeletal morphogenesis. These ciliopathies are caused by mutations affecting the EVC-EVC2 complex, a transmembrane protein heterodimer that regulates Hedgehog signaling from inside primary cilia. Despite the importance of this complex, the mechanisms underlying its stability, targeting and function are poorly understood. To address this, we characterized the endogenous EVC protein interactome in control and Evc-null cells. This proteomic screen confirmed EVC’s main known interactors (EVC2, IQCE, EFCAB7), while revealing new ones, including USP7, a deubiquitinating enzyme involved in Hedgehog signaling. We therefore looked at EVC-EVC2 complex ubiquitination. Such ubiquitination exists but is independent of USP7 (and of USP48, also involved in Hh signaling). We did find, however, that monoubiquitination of EVC-EVC2 cytosolic tails greatly reduces their protein levels. On the other hand, modification of EVC-EVC2 cytosolic tails with the small ubiquitin-related modifier SUMO3 has a different effect, enhancing complex accumulation at the EvC zone, immediately distal to the ciliary transition zone, possibly via increased binding to the EFCAB7-IQCE complex. Lastly, we find that EvC zone targeting of EVC-EVC2 depends on two separate EFCAB7-binding motifs within EVC2’s Weyers-deleted peptide. Only one of these motifs had been characterized previously, so we have mapped the second herein. Altogether, our data shed light on EVC-EVC2 complex regulatory mechanisms, with implications for ciliopathies., Peer reviewed

Ellis van Creveld syndrome and Weyers acrofacial dysostosis are two rare genetic diseases affecting skeletal development. They are both ciliopathies, as they are due to malfunction of primary cilia, microtubule-based plasma membrane protrusions that function as cellular antennae and are required for Hedgehog signaling, a key pathway during skeletal morphogenesis. These ciliopathies are caused by mutations affecting the EVC-EVC2 complex, a transmembrane protein heterodimer that regulates Hedgehog signaling from inside primary cilia. Despite the importance of this complex, the mechanisms underlying its stability, targeting and function are poorly understood. To address this, we characterized the endogenous EVC protein interactome in control and Evc-null cells. This proteomic screen confirmed EVC’s main known interactors (EVC2, IQCE, EFCAB7), while revealing new ones, including USP7, a deubiquitinating enzyme involved in Hedgehog signaling. We therefore looked at EVC-EVC2 complex ubiquitination. Such ubiquitination exists but is independent of USP7 (and of USP48, also involved in Hh signaling). We did find, however, that monoubiquitination of EVC-EVC2 cytosolic tails greatly reduces their protein levels. On the other hand, modification of EVC-EVC2 cytosolic tails with the small ubiquitin-related modifier SUMO3 has a different effect, enhancing complex accumulation at the EvC zone, immediately distal to the ciliary transition zone, possibly via increased binding to the EFCAB7-IQCE complex. Lastly, we find that EvC zone targeting of EVC-EVC2 depends on two separate EFCAB7-binding motifs within EVC2’s Weyers-deleted peptide. Only one of these motifs had been characterized previously, so we have mapped the second herein. Altogether, our data shed light on EVC-EVC2 complex regulatory mechanisms, with implications for ciliopathies., Peer reviewed

Ellis van Creveld syndrome and Weyers acrofacial dysostosis are two rare genetic diseases affecting skeletal development. They are both ciliopathies, as they are due to malfunction of primary cilia, microtubule-based plasma membrane protrusions that function as cellular antennae and are required for Hedgehog signaling, a key pathway during skeletal morphogenesis. These ciliopathies are caused by mutations affecting the EVC-EVC2 complex, a transmembrane protein heterodimer that regulates Hedgehog signaling from inside primary cilia. Despite the importance of this complex, the mechanisms underlying its stability, targeting and function are poorly understood. To address this, we characterized the endogenous EVC protein interactome in control and Evc-null cells. This proteomic screen confirmed EVC’s main known interactors (EVC2, IQCE, EFCAB7), while revealing new ones, including USP7, a deubiquitinating enzyme involved in Hedgehog signaling. We therefore looked at EVC-EVC2 complex ubiquitination. Such ubiquitination exists but is independent of USP7 (and of USP48, also involved in Hh signaling). We did find, however, that monoubiquitination of EVC-EVC2 cytosolic tails greatly reduces their protein levels. On the other hand, modification of EVC-EVC2 cytosolic tails with the small ubiquitin-related modifier SUMO3 has a different effect, enhancing complex accumulation at the EvC zone, immediately distal to the ciliary transition zone, possibly via increased binding to the EFCAB7-IQCE complex. Lastly, we find that EvC zone targeting of EVC-EVC2 depends on two separate EFCAB7-binding motifs within EVC2’s Weyers-deleted peptide. Only one of these motifs had been characterized previously, so we have mapped the second herein. Altogether, our data shed light on EVC-EVC2 complex regulatory mechanisms, with implications for ciliopathies., Peer reviewed

Ellis van Creveld syndrome and Weyers acrofacial dysostosis are two rare genetic diseases affecting skeletal development. They are both ciliopathies, as they are due to malfunction of primary cilia, microtubule-based plasma membrane protrusions that function as cellular antennae and are required for Hedgehog signaling, a key pathway during skeletal morphogenesis. These ciliopathies are caused by mutations affecting the EVC-EVC2 complex, a transmembrane protein heterodimer that regulates Hedgehog signaling from inside primary cilia. Despite the importance of this complex, the mechanisms underlying its stability, targeting and function are poorly understood. To address this, we characterized the endogenous EVC protein interactome in control and Evc-null cells. This proteomic screen confirmed EVC’s main known interactors (EVC2, IQCE, EFCAB7), while revealing new ones, including USP7, a deubiquitinating enzyme involved in Hedgehog signaling. We therefore looked at EVC-EVC2 complex ubiquitination. Such ubiquitination exists but is independent of USP7 (and of USP48, also involved in Hh signaling). We did find, however, that monoubiquitination of EVC-EVC2 cytosolic tails greatly reduces their protein levels. On the other hand, modification of EVC-EVC2 cytosolic tails with the small ubiquitin-related modifier SUMO3 has a different effect, enhancing complex accumulation at the EvC zone, immediately distal to the ciliary transition zone, possibly via increased binding to the EFCAB7-IQCE complex. Lastly, we find that EvC zone targeting of EVC-EVC2 depends on two separate EFCAB7-binding motifs within EVC2’s Weyers-deleted peptide. Only one of these motifs had been characterized previously, so we have mapped the second herein. Altogether, our data shed light on EVC-EVC2 complex regulatory mechanisms, with implications for ciliopathies., Peer reviewed