Análisis de los resultados de las Campañas de marcado de Atún rojo (Thunnus thynnus) del “Tagging GBYP-ICCAT 3ª Fase realizadas en el Golfo de León y Estrecho de Gibraltar durante 2011-12

In the Gulf of Lion Campaign 109 bluefin were tagged with conventional tags measuring between 74 cm and 108 cm fork length (LH). Five of these specimens had an electronic mark mini-patt placed on them. The campaign of the Strait of Gibraltar took place from 5/10/12 to 21/11/12 with 117 days at sea with a total of 1,477 bluefin marked of which 1,432 copies were marked, mainly with a double mainstream brand mark, 20 individuals with an electronic type pop-up (mini-pat) and 25 more fish with internal electronic tags. The tagged fish measured between 70 cm and 130 cm fork length (LH). Likewise, the biological samples which were scheduled were obtained for more than 40 samples of bluefin tuna of all sizes.Postprin

Campañas de marcado de atún rojo juvenil (Thunnus thynnus) juvenil coordinadas por el IEO, previstas en el Programa ICCAT-GBYP y realizadas en el Estrecho de Gibraltar durante Noviembre de 2011 y enero de 2012

This paper presents the results of conventional tagging surveys on juvenile bluefin tuna conducted in the Strait of Gibraltar during different periods of 2011 and 2012 with two vessels from the port of Algeciras that usually fish using pole and bait in that area. The campaigns were carried out within the framework of the Enhanced Research Program for Bluefin Tuna (Thunnus thynnus) (GBYP). In 36 days of activity, a total of 1389 bluefin tuna were tagged, weighing an average of approximately 15 kg, ranging between 7 and 40 kg. In 46% of the specimens, two different tags were placed, and the forecasts established in the Tagging Plan within the ICCAT-GBYP were achieved.GBYP-ICCATPostprin

Resultados de la encomienda de la SGP al IEO para el estudio del atún rojo (Thunnus thynnus) del stock del Atlántico este (que incluye el Mediterráneo) considerando las almadrabas españolas como observatorios científicos

During the years of 2010-2012 was a research project bluefin tuna traps using Spanish as scientific laboratories. The main objective was to keep the knowledge of the tendency of the index of abundance of bluefin tuna caught with these nets, and it is the most significant index used in the stock assessment process East Atlantic, including the Mediterranean. Likewise studies were developed bluefin tuna biological parameters such as growth, feeding, reproduction, stock structure and migration patterns, the results provide an important advance in the understanding of the biology and behavior of this species.Versión del edito

Preliminary study on the feeding of bluefin tuna (Thunnus thynnus) in the Mediterranean and the Strait of Gibraltar area

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PARP-1 Regulates Metastatic Melanoma through Modulation of Vimentin-induced Malignant Transformation

PARP inhibition can induce anti-neoplastic effects when used as monotherapy or in combination with chemo- or radiotherapy in various tumor settings; however, the basis for the anti-metastasic activities resulting from PARP inhibition remains unknown. PARP inhibitors may also act as modulators of tumor angiogenesis. Proteomic analysis of endothelial cells revealed that vimentin, an intermediary filament involved in angiogenesis and a specific hallmark of EndoMT (endothelial to mesenchymal transition) transformation, was down-regulated following loss of PARP-1 function in endothelial cells. VE-cadherin, an endothelial marker of vascular normalization, was up-regulated in HUVEC treated with PARP inhibitors or following PARP-1 silencing; vimentin over-expression was sufficient to drive to an EndoMT phenotype. In melanoma cells, PARP inhibition reduced pro-metastatic markers, including vasculogenic mimicry. We also demonstrated that vimentin expression was sufficient to induce increased mesenchymal/pro-metastasic phenotypic changes in melanoma cells, including ILK/GSK3-β-dependent E-cadherin down-regulation, Snail1 activation and increased cell motility and migration. In a murine model of metastatic melanoma, PARP inhibition counteracted the ability of melanoma cells to metastasize to the lung. These results suggest that inhibition of PARP interferes with key metastasis-promoting processes, leading to suppression of invasion and colonization of distal organs by aggressive metastatic cells.This work was supported by Ministerio de Ciencia e Innovación SAF2006-01094, SAF2009-13281-C02-01, Fundación La Caixa BM06-219-0 and Junta de Andalucía P07-CTS-0239 and CTS-6602 to FJO, Ministerio de Educación y Ciencia SAF2007-64597; CICYT: SAF2009-13281-C02-02; Junta de Andalucía, P06-CTS-01385 to JMRdA and grants CEIC (P10-CTS5865) and FEDER-ISCIII (PI10/00883) to JCR-M. AGdH has been funded by grants from “Fundación Científica de la Asociación Española Contra el Cáncer”, Ministerio de Ciencia y Tecnología SAF2010-16089, and “Fundación La Marató de TV3”. JCR-M has been funded by Grants CEIC (P1 = -CTS5865) and FEDER-ISCIII (PI10/00883)

PARP-1 Regulates Metastatic Melanoma through Modulation of Vimentin-induced Malignant Transformation

PARP inhibition can induce anti-neoplastic effects when used as monotherapy or in combination with chemo- or radiotherapy in various tumor settings; however, the basis for the anti-metastasic activities resulting from PARP inhibition remains unknown. PARP inhibitors may also act as modulators of tumor angiogenesis. Proteomic analysis of endothelial cells revealed that vimentin, an intermediary filament involved in angiogenesis and a specific hallmark of EndoMT (endothelial to mesenchymal transition) transformation, was down-regulated following loss of PARP-1 function in endothelial cells. VE-cadherin, an endothelial marker of vascular normalization, was up-regulated in HUVEC treated with PARP inhibitors or following PARP-1 silencing; vimentin over-expression was sufficient to drive to an EndoMT phenotype. In melanoma cells, PARP inhibition reduced pro-metastatic markers, including vasculogenic mimicry. We also demonstrated that vimentin expression was sufficient to induce increased mesenchymal/pro-metastasic phenotypic changes in melanoma cells, including ILK/GSK3-β-dependent E-cadherin down-regulation, Snail1 activation and increased cell motility and migration. In a murine model of metastatic melanoma, PARP inhibition counteracted the ability of melanoma cells to metastasize to the lung. These results suggest that inhibition of PARP interferes with key metastasis-promoting processes, leading to suppression of invasion and colonization of distal organs by aggressive metastatic cells.This work was supported by Ministerio de Ciencia e Innovación SAF2006-01094, SAF2009-13281-C02-01, Fundación La Caixa BM06-219-0 and Junta de Andalucía P07-CTS-0239 and CTS-6602 to FJO, Ministerio de Educación y Ciencia SAF2007-64597; CICYT: SAF2009-13281-C02-02; Junta de Andalucía, P06-CTS-01385 to JMRdA and grants CEIC (P10-CTS5865) and FEDER-ISCIII (PI10/00883) to JCR-M. AGdH has been funded by grants from “Fundación Científica de la Asociación Española Contra el Cáncer”, Ministerio de Ciencia y Tecnología SAF2010-16089, and “Fundación La Marató de TV3”. JCR-M has been funded by Grants CEIC (P1 = -CTS5865) and FEDER-ISCIII (PI10/00883)

Autophagy requires poly(adp-ribosyl)ation-dependent AMPK nuclear export

AMPK is a central energy sensor linking extracellular milieu fluctuations with the autophagic machinery. In the current study we uncover that Poly(ADP-ribosyl)ation (PARylation), a post-translational modification (PTM) of proteins, accounts for the spatial and temporal regulation of autophagy by modulating AMPK subcellular localisation and activation. More particularly, we show that the minority AMPK pool needs to be exported to the cytosol in a PARylation-dependent manner for optimal induction of autophagy, including ULK1 phosphorylation and mTORC1 inactivation. PARP-1 forms a molecular complex with AMPK in the nucleus in non-starved cells. In response to nutrient deprivation, PARP-1 catalysed PARylation, induced the dissociation of the PARP-1/AMPK complex and the export of free PARylated nuclear AMPK to the cytoplasm to activate autophagy. PARP inhibition, its silencing or the expression of PARylation-deficient AMPK mutants prevented not only the AMPK nuclear-cytosolic export but also affected the activation of the cytosolic AMPK pool and autophagosome formation. These results demonstrate that PARylation of AMPK is a key early signal to efficiently convey extracellular nutrient perturbations with downstream events needed for the cell to optimize autophagic commitment before autophagosome formation