Mitochondrial Na+ controls oxidative phosphorylation and hypoxic redox signalling

All metazoans depend on O2 delivery and consumption by the mitochondrial oxidative phosphorylation (OXPHOS) system to produce energy. A decrease in O2 availability (hypoxia) leads to profound metabolic rewiring. In addition, OXPHOS uses O2 to produce reactive oxygen species (ROS) that can drive cell adaptations through redox signalling, but also trigger cell damage1–4, and both phenomena occur in hypoxia4–8. However, the precise mechanism by which acute hypoxia triggers mitochondrial ROS production is still unknown. Ca2+ is one of the best known examples of an ion acting as a second messenger9, yet the role ascribed to Na+ is to serve as a mere mediator of membrane potential and collaborating in ion transport10. Here we show that Na+ acts as a second messenger regulating OXPHOS function and ROS production by modulating fluidity of the inner mitochondrial membrane (IMM). We found that a conformational shift in mitochondrial complex I during acute hypoxia11 drives the acidification of the matrix and solubilization of calcium phosphate precipitates. The concomitant increase in matrix free-Ca2+ activates the mitochondrial Na+/Ca2+ exchanger (NCLX), which imports Na+ into the matrix. Na+ interacts with phospholipids reducing IMM fluidity and mobility of free ubiquinone between complex II and complex III, but not inside supercomplexes. As a consequence, superoxide is produced at complex III, generating a redox signal. Inhibition of mitochondrial Na+ import through NCLX is sufficient to block this pathway, preventing adaptation to hypoxia. These results reveal that Na+ import into the mitochondrial matrix controls OXPHOS function and redox signalling through an unexpected interaction with phospholipids, with profound consequences in cellular metabolism

Thermotolerance responses in ripening berries of vitis vinifera l. cv muscat hamburg

Berry organoleptic properties are highly influenced by ripening environmental conditions. In this study, we used grapevine fruiting cuttings to follow berry ripening under different controlled conditions of temperature and irradiation intensity. Berries ripened at higher temperatures showed reduced anthocyanin accumulation and hastened ripening, leading to a characteristic drop in malic acid and total acidity. The GrapeGen GeneChip® combined with a newly developed GrapeGen 12Xv1 MapMan version were utilized for the functional analysis of berry transcriptomic differences after 2 week treatments from veraison onset. These analyses revealed the establishment of a thermotolerance response in berries under high temperatures marked by the induction of heat shock protein (HSP) chaperones and the repression of transmembrane transporter-encoding transcripts. The thermotolerance response was coincident with up-regulation of ERF subfamily transcription factors and increased ABA levels, suggesting their participation in the maintenance of the acclimation response. Lower expression of amino acid transporter-encoding transcripts at high temperature correlated with balanced amino acid content, suggesting a transcriptional compensation of temperature effects on protein and membrane stability to allow for completion of berry ripening. In contrast, the lower accumulation of anthocyanins and higher malate metabolization measured under high temperature might partly result from imbalance in the expression and function of their specific transmembrane transporters and expression changes in genes involved in their metabolic pathways. These results open up new views to improve our understanding of berry ripening under high temperatures. © 2013 The Author.This study was supported by Genoma España [within a collaborative agreement with Genome Canada (Grapegen Project)]; the Spanish Ministry of Science and Innovation [grant Nos. BIO2008-03892, BIO2011-26229]; a bilateral collaborative grant with the University of Cuyo (Mendoza, Argentina) [grant No. AR2009-0021].Peer Reviewe

High temperature acclimation of berry ripening in Muscat Hamburg grapevine cultivar

Póster presentado en el IX International Symposium on Grapevine Physiology and Biotechnology, celebrado en La Serena (Chile) del 21 al 26 de abril de 2013.Berry organoleptic properties are highly influenced by ripening environmental conditions. In this study, we used grapevine fruiting cuttings to follow berry ripening under different conditions of temperature and irradiation. Berries ripened at higher temperatures showed reduced anthocyanin accumulation and hastened ripening leading to characteristic malic acid and total acidity drop. The GrapeGen GeneChip combined with a newly developed GrapeGen 12Xv1 MapMan version were used for the functional analysis of berry transcriptomic differences after two weeks treatments from veraison onset. These analyses revealed the establishment of a thermotolerance response dominated by the induction of HSP chaperones and the repression of transmembrane transporter encoding transcripts. The thermotolerance response was coincident with up-regulation of ERF subfamily transcription factors and increased ABA levels suggesting their participation in the acclimation response maintenance. Lower expression of amino acid transporter encoding transcripts at high temperature was able to balance amino acid content suggesting a transcriptional compensation of temperature effects on protein and membrane stability to allow completion of berry ripening. By contrast, the lower anthocyanin accumulation and higher malate metabolization measured under high temperature might partly result from imbalance in the expression and function of their specific transmembrane transporters.Acknowledgments: Project GrapeGen (Fundación Genoma España).Peer Reviewe

Guía para el control de enterobacterias productoras de carbapenemasas. Protocolo clínico PTC-XI-23

Establecer os mecanismos para a detección de casos de Enterobacterias produtoras de Carbapenemasas (EPC), así como o manexo dos pacientes afectados, os seus contactos e o alta do paciente.Establecer los mecanismos para la detección de casos de Enterobacterias productoras de Carbapenemasas (EPC), así como el manejo de los pacientes afectados, sus contactos y el alta del paciente

Volatile compounds other than CO2 emitted by different microorganisms promote distinct posttranscriptionally regulated responses in plants

A “box‐in‐box” cocultivation system was used to investigate plant responses to microbial volatile compounds (VCs) and to evaluate the contributions of organic and inorganic VCs (VOCs and VICs, respectively) to these responses. Arabidopsis plants were exposed to VCs emitted by adjacent Alternaria alternata and Penicillium aurantiogriseum cultures, with and without charcoal filtration. No VOCs were detected in the headspace of growth chambers containing fungal cultures with charcoal filters. However, these growth chambers exhibited elevated CO2 and bioactive CO and NO headspace concentrations. Independently of charcoal filtration, VCs from both fungal phytopathogens promoted growth and distinct developmental changes. Plants cultured at CO2 levels observed in growth boxes containing fungal cultures were identical to those cultured at ambient CO2. Plants exposed to charcoal‐filtered fungal VCs, nonfiltered VCs, or superelevated CO2 levels exhibited transcriptional changes resembling those induced by increased irradiance. Thus, in the “box‐in‐box” system, (a) fungal VICs other than CO2 and/or VOCs not detected by our analytical systems strongly influence the plants' responses to fungal VCs, (b) different microorganisms release VCs with distinct action potentials, (c) transcriptional changes in VC‐exposed plants are mainly due to enhanced photosynthesis signaling, and (d) regulation of some plant responses to fungal VCs is primarily posttranscriptional.This work was partially supported by the Comisión Interministerial de Ciencia y Tecnología and Fondo Europeo de Desarrollo Regional (Spain; grants BIO2013‐49125‐C2‐1‐P and BIO2016‐78747‐P) and the Government of Navarra (refs. P1044 AGROESTI and P1004 PROMEBIO).Peer reviewe

El legado de la familia Betancourt. Aliciente académico, patrimonial y turístico en Tenerife

El presente libro es un compendio de los resultados obtenidos en el proyecto de investigación Los hermanos José y Agustín de Betancourt. Recuperación de su obra gráfica en los inicios de la época Contemporánea. Aliciente académico, patrimonial y turístico [2016/UEM21]. Seleccionado en la convocatoria nacional de proyectos de investigación con financiación interna, correspondientes a la Universidad Europea durante el curso 2016-2017, desde una perspectiva multidisciplinar, teórica, histórica y práctica, ha aspirado a ofrecer un camino para su aplicación docente y la utilidad para repercutir como producto patrimonial y turístico. De acuerdo a esos fines, este proyecto de investigación ha rescatado la figura histórica de Agustín de Betancourt y sus hermanos insistiendo en una premisa básica para nuestro tiempo: dar valor de presente a sucesos y personajes del pasado y enaltecer, reconocer y revitalizar la representación histórica de las bases culturales que han construido la sociedad canaria.Universidad Europea de Canarias 2016/UEM21. Gobierno de Canarias.No data 2018UE

Na+ controls hypoxic signalling by the mitochondrial respiratory chain

All metazoans depend on the consumption of O2 by the mitochondrial oxidative phosphorylation system (OXPHOS) to produce energy. In addition, the OXPHOS uses O2 to produce reactive oxygen species that can drive cell adaptations1-4, a phenomenon that occurs in hypoxia4-8 and whose precise mechanism remains unknown. Ca2+ is the best known ion that acts as a second messenger9, yet the role ascribed to Na+ is to serve as a mere mediator of membrane potential10. Here we show that Na+ acts as a second messenger that regulates OXPHOS function and the production of reactive oxygen species by modulating the fluidity of the inner mitochondrial membrane. A conformational shift in mitochondrial complex I during acute hypoxia11 drives acidification of the matrix and the release of free Ca2+ from calcium phosphate (CaP) precipitates. The concomitant activation of the mitochondrial Na+/Ca2+ exchanger promotes the import of Na+ into the matrix. Na+ interacts with phospholipids, reducing inner mitochondrial membrane fluidity and the mobility of free ubiquinone between complex II and complex III, but not inside supercomplexes. As a consequence, superoxide is produced at complex III. The inhibition of Na+ import through the Na+/Ca2+ exchanger is sufficient to block this pathway, preventing adaptation to hypoxia. These results reveal that Na+ controls OXPHOS function and redox signalling through an unexpected interaction with phospholipids, with profound consequences for cellular metabolism

Na+ controls hypoxic signalling by the mitochondrial respiratory chain

All metazoans depend on O2 delivery and consumption by the mitochondrial oxidative phosphorylation (OXPHOS) system to produce energy. A decrease in O2 availability (hypoxia) leads to profound metabolic rewiring. In addition, OXPHOS uses O2 to produce reactive oxygen species (ROS) that can drive cell adaptations through redox signalling, but also trigger cell damage1–4, and both phenomena occur in hypoxia4–8. However, the precise mechanism by which acute hypoxia triggers mitochondrial ROS production is still unknown. Ca2+ is one of the best known examples of an ion acting as a second messenger9, yet the role ascribed to Na+ is to serve as a mere mediator of membrane potential and collaborating in ion transport10. Here we show that Na+ acts as a second messenger regulating OXPHOS function and ROS production by modulating fluidity of the inner mitochondrial membrane (IMM). We found that a conformational shift in mitochondrial complex I during acute hypoxia11 drives the acidification of the matrix and solubilization of calcium phosphate precipitates. The concomitant increase in matrix free-Ca2+ activates the mitochondrial Na+/Ca2+ exchanger (NCLX), which imports Na+ into the matrix. Na+ interacts with phospholipids reducing IMM fluidity and mobility of free ubiquinone between complex II and complex III, but not inside supercomplexes. As a consequence, superoxide is produced at complex III, generating a redox signal. Inhibition of mitochondrial Na+ import through NCLX is sufficient to block this pathway, preventing adaptation to hypoxia. These results reveal that Na+ import into the mitochondrial matrix controls OXPHOS function and redox signalling through an unexpected interaction with phospholipids, with profound consequences in cellular metabolism