149 research outputs found

    Understanding Degassing Pathways Along the 1886 Tarawera (New Zealand) Volcanic Fissure by Combining Soil and Lake CO₂ Fluxes

    Get PDF
    CO₂ flux measurements are often used to monitor volcanic systems, understand the cause of volcanic unrest, and map sub-surface structures. Currently, such measurements are incomplete at Tarawera (New Zealand), which erupted with little warning in 1886 and produced a ∼17 km long fissure. We combine new soil CO₂ flux and C isotope measurements of Tarawera with previous data from Rotomahana and Waimangu (regions also along the 1886 fissure) to fingerprint the CO₂ source, understand the current pathways for degassing, quantify the CO₂ released along the entire fissure, and provide a baseline survey. The total CO₂ emissions from the fissure are 1227 t⋅d⁻¹ (742–3398 t⋅d⁻¹ 90 % confidence interval), similar to other regions in the Taupō Volcanic Zone. The CO₂ flux from Waimangu and Rotomahana is far higher than from Tarawera (>549 vs. ∼4 t⋅d⁻¹ CO₂), likely influenced by a shallow silicic body at depth and Okataina caldera rim faults increasing permeability at the southern end of the fissure. Highly localized regions of elevated CO2 flux occur along the fissure and are likely caused by cross-cutting faults that focus the flow. One of these areas occurs on Tarawera, which is emitting ∼1 t⋅d⁻¹ CO₂ with a δ¹³CO₂ of −5.5 ± 0.5 ‰, and comparison with previous observations shows that activity is declining over time. This region highlights the spatial and temporal complexity of degassing pathways at volcanoes and that sub-surface structures exert a primary control on the magnitude of CO₂ flux in comparison to the surface mechanism (i.e., CO₂ released through the soil or lake surface)

    Identification and characterization of DGA2, an acyltransferase of the DGAT1 acyl-CoA:diacylglycerol acyltransferase family in the oleaginous yeast Yarrowia lipolytica. New insights into the storage lipid metabolism of oleaginous yeasts

    Get PDF
    Triacylglycerols (TAG) and steryl esters (SE) are the principal storage lipids in all eukaryotic cells. In yeasts, these storage lipids accumulate within special organelles known as lipid bodies (LB). In the lipid accumulation-oriented metabolism of the oleaginous yeast Yarrowia lipolytica, storage lipids are mostly found in the form of TAG, and only small amounts of SE accumulate. We report here the identification of a new DAG acyltransferase gene, DGA2, homologous to the ARE genes of Saccharomyces cerevisiae. This gene encodes a member of the type 1 acyl-CoA:diacylglycerol acyltransferase family (DGAT1), which has not previously been identified in yeasts, but is commonly found in mammals and plants. Unlike the Are proteins in S. cerevisiae, Dga2p makes a major contribution to TAG synthesis via an acyl-CoA-dependent mechanism and is not involved in SE synthesis. This enzyme appears to affect the size and morphology of LB, suggesting a direct role of storage lipid proteins in LB formation. We report that the Are1p of Y. lipolytica was essential for sterol esterification, as deletion of the encoding gene (ARE1) completely abolished SE synthesis. Unlike its homologs in yeasts, YlARE1 has no DAG acyltransferase activity. We also reconsider the role and function of all four acyltransferase enzymes involved in the final step of neutral lipid synthesis in this oleaginous yeast

    Biliary atresia

    Get PDF
    Biliary atresia (BA) is a rare disease characterised by a biliary obstruction of unknown origin that presents in the neonatal period. It is the most frequent surgical cause of cholestatic jaundice in this age group. BA occurs in approximately 1/18,000 live births in Western Europe. In the world, the reported incidence varies from 5/100,000 to 32/100,000 live births, and is highest in Asia and the Pacific region. Females are affected slightly more often than males. The common histopathological picture is one of inflammatory damage to the intra- and extrahepatic bile ducts with sclerosis and narrowing or even obliteration of the biliary tree. Untreated, this condition leads to cirrhosis and death within the first years of life. BA is not known to be a hereditary condition. No primary medical treatment is relevant for the management of BA. Once BA suspected, surgical intervention (Kasai portoenterostomy) should be performed as soon as possible as operations performed early in life is more likely to be successful. Liver transplantation may be needed later if the Kasai operation fails to restore the biliary flow or if cirrhotic complications occur. At present, approximately 90% of BA patients survive and the majority have normal quality of life

    Molecular and biochemical characterisation of a novel mutation in POLG associated with Alpers syndrome

    Get PDF
    <p>Abstract</p> <p>Background</p> <p>DNA polymerase γ (<it>POLG</it>) is the only known mitochondrial DNA (mtDNA) polymerase. It mediates mtDNA replication and base excision repair. Mutations in the <it>POLG </it>gene lead to reduction of functional mtDNA (mtDNA depletion and/or deletions) and are therefore predicted to result in defective oxidative phosphorylation (OXPHOS). Many mutations map to the polymerase and exonuclease domains of the enzyme and produce a broad clinical spectrum. The most frequent mutation p.A467T is localised in the linker region between these domains. In compound heterozygote patients the p.A467T mutation has been described to be associated amongst others with fatal childhood encephalopathy. These patients have a poorer survival rate compared to homozygotes.</p> <p>Methods</p> <p>mtDNA content in various tissues (fibroblasts, muscle and liver) was quantified using quantitative PCR (qPCR). OXPHOS activities in the same tissues were assessed using spectrophotometric methods and catalytic stain of BN-PAGE.</p> <p>Results</p> <p>We characterise a novel splice site mutation in <it>POLG </it>found <it>in trans </it>with the p.A467T mutation in a 3.5 years old boy with valproic acid induced acute liver failure (Alpers-Huttenlocher syndrome). These mutations result in a tissue specific depletion of the mtDNA which correlates with the OXPHOS-activities.</p> <p>Conclusions</p> <p>mtDNA depletion can be expressed in a high tissue-specific manner and confirms the need to analyse primary tissue. Furthermore<it>, POLG </it>analysis optimises clinical management in the early stages of disease and reinforces the need for its evaluation before starting valproic acid treatment.</p

    Ion homeostasis in the Chloroplast

    Full text link
    peer reviewedThe chloroplast is an organelle of high demand for macro- and micro-nutrient ions, which are required for the maintenance of the photosynthetic process. To avoid deficiency while preventing excess, homeostasis mechanisms must be tightly regulated. Here, we describe the needs for nutrient ions in the chloroplast and briefly highlight their functions in the chloroplastidial metabolism. We further discuss the impact of nutrient deficiency on chloroplasts and the acclimation mechanisms that evolved to preserve the photosynthetic apparatus. We finally present what is known about import and export mechanisms for these ions. Whenever possible, a comparison between cyanobacteria, algae and plants is provided to add an evolutionary perspective to the description of ion homeostasis mechanisms in photosynthesis
    corecore