| 1. |
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- 2019
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Tidskriftsartikel (refereegranskat)
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| 2. |
- Clarke, A. L., et al.
(författare)
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Long-Term Trends in Eutrophication and Nutrients in the Coastal Zone
- 2006
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Ingår i: Limnology and Oceanography. - 0024-3590 .- 1939-5590. ; 51:1, s. 385-397
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Tidskriftsartikel (refereegranskat)abstract
- We used high-resolution paleoecological records of environmental change to study the rate and magnitude of eutrophication over the last century in two contrasting coastal ecosystems. A multiproxy approach using geochemical and biological indicators and diatom-based transfer functions provides a long-term perspective on changes in nutrient concentrations and the corresponding biological and sedimentary responses. In Roskilde Fjord, Denmark, total nitrogen (TN) increased 85% during the last century, with the most rapid increase occurring after the 1950s, corresponding to the postwar increase in N fertilizer use. In Laajalahti Bay, an urban embayment near Helsinki, Finland, total dissolved nitrogen (TDN) increased with growing wastewater inputs and decreased with the remedial actions taken to reduce these discharges. These changes are small relative to the order of magnitude increases in nutrient loading that have occurred in northwestern Europe, where the dissolved inorganic nitrogen (DIN) load has increased more than threefold in certain areas.
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| 3. |
- Nicholls, Thomas J., et al.
(författare)
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Dinucleotide Degradation by REXO2 Maintains Promoter Specificity in Mammalian Mitochondria
- 2019
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Ingår i: Molecular Cell. - : Elsevier BV. - 1097-2765 .- 1097-4164. ; 76:5
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Tidskriftsartikel (refereegranskat)abstract
- Oligoribonucleases are conserved enzymes that degrade short RNA molecules of up to 5 nt in length and are assumed to constitute the final stage of RNA turnover. Here we demonstrate that REXO2 is a specialized dinucleotide-degrading enzyme that shows no preference between RNA and DNA dinucleotide substrates. A heart- and skeletal-muscle-specific knockout mouse displays elevated dinucleotide levels and alterations in gene expression patterns indicative of aberrant dinucleotide-primed transcription initiation. We find that dinucleotides act as potent stimulators of mitochondrial transcription initiation in vitro. Our data demonstrate that increased levels of dinucleotides can be used to initiate transcription, leading to an increase in transcription levels from both mitochondrial promoters and other, nonspecific sequence elements in mitochondrial DNA. Efficient RNA turnover by REXO2 is thus required to maintain promoter specificity and proper regulation of transcription in mammalian mitochondria.
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| 4. |
- Siibak, Triinu, et al.
(författare)
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A multi-systemic mitochondrial disorder due to a dominant p.Y955H disease variant in DNA polymerase gamma
- 2017
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Ingår i: Human Molecular Genetics. - : Oxford University Press (OUP). - 0964-6906 .- 1460-2083. ; 26:13, s. 2515-2525
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Tidskriftsartikel (refereegranskat)abstract
- Mutations in the mitochondrial DNA polymerase, POLG, are associated with a variety of clinical presentations, ranging from early onset fatal brain disease in Alpers syndrome to chronic progressive external ophthalmoplegia. The majority of mutations are linked with disturbances of mitochondrial DNA (mtDNA) integrity and maintenance. On a molecular level, depending on their location within the enzyme, mutations either lead to mtDNA depletion or the accumulation of multiple mtDNA deletions, and in some cases these molecular changes can be correlated to the clinical presentation. We identified a patient with a dominant p.Y955H mutation in POLG, presenting with a severe, early-onset multi-systemic mitochondrial disease with bilateral sensorineural hearing loss, cataract, myopathy, and liver failure. Using a combination of disease models of Drosophila melanogaster and in vitro biochemistry analysis, we compare the molecular consequences of the p.Y955H mutation to the well-documented p.Y955C mutation. We demonstrate that both mutations affect mtDNA replication and display a dominant negative effect, with the p.Y955H allele resulting in a more severe polymerase dysfunction.
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