| 1. |
- Kanai, M, et al.
(författare)
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- 2023
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swepub:Mat__t
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| 2. |
- Niemi, MEK, et al.
(författare)
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- 2021
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swepub:Mat__t
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| 3. |
- Suggitt, Andrew J., et al.
(författare)
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Extinction risk from climate change is reduced by microclimatic buffering
- 2018
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Ingår i: Nature Climate Change. - : Springer Science and Business Media LLC. - 1758-678X .- 1758-6798. ; 8:8, s. 713-
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Tidskriftsartikel (refereegranskat)abstract
- Protecting biodiversity against the impacts of climate change requires effective conservation strategies that safeguard species at risk of extinction(1). Microrefugia allowed populations to survive adverse climatic conditions in the past(2,3), but their potential to reduce extinction risk from anthropogenic warming is poorly understood(3-5), hindering our capacity to develop robust in situ measures to adapt conservation to climate change(6). Here, we show that microclimatic heterogeneity has strongly buffered species against regional extirpations linked to recent climate change. Using more than five million distribution records for 430 climate-threatened and range-declining species, population losses across England are found to be reduced in areas where topography generated greater variation in the microclimate. The buffering effect of topographic microclimates was strongest for those species adversely affected by warming and in areas that experienced the highest levels of warming: in such conditions, extirpation risk was reduced by 22% for plants and by 9% for insects. Our results indicate the critical role of topographic variation in creating microrefugia, and provide empirical evidence that microclimatic heterogeneity can substantially reduce extinction risk from climate change.
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| 4. |
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| 5. |
- Peiris, Heshan, et al.
(författare)
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A Syntenic Cross Species Aneuploidy Genetic Screen Links RCAN1 Expression to β-Cell Mitochondrial Dysfunction in Type 2 Diabetes
- 2016
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Ingår i: PLoS Genetics. - : Public Library of Science (PLoS). - 1553-7390 .- 1553-7404. ; 12:5
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Tidskriftsartikel (refereegranskat)abstract
- Type 2 diabetes (T2D) is a complex metabolic disease associated with obesity, insulin resistance and hypoinsulinemia due to pancreatic β-cell dysfunction. Reduced mitochondrial function is thought to be central to β-cell dysfunction. Mitochondrial dysfunction and reduced insulin secretion are also observed in β-cells of humans with the most common human genetic disorder, Down syndrome (DS, Trisomy 21). To identify regions of chromosome 21 that may be associated with perturbed glucose homeostasis we profiled the glycaemic status of different DS mouse models. The Ts65Dn and Dp16 DS mouse lines were hyperglycemic, while Tc1 and Ts1Rhr mice were not, providing us with a region of chromosome 21 containing genes that cause hyperglycemia. We then examined whether any of these genes were upregulated in a set of ~5,000 gene expression changes we had identified in a large gene expression analysis of human T2D β-cells. This approach produced a single gene, RCAN1, as a candidate gene linking hyperglycemia and functional changes in T2D β-cells. Further investigations demonstrated that RCAN1 methylation is reduced in human T2D islets at multiple sites, correlating with increased expression. RCAN1 protein expression was also increased in db/db mouse islets and in human and mouse islets exposed to high glucose. Mice overexpressing RCAN1 had reduced in vivo glucose-stimulated insulin secretion and their β-cells displayed mitochondrial dysfunction including hyperpolarised membrane potential, reduced oxidative phosphorylation and low ATP production. This lack of β-cell ATP had functional consequences by negatively affecting both glucose-stimulated membrane depolarisation and ATP-dependent insulin granule exocytosis. Thus, from amongst the myriad of gene expression changes occurring in T2D β-cells where we had little knowledge of which changes cause β-cell dysfunction, we applied a trisomy 21 screening approach which linked RCAN1 to β-cell mitochondrial dysfunction in T2D.
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