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111.
Anže Žerdoner Čalasan Juliane Kretschmann Marc Gottschling 《Organisms Diversity & Evolution》2018,18(1):29-38
Tertiary endosymbiosis is proven through dinophytes, some of which (i.e. Kryptoperidiniaceae) have engulfed diatom algae containing a secondary plastid. Chloroplasts are usually inherited together permanently with the host cell, leading to co-phylogeny. We compiled a diatom sequence data matrix of two nuclear and two chloroplast loci. Almost all endosymbionts of Kryptoperidiniaceae found their closest relatives in free-living diatoms and not in other harboured algae, rejecting co-phylogeny and indicating that resident diatoms were taken up by dinophytes multiple times independently. Almost intact ultrastructure and insignificant genome reduction are supportive for young, if not recent events of diatom capture. With their selective specificity on the one hand and extraordinary degree of endosymbiotic flexibility on the other hand, dinophytes hosting diatoms share more traits with lichens or facultatively phototrophic ciliates than with green algae and land plants. Time estimates indicate the dinophyte lineages as consistently older than the hosted diatom lineages, thus also favouring a repeated uptake of endosymbionts. The complex ecological role of dinophytes employing a variety of organismic interactions may explain their high potential and plasticity in acquiring a great diversity of plastids. 相似文献
112.
Irene Pila-Castellanos Diana Molino Joe McKellar Laetitia Lines Juliane Da Graca Marine Tauziet Laurent Chanteloup Ivan Mikaelian Laurne Meyniel-Schicklin Patrice Codogno Jacky Vonderscher Cdric Delevoye Olivier Moncorg Eric Meldrum Caroline Goujon Etienne Morel Benoit de Chassey 《PLoS pathogens》2021,17(2)
Influenza virus infections are major public health threats due to their high rates of morbidity and mortality. Upon influenza virus entry, host cells experience modifications of endomembranes, including those used for virus trafficking and replication. Here we report that influenza virus infection modifies mitochondrial morphodynamics by promoting mitochondria elongation and altering endoplasmic reticulum-mitochondria tethering in host cells. Expression of the viral RNA recapitulates these modifications inside cells. Virus induced mitochondria hyper-elongation was promoted by fission associated protein DRP1 relocalization to the cytosol, enhancing a pro-fusion status. We show that altering mitochondrial hyper-fusion with Mito-C, a novel pro-fission compound, not only restores mitochondrial morphodynamics and endoplasmic reticulum-mitochondria contact sites but also dramatically reduces influenza replication. Finally, we demonstrate that the observed Mito-C antiviral property is directly connected with the innate immunity signaling RIG-I complex at mitochondria. Our data highlight the importance of a functional interchange between mitochondrial morphodynamics and innate immunity machineries in the context of influenza viral infection. 相似文献
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Background aims
In vitro engineered adipose tissue is in great demand to treat lost or damaged soft tissue or to screen for new drugs, among other applications. However, today most attempts depend on the use of animal-derived sera. To pave the way for the application of adipose tissue–engineered products in clinical trials or as reliable and robust in vitro test systems, sera should be completely excluded from the production process. In this study, we aimed to develop an in vitro adipose tissue model in the absence of sera and maintain its function long-term.Methods
Human adipose tissue–derived stem cells were expanded and characterized in a xeno- and serum-free environment. Adipogenic differentiation was induced using a completely defined medium. Developed adipocytes were maintained in a completely defined maturation medium for additional 28 days. In addition to cell viability and adherence, adipocyte-specific markers such as perilipin A expression or leptin release were evaluated.Results
The defined differentiation medium enhanced cell adherence and lipid accumulation at a significant level compared with the corresponding negative control. The defined maturation medium also significantly supported cell adherence and functional adipocyte maturation during the long-term culture period.Conclusions
The process described here enables functional adipocyte generation and maintenance without the addition of unknown or animal-derived constituents, achieving an important milestone in the introduction of adipose tissue–engineered products into clinical trials or in vitro screening. 相似文献115.
Cross‐talk between monocyte invasion and astrocyte proliferation regulates scarring in brain injury 下载免费PDF全文
Jesica Frik Juliane Merl‐Pham Nikolaus Plesnila Nicola Mattugini Jacob Kjell Jonas Kraska Ricardo M Gómez Stefanie M Hauck Swetlana Sirko Magdalena Götz 《EMBO reports》2018,19(5)
Scar formation after brain injury is still poorly understood. To further elucidate such processes, here, we examine the interplay between astrocyte proliferation taking place predominantly at the vascular interface and monocyte invasion. Using genetic mouse models that decrease or increase reactive astrocyte proliferation, we demonstrate inverse effects on monocyte numbers in the injury site. Conversely, reducing monocyte invasion using CCR2?/? mice causes a strong increase in astrocyte proliferation, demonstrating an intriguing negative cross‐regulation between these cell types at the vascular interface. CCR2?/? mice show reduced scar formation with less extracellular matrix deposition, smaller lesion site and increased neuronal coverage. Surprisingly, the GFAP+ scar area in these mice is also significantly decreased despite increased astrocyte proliferation. Proteomic analysis at the peak of increased astrocyte proliferation reveals a decrease in extracellular matrix synthesizing enzymes in the injury sites of CCR2?/? mice, highlighting how early key aspects of scar formation are initiated. Taken together, we provide novel insights into the cross‐regulation of juxtavascular proliferating astrocytes and invading monocytes as a crucial mechanism of scar formation upon brain injury. 相似文献
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Aor Pranchai Michael Jenke Juliane Vogt Uwe Grueters Lin Yue Ulf Mehlig Moirah Machado de Menezes Sven Wagner Uta Berger 《Wetlands Ecology and Management》2018,26(2):139-150
The global effort to rehabilitate and restore destroyed mangrove forests is unable to keep up with the high mangrove deforestation rates, which exceed the average pace of global deforestation. Although facilitation theory presents new possibilities for the restoration of heavily degraded mangrove sites, knowledge of tree–tree interactions in stressed mangrove forest ecosystems is too limited to utilize facilitation appropriately. The aim was to determine the mode of local interaction among stressed mangrove trees by investigating the effect of clustering on tree size and crown morphology under contrasting stand densities. The study was conducted in a dwarf Avicennia germinans forest in Northern Brazil, in which tree growth is limited by infrequent inundation and high pore-water salinity. Autoregressive regression, Voronoi tessellation and spatial point pattern statistics were used to address the spatial processes underlying tree interaction. Under low stand density (1.2 trees m?2) dwarf trees which grew in clustered cohorts of A. germinans had a less stunted crown morphology revealing the dominance of a positive neighborhood influence among plants. In contrast, dwarf trees in the denser forest stand (2.7 trees m?2) were interacting competitively as indicated by the more negative effect of neighbors on crown morphology and size. The shift from facilitative to competitive interactions is an important feature of mangrove forest regeneration under harsh environmental conditions. If mangrove trees are unable to regenerate naturally on severely degraded sites, intraspecific facilitation could be used to assist regeneration by planting seedlings in clusters and not evenly spaced. 相似文献
119.
Leucio D. Vieira Juliane S. Farias Diego B. de Queiroz Edjair V. Cabral Manoel M. Lima-Filho Bruna R.M. SantHelena Regina S. Aires Valdilene S. Ribeiro Juliana Santos-Rocha Fabiano E. Xavier Ana D. Paix?o 《生物化学与生物物理学报:疾病的分子基础》2018,1864(12):3577-3587
We investigated whether hypertension induced by maternal lipopolysaccharide (LPS) administration during gestation is linked to peripheral vascular and renal hemodynamic regulation, through angiotensin II?→?NADPH-oxidase signalling, and whether these changes are directly linked to intrauterine oxidative stress. Female Wistar rats were submitted to LPS, in the absence or presence of α-tocopherol during pregnancy. Malondialdehyde in placenta and in livers from dams and foetuses was enhanced by LPS. Tail-cuff systolic blood pressure (tcSBP) was elevated in the 16-week-old LPS offspring. Renal malondialdeyde and protein expression of NADPH oxidase isoform 2 were elevated in these animals at 20?weeks of age. Maternal α-tocopherol treatment prevented the elevation in malondialdehyde induced by LPS on placenta and livers from dams and foetuses, as well as prevented the elevation in tcSBP and the elevation in renal malondialdehyde in adult life. LPS offspring presented impairment of endothelium-dependent relaxation in aorta and mesenteric rings, which was blunted by angiotensin type 1 receptor (AT1R) blockade and NADPH oxidase inhibition. At age of 32?weeks, renal hemodynamic parameters were unchanged in anaesthetised LPS offspring, but angiotensin II infusion led to an increased glomerular filtration rate paralleled by filtration fraction elevation. The renal haemodynamic changes provoked by angiotensin II was prevented by early treatment with α-tocopherol and by late treatment with NADPH oxidase inhibitor. These results point to oxidative stress as a mediator of offspring hypertension programmed by maternal inflammation and to the angiotensin II?→?NADPH oxidase signalling pathway as accountable for vascular and renal dysfunctions that starts and maintains hypertension. 相似文献
120.
Fine Root Production across a Primary Successional Ecosystem Chronosequence at Mt. Shasta,California 总被引:1,自引:0,他引:1
Estimating changes in belowground biomass and production is essential for understanding fundamental patterns and processes
during ecosystem development. We examined patterns of fine root production, aboveground litterfall, and forest floor accumulation
during forest primary succession at the Mt. Shasta Mudflows ecosystem chronosequence. Fine root production was measured using
the root ingrowth cores method over 1 year, and aboveground litterfall was collected over 2 years. Fine root production increased
significantly with ecosystem age, but only the youngest ecosystem was significantly different from all of the older ecosystems.
Root production was 44.5 ± 13.3, 168.3 ± 20.6, 190.5 ± 33.8, and 236.3 ± 65.4 g m−2 y−1 in the 77, 255, 616, and >850-year-old ecosystems, respectively. Generally, aboveground litterfall and forest floor accumulation
did not follow the same pattern as root production. The relative contribution of fine root production to total fine detrital
production increased significantly with ecosystem age, from 14 to 49%, but only the youngest ecosystem was significantly different
from all of the older ecosystems. Fine root production was significantly correlated with some measures of soil fertility but
was not correlated with leaf or total litterfall, or forest floor accumulation. It was best predicted by soil N concentration
alone, but this relationship may not be causal, as soil N concentration was also correlated with ecosystem age. For the oldest
ecosystem, fine root production was also measured using the sequential intact cores/compartment-flow model method, and the
difference between the two estimates was not significant. Our study suggests that the relative contribution of fine roots
to fine detrital production, and hence to soil organic matter accumulation, may increase during forest primary succession. 相似文献