42 research outputs found

    Arabidopsis inositol phosphate kinases, IPK1 and ITPK1, constitute a metabolic pathway in maintaining phosphate homeostasis

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    Emerging studies have implicated a close link between inositol phosphate (InsP) metabolism and cellular phosphate (Pi) homeostasis in eukaryotes; however, whether a common InsP species is deployed as an evolutionarily conserved metabolic messenger to mediate Pi signaling remains unknown. Here, using genetics and InsP profiling combined with Pi starvation response (PSR) analysis in Arabidopsis thaliana, we showed that the kinase activity of inositol pentakisphosphate 2‐kinase (IPK1), an enzyme required for phytate (inositol hexakisphosphates; InsP6) synthesis, is indispensable for maintaining Pi homeostasis under Pi‐replete conditions, and inositol 1,3,4‐trisphosphate 5/6‐kinase 1 (ITPK1) plays an equivalent role. Although both ipk1‐1 and itpk1 mutants exhibited decreased levels of InsP6 and diphosphoinositol pentakisphosphate (PP‐InsP5; InsP7), disruption of another ITPK family enzyme, ITPK4, which correspondingly caused depletion of InsP6 and InsP7, did not display similar Pi‐related phenotypes, which precludes these InsP species as effectors. Notably, the level of D/L‐Ins(3,4,5,6)P4 was concurrently elevated in both ipk1‐1 and itpk1 mutants, which showed a specific correlation to the misregulated Pi phenotypes. However, the level of D/L‐Ins(3,4,5,6)P4 is not responsive to Pi starvation that instead manifests a shoot‐specific increase in InsP7 level. This study demonstrates a more nuanced picture of the intersection of InsP metabolism and Pi homeostasis and PSR than has previously been elaborated and additionally establishes intermediate steps to phytate biosynthesis in plant vegetative tissues

    Konzeption und Umsetzung eines Blogs zum Thema Nachhaltigkeit und "Low Impact"-Leben

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    Die vorliegende Bachelorarbeit beschreibt die Konzeption und anschließende medienpraktische Umsetzung des persönlichen Online-Blogs www.thegreenie.eu zum Thema Nachhaltigkeit und einem “Low Impact”-Leben. Dieser bietet aufbereitete Informationen und Handlungstipps fĂŒr einen nachhaltigeren Lebensstil. Die Konzeption umfasst die Navigationsstruktur, den Aufbau der Site und das Design. Auch die Blog-Inhalte und deren Produktion wurden konzeptionell ausgearbeitet und dokumentiert. Die Konzeption basiert dabei auf einer Analyse potentieller Nutzer, dem Suchverhalten dieser und einer Benchmark-Analyse themenverwandter Websites. Die Umsetzung des Blogs erfolgte mit dem Content-Management-System Wordpress​. Die Dokumentation der vorliegenden Arbeit beschreibt die Auswahl eines Themes und technische Einbindung des Blogs. Außerdem geht daraus hervor, wie der Blog durch integrierte Anpassungsmöglichkeiten im Theme, Plugins und Änderungen im Quellcode personalisiert und dem Zweck angepasst wurde. Um Traffic zu generieren, wurde die Sichtbarkeit der Website durch Suchmaschinenoptimierung und die Einbindung sozialer Netzwerke erhöht. Die entsprechenden Maßnahmen sind ebenfalls in der Arbeit dokumentiert

    CD39 is upregulated during activation of mouse and human T cells and attenuates the immune response to <i>Listeria monocytogenes</i>

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    <div><p>The ectoenzymes CD39 and CD73 degrade extracellular ATP to adenosine. ATP is released by stressed or damaged cells and provides pro-inflammatory signals to immune cells through P2 receptors. Adenosine, on the other hand, suppresses immune cells by stimulating P1 receptors. Thus, CD39 and CD73 can shape the quality of immune responses. Here we demonstrate that upregulation of CD39 is a consistent feature of activated conventional CD4<sup>+</sup> and CD8<sup>+</sup> T cells. Following stimulation <i>in vitro</i>, CD4<sup>+</sup> and CD8<sup>+</sup> T cells from human blood gained surface expression of CD39 but displayed only low levels of CD73. Activated human T cells from inflamed joints largely presented with a CD39<sup>+</sup>CD73<sup>—</sup> phenotype. In line, in spleens of mice with acute <i>Listeria monocytogenes</i>, listeria-specific CD4<sup>+</sup> and CD8<sup>+</sup> T cells acquired a CD39<sup>+</sup>CD73<sup>—</sup> phenotype. To test the function of CD39 in control of bacterial infection, CD39-deficient (CD39<sup>-/-</sup>) mice were infected with <i>L</i>. <i>monocytogenes</i>. CD39<sup>-/-</sup> mice showed better initial control of <i>L</i>. <i>monocytogenes</i>, which was associated with enhanced production of inflammatory cytokines. In the late stage of infection, CD39<sup>-/-</sup> mice accumulated more listeria-specific CD8<sup>+</sup> T cells in the spleen than wildtype animals suggesting that CD39 attenuates the CD8<sup>+</sup> T-cell response to infection. In conclusion, our results demonstrate that CD39 is upregulated on conventional CD4<sup>+</sup> and CD8<sup>+</sup> T cells at sites of acute infection and inflammation, and that CD39 dampens responses to bacterial infection.</p></div
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