1,435 research outputs found

    Observer et évaluer les usages de Gallica. Réflexion épistémologique et stratégique

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    Ce rapport rend compte d\u27une étude menée en partenariat avec la BnF et le département SES de Telecom ParisTech. Il est composé de deux axes : un état de l\u27art des nouveaux enjeux scientifiques et organisationnels de l\u27analyse des usages en ligne face aux profondes transformations des services et des pratiques numériques ; une enquête qualitative sur la manière dont les publics et les usages de Gallica sont envisagés et questionnés au sein de la BnF. Il s\u27achève sur une série de recommandations d\u27ordre général quant aux types de problématiques et d\u27études que la BnF pourrait développer dans les prochaines années

    Internal Ca2+ release in yeast is triggered by hypertonic shock and mediated by a TRP channel homologue

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    Calcium ions, present inside all eukaryotic cells, are important second messengers in the transduction of biological signals. In mammalian cells, the release of Ca2+ from intracellular compartments is required for signaling and involves the regulated opening of ryanodine and inositol-1,4,5-trisphosphate (IP3) receptors. However, in budding yeast, no signaling pathway has been shown to involve Ca2+ release from internal stores, and no homologues of ryanodine or IP3 receptors exist in the genome. Here we show that hyperosmotic shock provokes a transient increase in cytosolic Ca2+ in vivo. Vacuolar Ca2+, which is the major intracellular Ca2+ store in yeast, is required for this response, whereas extracellular Ca2+ is not. We aimed to identify the channel responsible for this regulated vacuolar Ca2+ release. Here we report that Yvc1p, a vacuolar membrane protein with homology to transient receptor potential (TRP) channels, mediates the hyperosmolarity induced Ca2+ release. After this release, low cytosolic Ca2+ is restored and vacuolar Ca2+ is replenished through the activity of Vcx1p, a Ca2+/H+ exchanger. These studies reveal a novel mechanism of internal Ca2+ release and establish a new function for TRP channels
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