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Chronic dysfunction of Store-operated calcium entry by pulsed RNAi induction in fat tissue impairs organismal energy homeostasis in Drosophila

ABSTRACT: The purpose is to have a overview on how chronic dysfunction of store-operated calcium entry change transcription profiles of adult fly fat tissue. Methods:To achieve chronic dysfunction of store-operated calcium entry, we carried out the Temperature-caused RNAi Pulse Induction of Stim (29 celcius degree incubation, Stim-TRiPI, or Stim-TRIP in data file) in fat storage tissue of 6 days old adult male flies. At day 10 and 11 after Stim-TRiPI (Stim-TRIP), we isolated the fat tissues and carried out RNAseq analysis based gene-level read counts.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE112689 | GEO | 2019/05/07

REPOSITORIES: GEO

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Selective modulation of gene expression in activated normal human peripheral blood mononuclear cells by store-operated calcium entry blocker BTP2

Project description:Calcium is a critical signaling molecule in many cell types including immune cells. The calcium-release activated calcium channels (CRAC) responsible for store-operated calcium entry (SOCE) in immune cells are gated by STIM family members functioning as sensors of Ca2+ store content in the endoplasmic reticulum. We investigated the effect of SOCE blocker BTP2 on human peripheral blood mononuclear cells (PBMC) stimulated with the mitogen phytohemagglutinin (PHA).

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Project description:Calcium signals are initiated in immune cells by the process of store-operated calcium entry (SOCE), where receptor activation triggers transient calcium release from the endoplasmic reticulum, followed by opening of plasma membrane calcium-release activated calcium (CRAC) channels. ORAI1, ORAI2 and ORAI3 are known to comprise the CRAC channel, however the contributions of individual isoforms to neutrophil function is not well understood. Here we show that loss of ORAI1 partially decreases calcium influx while loss of both ORAI1 and ORAI2 completely abolishes store-operated calcium entry. In other immune cell types, loss of ORAI2 enhances SOCE. In contrast, we find that ORAI2-deficient neutrophils display decreased calcium influx, which is correlated with measurable differences in regulation of neutrophil membrane potential via KCa3.1. Decreased SOCE in ORAI1-, ORAI2- and ORAI1/2-deficient neutrophils impairs multiple neutrophil functions including phagocytosis, degranulation, leukotriene and ROS production, rendering ORAI1/2-deficient mice highly susceptible to staphylococcal infection. This study demonstrates that ORAI1 and ORAI2 are the primary components of the neutrophil CRAC channel and identifies novel subpopulations of neutrophils where cell membrane potential functions as a rheostat to modulate the SOCE response. These findings have implications for new mechanisms that modulate neutrophil function during infection, acute and chronic inflammatory conditions, and cancer.

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Project description:Differential regulation of membrane potential during store-operated calcium entry in neutrophil subsets

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Store-operated Ca2+ entry in follicular T cells controls humoral immune responses and autoimmunity

Project description:T follicular helper (TFH) cells promote affinity maturation of B cells in germinal centers (GCs), whereas T follicular regulatory (TFR) cells limit GC reaction. Store-operated Ca2+ entry (SOCE) through Ca2+ release-activated Ca2+ (CRAC) channels mediated by STIM and ORAI proteins is a fundamental signaling pathway in T lymphocytes. Here we show that SOCE is required for the differentiation and function of both TFH and TFR cells. Conditional deletion of Stim1 and Stim2 genes in T cells or Treg cells results in spontaneous autoantibody production and humoral autoimmunity. Conversely, antibody-mediated immune responses following viral infection critically depend on SOCE in TFH cells. Mechanistically, STIM1 and STIM2 control early TFR and TFH cell differentiation through NFAT-mediated IRF4, BATF and Bcl-6 expression. SOCE plays a dual role in GC response by controlling TFH and TFR cell function, thus enabling protective B cell responses and preventing humoral autoimmunity. RNAseq analyses of WT and Stim1Stim2 DKO follicular T cells and non-follicular T cells; 4-6 mice per cohort in duplicates. Mice were infected for 10 days with LCMV.

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Store-operated Ca2+ entry in follicular T cells controls humoral immune responses and autoimmunity

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Chronic dysfunction of Store-operated calcium entry by pulsed RNAi induction in fat tissue impairs organismal energy homeostasis in Drosophila

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Transcriptomic screen to identify genes regulated by Store-operated calcium entry in Drosophila pupal nervous system

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Gene expession profiles for monoclonal cell lines with high or low levels of store-operated Ca2+ entry.

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Project description:Transcriptomic screen to identify genes regulated by Store-operated calcium entry in Drosophila pupal nervous system

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