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Analysis of gene expression regulated by Drosophila melanogaster Tis11

ABSTRACT: In mammalian cells, AU-rich elements (AREs) are well known regulatory sequences located in the 3' untranslated region (UTR) of many short-lived mRNAs that suppress gene expression at the posttranscriptional level. Tis11, a zinc finger RNA-binding protein homologous to mammalian tristetraprolin, targets ARE-containing reporter mRNAs for rapid degradation in SL2 cells. To identify Drosophila mRNA targets of Tis11, we performed genome-wide expression profiling after dsRNA-mediated depletion of endogenous Tis11 in SL2 cells. Furthermore, we studied the involvement of Tis11 in regulating the Drosophila immune response by profiling mRNA expression after LPS treatment, in the presence or absence of Tis11.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE28147 | GEO | 2011/03/25

SECONDARY ACCESSION(S): PRJNA139383

REPOSITORIES: GEO

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Analysis of gene expression regulated by Drosophila melanogaster Tis11

Project description:In mammalian cells, AU-rich elements (AREs) are well known regulatory sequences located in the 3' untranslated region (UTR) of many short-lived mRNAs that suppress gene expression at the posttranscriptional level. Tis11, a zinc finger RNA-binding protein homologous to mammalian tristetraprolin, targets ARE-containing reporter mRNAs for rapid degradation in SL2 cells. To identify Drosophila mRNA targets of Tis11, we performed genome-wide expression profiling after dsRNA-mediated depletion of endogenous Tis11 in SL2 cells. Furthermore, we studied the involvement of Tis11 in regulating the Drosophila immune response by profiling mRNA expression after LPS treatment, in the presence or absence of Tis11. SL2 cells were treated with either dsRNA against Tis11 or dsRNA against GFP (control). After 4 days of treatment with 12.5 microgram dsRNA / ml medium, total RNA was extracted and hybridized to Drosophila Genome 2.0 Arrays (Affymetrix, Cat. No. 900531). Where indicated, cells were treated with lipopolysaccharide (LPS, Sigma, O55:B5) at a concentration of 10 microgram / ml for 4 hours before lysis. All experiments were performed in 3 biological replicates.

2011-03-24 | E-GEOD-28147 | biostudies-arrayexpress

The Drosophila Tis11 protein and its effects on mRNA expression in flies

Project description:Insects generally express one tristetraprolin family member, proteins that in mammals promote mRNA decay. The Drosophila protein, Tis11, can promote mRNA decay in cells, and its deficiency in flies results in major changes in mRNA levels. Tis11 deficiency in Drosophila results in accumulation of potentialtarget transcripts. Tis11 can affect post- transcriptional gene expression in adult flies by regulating mRNA decay.

2014-10-23 | GSE58937 | GEO

The Drosophila Tis11 protein and its effects on mRNA expression in flies

2014-10-23 | E-GEOD-58937 | biostudies-arrayexpress

Translational repression of pre-formed cytokine mRNA prevents chronic activation of memory T cells

Project description:Memory T cells are critical to protect us from recurring infections. Their instantaneous reactivity to pathogens is empowered by persistent expression of cytokine mRNA. How aberrant protein production of this pre-formed mRNA is prevented in the absence of infection, however, remains unresolved. We show that protein production in memory T cells is blocked through a 3’untranslated region (3’UTR)-mediated process, and that AU-rich elements (AREs) are key herein. Germ-line deletion of AREs leads to chronic IFN- production in bona fide memory T cells. Strikingly, the aberrant protein production does not result from increased mRNA levels and/or half-life. Rather, AREs block the recruitment of cytokine mRNA to ribosomes, a process that is mediated by the ARE-binding protein ZFP36L2. Thus, AREs are crucial elements for translational repression that allow murine and human memory T cells to contain pre-formed cytokine mRNAs, while preventing undesirable protein production in the absence of infection.

2018-05-15 | PXD008051 | Pride

Tristetraprolin is a tumor suppressor that impairs Myc-induced lymphoma and abolishes the malignant state [Lymphoma].

Project description:Myc oncoproteins directly regulate transcription by binding to target genes, yet this only explains a fraction of the genes affected by Myc. mRNA turnover is controlled via AU-binding proteins (AUBPs) that recognize AU-rich elements (AREs) found within many transcripts. Analyses of precancerous and malignant Myc-expressing B cells revealed that Myc regulates hundreds of ARE-containing (ARED) genes and select AUBPs. Notably, Myc directly suppresses transcription of Tristetraprolin (TTP/ZFP36), an mRNA-destabilizing AUBP, and this circuit is also operational during B lymphopoiesis and IL7 signaling. Importantly, TTP suppression is a hallmark of cancers with MYC involvement, and restoring TTP impairs Myc-induced lymphomagenesis and abolishes maintenance of the malignant state. Further, there is a selection for TTP loss in malignancy; thus, TTP functions as a tumor suppressor. Finally, Myc/TTP-directed control of select cancer-associated ARED genes is disabled during lymphomagenesis. Thus, Myc targets AUBPs to regulate ARED genes that control tumorigenesis. Lymphomas collected from EÎ¼-Myc and EÎ¼-Myc;EÂµ-TTP-1 transgenic mice were investigated. These samples were used for subsequent RNA purification, labeling and hybridization to MOE430 2.0 Affymetrix arrays.

2012-08-01 | E-GEOD-37790 | biostudies-arrayexpress

TTP-dependent mRNA decay in LPS-stimulated macrophages

Project description:Controlled decay of cytokine and chemokine mRNAs restrains the time and amplitude of inflammatory responses. Tristetraprolin (TTP) binds to AU-rich elements in 3´ untranslated regions of mRNA and targets the bound mRNA for degradation. We have addressed here the function of TTP in balancing the macrophage activation state by a comprehensive analysis of TTP-dependent mRNA decay in LPS-stimulated macrophages from WT and TTP-deficient mice.

2011-12-15 | GSE28880 | GEO

Tristetraprolin is a tumor suppressor that impairs Myc-induced lymphoma and abolishes the malignant state [Lymphoma].

2012-08-02 | GSE37790 | GEO

Tristetraprolin is a tumor suppressor that impairs Myc-induced lymphoma and abolishes the malignant state [bone marrow B cells].

2012-08-02 | GSE33474 | GEO

Tristetraprolin is a tumor suppressor that impairs Myc-induced lymphoma and abolishes the malignant state [retrovirally infected ex vivo lymphoma]

2012-08-02 | GSE37791 | GEO

Tristetraprolin is a tumor suppressor that impairs Myc-induced lymphoma and abolishes the malignant state [retrovirally infected ex vivo lymphoma]

Project description:Myc oncoproteins directly regulate transcription by binding to target genes, yet this only explains a fraction of the genes affected by Myc. mRNA turnover is controlled via AU-binding proteins (AUBPs) that recognize AU-rich elements (AREs) found within many transcripts. Analyses of precancerous and malignant Myc-expressing B cells revealed that Myc regulates hundreds of ARE-containing (ARED) genes and select AUBPs. Notably, Myc directly suppresses transcription of Tristetraprolin (TTP/ZFP36), an mRNA-destabilizing AUBP, and this circuit is also operational during B lymphopoiesis and IL7 signaling. Importantly, TTP suppression is a hallmark of cancers with MYC involvement, and restoring TTP impairs Myc-induced lymphomagenesis and abolishes maintenance of the malignant state. Further, there is a selection for TTP loss in malignancy; thus, TTP functions as a tumor suppressor. Finally, Myc/TTP-directed control of select cancer-associated ARED genes is disabled during lymphomagenesis. Thus, Myc targets AUBPs to regulate ARED genes that control tumorigenesis. Ex vivo Eμ-Myc lymphoma cells were infected with MSCV-I-dsRed2 (RFP) and FACS sorted for dsRed2+ cells. These cells were then infected with MSCV-TTP-I-GFP and FACS sorted for GFP expression (TTP-GFP- or TTP-GFP+). These cells were used for subsequent RNA purification, labeling and hybridization to MOE430 2.0 Affymetrix arrays.

2012-08-01 | E-GEOD-37791 | biostudies-arrayexpress

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