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Transcriptome analysis of activated CD4+ T cells deficient for Zfp36 or Zfp36l1

ABSTRACT: Characterisation of the effects on the transcriptome of deleting the Zfp36 or Zfp36l1 genes in activated CD4+ T cells

ORGANISM(S): Mus musculus

PROVIDER: GSE214350 | GEO | 2022/10/01

REPOSITORIES: GEO

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Transcriptome analysis of activated CD4+ T cells deficient for Zfp36 or Zfp36l1

Project description:Transcriptome analysis of activated CD4+ T cells deficient for Zfp36 or Zfp36l1

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Multiomics analysis couples mRNA turnover and translational control of glutamine metabolism to the differentiation of the activated CD4+ T cell

Project description:The ZFP36 family of RNA-binding proteins acts post-transcriptionally to repress translation and promote RNA decay. Studies of genes and pathways regulated by the ZFP36 family in CD4+ T cells have focussed largely on cytokines, but their impact on metabolic reprogramming and differentiation is unclear. Using CD4+ T cells lacking Zfp36 and Zfp36l1, we combined the quantification of mRNA transcription, stability, abundance and translation with crosslinking immunoprecipitation and metabolic profiling to determine how they regulate T cell metabolism and differentiation. Our results suggest that ZFP36 and ZFP36L1 act directly to limit the expression of genes driving anabolic processes by two distinct routes: by targeting transcription factors and by targeting transcripts encoding rate-limiting enzymes. These enzymes span numerous metabolic pathways including glycolysis, one-carbon metabolism and glutaminolysis. Direct binding and repression of transcripts encoding glutamine transporter SLC38A2 correlated with increased cellular glutamine content in ZFP36/ZFP36L1-deficient T cells. Increased conversion of glutamine to α-ketoglutarate in these cells was consistent with direct binding of ZFP36/ZFP36L1 to Gls (encoding glutaminase) and Glud1 (encoding glutamate dehydrogenase). We propose that ZFP36 and ZFP36L1 as well as glutamine and α-ketoglutarate are limiting factors for the acquisition of the cytotoxic CD4+ T cell fate. Our data implicate ZFP36 and ZFP36L1 in limiting glutamine anaplerosis and differentiation of activated CD4+ T cells, likely mediated by direct binding to transcripts of critical genes that drive these processes.

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Transcriptome of Zfp36l1-deficient MZ B cells, WT MZ B cells and WT FO B cells.

Project description:Purpose: to identify the effects on the transcriptome of deleting ZFP36L1 in MZ B cells

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Zfp36l1 overexpression/knockdown effect on primary mouse articular chondrocytes

Project description:Gene expression profiling of primary mouse articular chondrocyte infected with recombinant adenovirus expressing mouse ZFP36 Ring Finger Protein Like 1(Zfp36l1) or recombinant adenovirus expressing mouse small hairpin RNA of Zfp36l1. In this study, we have attempted to explore the effects of Zfp36l1 gene overexpression or knockdown on mouse transcriptome and have identified numerous genes which are involved in osteoarthritis pathogenesis.

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Transcriptome of ZFP36L1-sufficient and ZFP36L1-deficient Fo B cells

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ZFP36L1

Project description:ZFP36L1

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The effect of ZFP36L1 deficiency on gene expression in the U2OS osteosarcoma cancer cell line

Project description:Post-transcriptional regulation of gene expression by RNA binding proteins (RBPs), one of the major classes of proteins encoded by the human genome, is well established. ZFP36L1 and its protein family members, ZFP36 and ZFP36L2, function as RBPs that primarily regulate gene expression at the post-transcriptional level by binding to adenine uridine (AU) rich elements (AREs) in the 3′ untranslated region (3′UTR) of certain mRNAs and mediating ARE-dependent mRNA decay. In this study, using CRISPR/Cas9 ZFP36L1 gene-editing, we generated ZFP36L1 deficient U2OS cellular models. The aim of the RNASeq experiment was to compare the gene expression profile in wild-type U2OS cells compared to ZFP36L1 deficient U2OS cells. Loss of functional ZFP36L1 leads to widespread changes in gene expression that are associated with dysregulation of KRAS signalling.

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Transcriptome of ZFP36L1-sufficient and ZFP36L1-deficient Fo B cells

Project description:Transcriptome of ZFP36L1-sufficient and ZFP36L1-deficient Fo B cells

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Silencing of ZFP36L1 using siRNA

Project description:ZFP36L1 is a tandem zinc-finger RNA-binding protein that recognizes conserved Adenylate-Uridylate-rich Elements (AREs) located in 3' untranslated regions (UTRs) to mediate RNA decay. We hypothesized that ZFP36L1 is a negative regulator of a post-transcriptional hub involved in the RNA half-life regulation of cancer-related transcripts. Forced expression of ZFP36L1 in cancer cells markedly reduced cell proliferation in vitro and in vivo; whereas silencing of ZFP36L1 enhanced tumor cell growth. To identify direct downstream targets of ZFP36L1, systematic screening using RNA pull-down of wildtype and mutant ZFP36L1 as well as whole transcriptome sequencing of bladder cancer cells ± tet-on ZFP36L1, was performed. A network of 1,410 genes was identified as potential direct targets of ZFP36L1, including HIF1A, CCND1, and E2F1. ZFP36L1 specifically bound to the 3' UTRs of these targets for RNA degradation, thus suppressing their expression. Collectively, our findings reveal an indispensable role of ZFP36L1 as a post-transcriptional safeguard against aberrant hypoxic signaling and abnormal cell cycle progression.

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Roles of Zfp36l1 and Zfp36l1 in retinal development

Project description:Roles of Zfp36l1 and Zfp36l1 in retinal development

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