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MYC-deficiency impairs the development of effector/memory T lymphocytes

ABSTRACT: MYC-deficiency impairs the development of effector/memory T lymphocytes

PROVIDER: PRJNA716339 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14037860_1.fastq.gz	Fastqsanger.gz
	SRR14037860_2.fastq.gz	Fastqsanger.gz
	SRR14037861_1.fastq.gz	Fastqsanger.gz
	SRR14037861_2.fastq.gz	Fastqsanger.gz
	SRR14037862_1.fastq.gz	Fastqsanger.gz

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MYC-deficiency impairs the development of effector/memory T lymphocytes

Project description:Using scRNA-seq we investigate the impact of the absence of MYC on physio-pathological development of PTEN-proficient or PTEN-deficient T lymphocytes. We demonstrate that MYC-deficient effector/memory T cells is drastically reduced. MYC is then essential for effector/memory differentiation

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MYC deficiency impairs the development of effector/memory T lymphocytes.

Project description:In the thymus, T cell progenitors differentiate in order to generate naive T lymphocytes which migrate in the periphery where they will fulfill their function in the adaptive immune response. During thymopoiesis, genomic alterations in thymocytes can promote leukemia development. Among recurrent alteration is PTEN inactivation, which is associated to MYC overexpression. Herein, we used conditional Pten and Myc knockout mouse models and single-cell RNA-sequencing approach, to investigate the impact of MYC loss on physio-pathological development of PTEN-proficient or PTEN-deficient T lymphocytes. First, our results confirm that MYC is mandatory for PTEN loss-mediated leukemogenesis, while it is not required for terminal steps of thymopoiesis. In contrast, we uncovered that Myc ablation in CD4+CD8+ thymocytes disrupts T lymphocytes homeostasis in the spleen, notably by drastically reducing the number of MYC-deficient effector/memory T cells. Collectively, our data show that besides naive T cells proliferation, MYC is essential for effector/memory differentiation.

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

Project description:This SuperSeries is composed of the following subset Series: GSE33474: Tristetraprolin is a tumor suppressor that impairs Myc-induced lymphoma and abolishes the malignant state [bone marrow B cells]. GSE37790: Tristetraprolin is a tumor suppressor that impairs Myc-induced lymphoma and abolishes the malignant state [Lymphoma]. GSE37791: Tristetraprolin is a tumor suppressor that impairs Myc-induced lymphoma and abolishes the malignant state [retrovirally infected ex vivo lymphoma] Refer to individual Series

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Transcriptional impacts of Myc deficiency in murine bone marrow NK cells

Project description:Despite the function of Myc oncogene has been extensively studied, little is known concerning its role in Natural killer (NK) cells. By performing RNA-sequencing analyses comparing Myc-deficient to Myc-sufficient NK cells, we aim at determining the biological function of Myc in these innate lymphocytes.

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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.

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Project description:Differentiation of CD8+ T lymphocytes into effector and memory cells is key for an adequate immune response and relies on complex interplay of pathways that convey signals from cell surface to nucleus. In this study, we fractionated four CD8+ T cell subtypes; naÃ¯ve, recently activated effector, effector and memory cells into membrane, cytosol, soluble nucleus, chromatin-bound and cytoskeleton compartments. Using LC-MS/MS analysis, identified peptides were matched to human peptides/proteins (SwissProt). Compartment fractionation and gel-LC-MS separation identified 2399 proteins in total. Among these 735 were detected in all five, 241 in four, 257 in three, 368 in two and 798 found in only one fraction. Comparison between the two most different subsets, naÃ¯ve and effector, yielded 146 significantly regulated proteins.

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Compartment resolved reference map from highly purified naive, activated, effector and memory CD8+ cells

Project description:Differentiation of CD8+ T lymphocytes into effector and memory cells is key for an adequate immune response and relies on complex interplay of pathways that convey signals from cell surface to nucleus. In this study, we fractionated four CD8+ T cell subtypes; naïve, recently activated effector, effector and memory cells into membrane, cytosol, soluble nucleus, chromatin-bound and cytoskeleton compartments. Using LC-MS/MS analysis, identified peptides were matched to human peptides/proteins (SwissProt). Compartment fractionation and gel-LC-MS separation identified 2399 proteins in total. Among these 735 were detected in all five, 241 in four, 257 in three, 368 in two and 798 found in only one fraction. Comparison between the two most different subsets, naïve and effector, yielded 146 significantly regulated proteins.

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Influence of isolation procedure and storage condition on the ex vivo gene expression pattern in peripheral human effector/memory T helper lymphocytes

Project description:Gene expression profiling of cells isolated ex vivo is a unique tool to assess gene expression in vivo. Exemplified for CD4+CD45RO+ effector/memory T helper (T E/M) lymphocytes of human peripheral blood, we have analyzed different isolation procedures and storage conditions for the introduction of bias.

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

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. Wild type, Eµ-TTP-1, precancerous Eμ-Myc and precancerous Eμ-Myc;Eµ-TTP-1 transgenic bone marrow B cells (from 4-6 week old littermates; 94% C57BL/6) were investigated. These samples were used for subsequent RNA purification, labeling and hybridization to MOE430 2.0 Affymetrix arrays.

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