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Translation-dependent and independent mRNA decay occur through mutually exclusive pathways that are defined by ribosome density during T Cell activation [RNA-Seq]

ABSTRACT: Translation-dependent and independent mRNA decay occur through mutually exclusive pathways that are defined by ribosome density during T Cell activation [RNA-Seq]

PROVIDER: PRJNA668315 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12801100_1.fastq.gz	Fastqsanger.gz
	SRR12801100_2.fastq.gz	Fastqsanger.gz
	SRR12801101_1.fastq.gz	Fastqsanger.gz
	SRR12801101_2.fastq.gz	Fastqsanger.gz
	SRR12801102_1.fastq.gz	Fastqsanger.gz

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Translation-dependent and independent mRNA decay occur through mutually exclusive pathways that are defined by ribosome density during T Cell activation

Project description:Translation-dependent and independent mRNA decay occur through mutually exclusive pathways that are defined by ribosome density during T Cell activation

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Translation-dependent and independent mRNA decay occur through mutually exclusive pathways that are defined by ribosome density during T Cell activation [Ribo-Seq]

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Translation-dependent and independent mRNA decay occur through mutually exclusive pathways that are defined by ribosome density during T Cell activation [PAS-Seq]

Project description:Translation-dependent and independent mRNA decay occur through mutually exclusive pathways that are defined by ribosome density during T Cell activation [PAS-Seq]

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Translation-dependent and independent mRNA decay occur through mutually exclusive pathways that are defined by ribosome density during T Cell activation [Ribo-Seq]

Project description:Post-transcriptional control is crucial for regulating protein expression, both basally and in response to extracellular cues. Proper signal transduction requires tight control of both response induction and termination. One way protein expression might be attenuated is by targeting mRNAs to translation-dependent degradation (TDD), thus making any increase in protein expression self-limiting. However, the extent to which TDD is a general mechanism for limiting protein expression is currently unknown. Here we describe a comprehensive analysis of basal and signal-induced TDD in mouse primary CD4 T cells. Our data indicate that most cellular transcripts are decayed to some extent in a translation-dependent manner, both in resting and activated cells. Analysis of transcript features revealed that 3’UTR length and ribosome density are major determinants of the magnitude of TDD as well as GC content and amino acid identity. Consistently, upon T cell activation, all transcripts that undergo changes in ribosome density display a corresponding change in their level of TDD. Surprisingly, the amplitude of translation-independent mRNA decay appears as a mirror image of TDD. Moreover, translation-independent decay also responds to changes in ribosome density upon T cell activation but in the opposite direction to those observed for TDD. Our data demonstrate a strong interconnection between mRNA translation and decay in mammalian cells. Furthermore they indicate that ribosome loading is a major determinant of the pathway by which transcripts are degraded within cells

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Translation-dependent and independent mRNA decay occur through mutually exclusive pathways that are defined by ribosome density during T Cell activation

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Transcriptome-wide binding sites of mutually exclusive exon junction complexes

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Yap1/Birc, c-Met and N-ras DNA amplifications are mutually exclusive in mouse mammary tumors.

Project description:Tumors acquire somatic DNA copy number aberrations, leading to activation of oncogenes and inactivation of tumor suppressors. Many studies have focused on the analysis of single copy number aberrations and associated driver genes, but few studies have performed combinatorial analyses. We propose a genome-wide scoring framework to find mutually exclusive gains and losses. Mutually exclusive copy number aberrations can identify genes whose oncogenic function is redundant, either by functioning in the same pathway or in a parallel pathway. As one gene is aberrated the selective pressure for its partner is alleviated which leads to a mutually exclusive perturbation pattern. In a dataset of mouse models for invasive lobular carcinoma we found three mutually exclusive DNA amplifications, containing several well-known oncogenes: the Met proto-oncogene on chromosome 6, the cluster of Birc2, Birc3 and Yap1 genes on chromosome 9, and Nras on chromosome 3. Furthermore, gene expression or protein expression of these genes correlates very well with copy number data indicating that they are the target of the amplification. Although homologous amplifications in human tumors are rare, the mutual exclusivity of MET, BIRC/YAP1 and NRAS is maintained in a variety of cancer types. This suggests a novel function for YAP1 in the mitogen-activated signaling pathway by association with MET and NRAS, known players in this pathway. This function is independent to the propensity of YAP1 to cause Epithelial-to-Mesenchymal transition. aCGH data of 67 mouse mammary tumors from K14-Cre and WAP-Cre driven P53-F/F;Cdh1-F/F animals - tumor DNA hybridized against same-animal splenic DNA

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