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LIN37 dependent and independent TP53 response

ABSTRACT: Analysis of the TP53 activation response by DREAM component LIN37 knockout and rescue HCT116 cell lines

PROVIDER: PRJEB31044 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3138070.fastq.gz	Fastqsanger.gz
	ERR3138080.fastq.gz	Fastqsanger.gz
	ERR3138071.fastq.gz	Fastqsanger.gz
	ERR3138081.fastq.gz	Fastqsanger.gz
	ERR3138072.fastq.gz	Fastqsanger.gz

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nascent proteome analysis of HCT116 TP53 wild type and TP53 knockout cells treated with Neocarcinostatin (NCS) for 6h

Project description:In order to investigate the potential role of TP53 in regulating translation, HCT116 wild type and TP53 knockout cells were analyzed using both RNA sequencing, Ribosome sequencing and nascent proteome analysis. The cells were treated with 0.2 µg/ml Neocarcinostatin (NCS) to induce DNA damage and activate TP53.

2022-04-27 | PXD029512 | Pride

Lin37 is essential for repression of cell-cycle genes in quiescence

Project description:The DREAM complex represses cell-cycle gene transcription in quiescence. To investigate the role of the DREAM component Lin37, we created Lin37 knockout cells by CRISPR/Cas9-nickase. pRTS episomal vectors expressing luciferase or Lin37 were introduced in two independent knockout clones (411-27 and 632-2) to create Lin37 knockout and rescue cells. To exit the cell cycle and to enter quiescence, cells were serum starved for 60h. RNA-seq was applied to identify genes de-regulated by loss of Lin37 during quiescence.

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RNAseq of mutant TP53 HCT116 cell line clones generated via CRISPR editing

Project description:To compare the impact of several TP53 mutant variants in an isogenic setting, different TP53 mutations were introduced in HCT116 colorectal carcinoma cells. This parental cell line is wild-type for TP53 and shows a prototypical p53 response. To ensure unambigous genotype-phenotype correlations, the cell were haploidized prior to CRISPR-editing by introducing inactivating deletions of intronic splicing into one of the two TP53 alleles, leaving only one functional copy of TP53. The remaining TP53 allele was altered by inserting a LoxP-flanked transcriptional stop cassette (Lox-Stop-Lox, LSL) into intron 4, which allowed reversible silencing of TP53 expression. The LSL cassette was then specifically targeted with CRISPR/Cas9 to introduce a variety of different mutant p53 alleles. The competency of the mutated p53 allele to induce a p53 response upon activation using Nutlin-3a was then assessed in an RNAseq experiment.

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Next Generation Sequencing Facilitates Quantitative Analysis of TP53-WT and TP53-KO HCT116 cells transcriptomes [RNA-seq]

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare TP53-WT and TP53-KO HCT116 cells transcriptome profiling (RNA-seq) under 5-FU treatment condition and to evaluate the correlation between transcriptome profileing and chromatin accessibility under 5-FU treatment. Methods: HCT116 cell profiles of TP53-WT and TP53- KO were generated by deep sequencing, in duplicates, using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript isoform levels: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA). Conclusions: Our study represents the detailed analysis of TP53-WT and TP53-KO HCT116 cell transcriptomes under 5-FU treatment with different timepoint, with biologic replicates, generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles. Our results show that RNA-seq offers a comprehensive and more accurate quantitative and qualitative evaluation of mRNA content within a TP53-WT and TP53-KO cells with and without 5-FU treatment in different timepoint. We conclude that NGS based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions.

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SARS-CoV-2 spike sequence dictates host TP53 activity and COVID-19 pathogenicity

Project description:SARS-CoV-2 induces widespread transcriptomic changes in host cells upon infection, in part through activation and modulation of innate immunity pathways and downstream gene regulation. However, the mechanisms by which SARS-CoV-2 and its evolutionary variants differentially affect host cell transcriptomic states remain largely unclear. Through chromatin proteomic (iDAPT-MS) analysis, we found that although SARS-CoV-2 and other pathogenic coronaviruses exhibit similar proteomic shifts on chromatin, SARS-CoV-2 uniquely promotes TP53 nuclear accumulation and activation. Parallel assessment of SARS-CoV-2 viral protein expression on host chromatin states (ATAC-seq) identifies intracellular spike protein as a key determinant of virus-mediated chromatin accessibility changes. Multilevel chromatin profiling reveals increased TP53 nuclear accumulation, TP53-associated chromatin accessibility changes, and TP53 target gene activation upon expression of SARS-CoV-2 alpha (B.1.1.7) and delta (B.1.617.2) spike variants relative to the ancestral spike sequence. TP53, ACE2, and furin cleavage are required for these changes, driving decreased cellular proliferation, increased cellular senescence, and increased cytokine release. Finally, BA.1 but not BA.2, BA.2.12.1, nor BA.4/BA.5 spike expression leads to attenuated TP53 activity and fusogenicity relative to ancestral spike. Our findings implicate spike-mediated host TP53 activation as a “rheostat” of COVID-19 pathogenicity.

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