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Timecourse of gene expression in HeLa cells (parental cells and clonal knockouts of MED12 and MED24) following induction by TNFa or IL-1b

ABSTRACT: Timecourse of gene expression in HeLa cells (parental cells and clonal knockouts of MED12 and MED24) following induction by TNFa or IL-1b

PROVIDER: PRJNA548788 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9297180_1.fastq.gz	Fastqsanger.gz
	SRR9297180_2.fastq.gz	Fastqsanger.gz
	SRR9297190_1.fastq.gz	Fastqsanger.gz
	SRR9297190_2.fastq.gz	Fastqsanger.gz
	SRR9297200_1.fastq.gz	Fastqsanger.gz

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Timecourse of gene expression in HeLa cells (parental cells and clonal knockouts of MED12 and MED24) following induction by TNFa or IL-1b

Project description:Activation of nuclear factor kappa B (NF-kB) by inflammatory signals results in nuclear translocation of the transcription factor p65 and induction of gene expression. We identified MED12 and MED24 in an optical pooled CRISPR knockout screen in HeLa-Cas9 cells for genes affecting the activation and/or relaxation of p65 to the cytoplasm following induction by either TNFa or IL-1b. We generated isogenic clonal knockout HeLa-Cas9 lines using crRNA transfection and confirmed that loss of MED12 or MED24 results in delayed relaxation of p65, assayed by live-cell imaging of a p65-mNeonGreen fluorescent fusion.

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SM015 - Infection with SARS MA15 of C57BL/6J mice and Tnfrsf1a/1b knockouts

Project description:Comparing the host response of C57BL/6J mice to Tnfrsf1a/1b knockouts in the same strain of mice. Groups of 10-week-old C57BL/6 mice or Tnfrsf1a/1b knockout mice were infected with SARS MA15 at a dose of 10^5 PFU or mock infected. Mice were euthanized on days 4 and 7 post-infection to measure virus load and isolate samples for measurement of virus load, lung pathology, transcriptional analysis and proteomics analysis. Mock-infected animals were also harvested at each time point. Mice were weighed every 24 hours to measure general disease progression and any mouse approaching 30% weight loss was euthanized.

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Project description:Here, the goal of our study was to determine the protein-protein interactome of MED12 in resting and activated human T-cells. We immunoprecipitated endogenous MED12 and evaluated the protein interactome in comparison to an isotype-matched IgG as a control.

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Project description:We characterized the genome wide occupancy of Med12 and p300 in mouse HSPCs. We also characterize p300 occupancy upon shRNA against control or Med12. ChIP-seq analysis of Med12 and/or p300 in untreated HSPCs

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Project description:We characterized the genome wide occupancy of Med12 and p300 in mouse HSPCs. We also characterize p300 occupancy upon shRNA against control or Med12.

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Maternal Med12 safeguards trophoblast pluripotency and placental development

Project description:For a brief but critical period post-fertilization, the mammalian embryo is entirely dependent on maternal products inherited from the oocyte. Previous research showed that oocyte-specific loss of Med12, an X-linked gene and Mediator complex subunit, leads to female sterility despite normal folliculogenesis and ovulation. Here, we show that loss of maternal Med12 has minimal effect on the oocyte transcriptome and does not manifest in embryonic lethality until post-implantation. Implants derived from Med12-null oocytes demonstrate abnormal placentation at E9.5, with an overabundance of trophoblast giant cells (TGC). This phenotype associates with downregulation of trophoblast pluripotency markers (e.g. Cdx2) and activation of drivers of TGC identity (e.g. Stra13) in the E7.5 extraembryonic ectoderm, revealing a previously undescribed role for Med12 in trophoblast pluripotency maintenance. Notably, we find consistently low Med12 expression in embryos derived from Med12-null oocytes, potentially due to programmed paternal X chromosome inactivation (XCI). To isolate the consequences of maternal Med12 depletion, we introduced an autosomal Med12 transgene and show that embryonic expression of the transgene rescues development of Med12-null oocytes. We conclude that oocyte-specific deletion of Med12 produces a maternal-zygotic double knock-out in extraembryonic tissues due to paternal XCI, leading to loss of pluripotency in the trophoblast, placental malformation, and embryonic death.

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