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Nationwide Outbreak of invasive Listeriosis associated with Consumption of Meat Products in Health Care Facilities (HCF), Germany, 2014-2019

ABSTRACT: Nationwide Outbreak of invasive Listeriosis associated with Consumption of Meat Products in Health Care Facilities (HCF), Germany, 2014-2019

PROVIDER: PRJEB37937 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	ERR4057730.fastq.gz	Fastqsanger.gz
	ERR4057740.fastq.gz	Fastqsanger.gz
	ERR4057750_1.fastq.gz	Fastqsanger.gz
	ERR4057750_2.fastq.gz	Fastqsanger.gz

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Project description:Background and Aims: Host-cell factor 1 (HCF-1), encoded by the ubiquitously expressed X linked gene Hcfc1, is an epigenetic co-regulator important for mouse development and cell proliferation, including during liver regeneration. Here, we examine the role of HCF-1 in adult tissue physiology using, as model, the resting mouse liver. Methods: We used a hepatocyte-specific inducible Hcfc1 knock-out allele (called Hcfc1hepKO), to induce HCF-1 loss in hepatocytes of hemizygous Hcfc1 hepKO/Y males by four days. In heterozygous Hcfc1hepKO/+ females, owing to random X-chromosome inactivation, upon Hcfc1hepKO allele induction, a 50/50 mix of HCF-1 positive and negative hepatocyte clusters is engineered. Results: The livers with Hcfc1hepKO/Y hepatocytes displayed a 21 24-day terminal non-alcoholic fatty liver (NAFL) followed by non-alcoholic steatohepatitis (NASH) disease progression typical of severe NAFL disease (NAFLD). In contrast, in livers with heterozygous Hcfc1hepKO/+ hepatocytes, HCF-1-positive hepatocytes replaced HCF-1-negative hepatocytes and revealed only mild-NAFL development. Loss of HCF-1 led to loss of PGC1 alpha protein levels, probably owing to its destabilization, and deregulation of gene expression particularly of genes involved in mitochondrial structure and function, likely explaining the severe Hcfc1hepKO/Y liver pathology. Interestingly, although HCF-1 binds to over 5000 transcriptional start sites in the resting liver, expression of only a minor subset of the associated genes was affected by HCF-1 loss. Conclusion: HCF-1 is essential for proper liver physiology likely playing both transcriptional and non-transcriptional roles. These genetically-engineered loss-of-HCF-1 mice represent models for the study of NASH and NAFLD resolution.

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Project description:Here we study the effect of doxycycline induced expression of HCF-2 (the host-cell-factor 2) proteins - HCF-2WT and its mutant HCF-2Fn3nc* on the global gene expression in HEK-293 cells. We identified 7175 genes that were differentially expressed after day 1 in any of the HCF-2WT or HCF-2Fn3nc* samples (log2 (fold change) > 0.5 or < -0.5 and FDR < 0.05). The maximal gene-expression changes over time were on day 6 in each case, with more genes up-regulated (2199 vs. 1241) in the HCF-2WT samples and more genes down-regulated (2513 vs. 1555) in the HCF-2Fn3nc* samples after six days compared to day 1. Notably, there was little overlap between the genes affected by the induced synthesis of HCF-2WT or HCF-2Fn3nc* indicating that the HCF-2Fn3nc* mutation seriously disrupts HCF-2 function. In total, we found that up-regulated genes in HCF-2WT were associated with developmental and morphogenesis programs induction, whereas down-regulated genes were linked to the inhibition of cellular metabolism and proliferation.

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| S-EPMC7323541 | biostudies-literature

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