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The role of MLF1 on accessible chromatin in AC16 cell line

ABSTRACT: The role of MLF1 on accessible chromatin in AC16 cell line

PROVIDER: PRJNA857661 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20077382_1.fastq.gz	Fastqsanger.gz
	SRR20077382_2.fastq.gz	Fastqsanger.gz
	SRR20077383_1.fastq.gz	Fastqsanger.gz
	SRR20077383_2.fastq.gz	Fastqsanger.gz
	SRR20077384_1.fastq.gz	Fastqsanger.gz

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The role of MLF1 on accessible chromatin in AC16 cell line

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Project description:Cardiovascular diseases are associated with an altered cardiomyocyte metabolism. Due to a shortage of human heart tissue, experimental studies mostly rely on alternative approaches including animal and cell culture models. Since the use of isolated primary cardiomyocytes is limited, immortalized cardiomyocyte cell lines may represent a useful tool as they closely mimic human cardiomyocytes. This study is focused on the AC16 cell line generated from adult human ventricular cardiomyocytes. Despite an increasing number of articles employing AC16 cells, the comprehensive proteomic, bioenergetic and oxygen-sensing characterization of proliferating versus differentiated cells is still lacking. Here, we provide a comparison of these two stages, particularly emphasizing cell metabolism, mitochondrial function, and hypoxic signalling. The label-free quantitative mass spectrometry revealed a decrease in autophagy and cytoplasmic translation in differentiated AC16, confirming their phenotype. Cell differentiation led to the global increase in mitochondrial proteins (e.g. OXPHOS proteins, TFAM, VWA8, etc.) reflected by elevated mitochondrial respiration. Fatty acid oxidation proteins were increased in differentiated cells, while the expression levels of proteins associated with fatty acid synthesis were unchanged, and glycolytic proteins were decreased. There was a profound difference between proliferating and differentiated cells in their response to hypoxia and anoxia/reoxygenation. We conclude that AC16 differentiation leads to proteomic and metabolic shifts and altered cell response to oxygen deprivation. This underscores the requirement for proper selection of particular differentiation state during experimental planning.

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Targeted analysis of alternative protein isoforms in AC16 cells

Project description:AC16 cells (Human Cardiomyocyte Cell Line) were digested by trypsin and analyzed by parallel reaction monitoring.

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NPM and NPM-MLF1 interact with chromatin remodeling complexes and influence their recruitment to specific genes

Project description:Nucleophosmin (NPM1) is either frequently mutated or subjected to chromosomal translocation in acute myeloid leukemia (AML). NPM protein is primarily located in the nucleus, but the recurrent NPMc+ mutation is characterized by cytoplasmic localization and leukemogenic properties. Similarly, the NPM-MLF1 translocation product favors the partial cytoplasmic retention of NPM. Regardless of their common cellular distribution, NPM-MLF1 malignancies engender different effects on hematopoiesis compared to NPMc+ counterparts, highlighting possible aberrant nuclear function(s) of NPM in NPMc+ AML. We performed a proteomics analysis and found that NPM and NPM-MLF1 interact with chromatin remodeling complexes of the ISWI family, as well as with NuRD and P/BAF complexes. Accordingly, NPM and NPM-MLF1 are recruited to transcriptionally active or repressed genes along with NuRD and P/BAF elements. Although the overall gene expression program in NPM knockdown cells is similar to that resulting from NPMc+ and is consistent with loss of nuclear function of NPM, NPM-MLF1 expression differentially altered gene transcription regulated by NPM. The abnormal gene regulation imposed by NPM-MLF1 is characterized by enhanced recruitment of NuRD to gene regulatory regions. Thus, different mechanisms orchestrate the deregulation of NPM function in NPMc+- versus NPM1-MLF1-associated leukemia.

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