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The zebrafish heart harbors a thermogenic beige fat depot analog of human epicardial adipose tissue

ABSTRACT: The zebrafish heart harbors a thermogenic beige fat depot analog of human epicardial adipose tissue

PROVIDER: PRJNA946307 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23908258_1.fastq.gz	Fastqsanger.gz
	SRR23908258_2.fastq.gz	Fastqsanger.gz
	SRR23908259_1.fastq.gz	Fastqsanger.gz
	SRR23908259_2.fastq.gz	Fastqsanger.gz
	SRR23908260_1.fastq.gz	Fastqsanger.gz

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The zebrafish heart harbors a thermogenic beige fat depot analog of human epicardial adipose tissue

Project description:The main goal of this study was to examine the presence and specific transcriptomic profile of epicardial adipose tissue (eAT) in zebrafish. We assessed how cold treatment affects the epicardial adipose tissue. Additional we provided some key differences between human, mouse and zebrafish epicardial adipose tissue.

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Project description:Background: The beneficial effect of thermogenic adipocytes in maintaining body weight and protecting against metabolic disorders has raised interest in understanding the regulatory mechanisms defining white and beige adipocyte identity. Although alternative splicing has been shown to propagate adipose browning signals in mice, this has yet to be thoroughly investigated in human adipocytes. Methods: We performed parallel white and beige adipogenic differentiation using primary adipose stem cells from 6 unrelated healthy subjects, and assessed differential gene and isoform expression in mature adipocytes by RNA sequencing. Results: We find 693 exon junctions with robust differential usage between white and beige adipocytes in all 6 subjects, mapping to 507 genes. Importantly, only 8% of these differentially spliced genes are also differentially expressed, indicating that alternative splicing constitutes an additional layer of gene expression regulation during beige adipocyte adipogenic differentiation. Functional classification of alternative isoforms point to a gain of function for key thermogenic regulators such as PPARG, CITED1 and PEMT. We find that a large majority of the splice variants arise from differential usage of transcription start sites (TSSs), with beige-specific TSSs being enriched for PPARγ and MED1 binding compared to white-specific TSSs. Finally, we validate beige specific isoform expression at the protein level for two thermogenic regulators, PPARγ and PEMT. Discussion: These results indicate that differential isoform expression through alternative TSS usage is an important regulatory mechanism for human adipocyte thermogenic specification.

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