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Exploring the Dynamics and Consequences of Differential Transcript Usage in Cardiomyocyte Fate Specification

ABSTRACT: Exploring the Dynamics and Consequences of Differential Transcript Usage in Cardiomyocyte Fate Specification

PROVIDER: PRJNA1147591 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30220900_1.fastq.gz	Fastqsanger.gz
	SRR30220900_2.fastq.gz	Fastqsanger.gz
	SRR30220901_1.fastq.gz	Fastqsanger.gz
	SRR30220901_2.fastq.gz	Fastqsanger.gz
	SRR30220902_1.fastq.gz	Fastqsanger.gz

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Exploring the Dynamics and Consequences of Differential Transcript Usage in Cardiomyocyte Fate Specification

Project description:Cardiovascular research often relies on in vitro models using induced pluripotent stem cells (iPSCs) differentiating into induced cardiomyocytes (iCM). Little is known about the changes in transcript variants, termed differential transcript usage (DTU), which greatly influence cellular programs. In this study, we explored the DTU landscape during the iPSC-to-iCM differentiation and its relation to iCM fate. We found that DTU is consistently displayed by a subset of genes during iCM differentiation. DTU largely operates on a distinct set of genes than DGE, and both impact different biological processes. The DTU is used more often by protein coding in the late stage of iCM differentiation. The DTU-displaying genes are linked with functions specific to CMs, including ion signaling and cell junction organization, and their expression is cell-type specific. The RNA binding proteins (RBPs) involved in shaping the alternative splicing during the iCM differentiation experience early directed gene expression changes in their expression. Our research emphasizes that analyzing transcript variant expression levels is crucial for uncovering novel genes and functions, and for mapping fine-tuning gene expression and cardiomyocyte-specific functions during cell differentiation.

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Tmem88a Mediates GATA-dependent Specification of Cardiomyocyte Progenitors by Restricting Canonical WNT Signaling

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Transcriptomic, proteomic and functional consequences of codon usage bias in human cells

Project description:Differences in codon frequency between genomes, genes, or positions along a gene, modulate transcription and translation efficiency, leading to phenotypic and functional differences. Integrative studies quantifying the phenotypic consequences of codon usage bias at different molecular and cellular levels in human cells are lacking. Here, we present a multiscale analysis of the effects of synonymous codon recoding during heterologous gene expression in human cells. Six synonymous versions of an antibiotic resistance gene were generated, fused to a fluorescent reporter, and independently expressed in HEK293 cells. Multiscale phenotype was analysed by means of: quantitative transcriptome and proteome assessment, as proxies for gene expression; cellular fluorescence, as a proxy for single-cell level expression; and real-time cell proliferation in absence or presence of antibiotic, as a proxy for the cell fitness. We show that differences in codon usage bias strongly impact the molecular and cellular phenotype: (i) they result in large differences in mRNA and in protein levels, as well in mRNA-to-protein ratio; (ii) they introduce unpredicted splicing events; (iii) they lead to reproducible phenotypic heterogeneity; and (iv) they lead to a trade-off between the benefit of antibiotic resistance and the burden of heterologous expression. In human cells in culture, codon usage bias modulates gene expression by modifying mRNA availability and suitability for translation, leading to differences in protein levels and eventually eliciting functional phenotypic changes.

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Transcriptional specification of early cardiac precursor cells at single cell resolution

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