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Charged tRNA profiling of mcf10a, HCC1806 cells, polysome profiling, RNA-Seq and Ribo-Seq in 4T07 cells upon LARS knockdown by shRNA, and RNA-Seq of ribosome-associated RNAs in Lars depleted PyMT tumors

ABSTRACT: Charged tRNA profiling of mcf10a, HCC1806 cells, polysome profiling, RNA-Seq and Ribo-Seq in 4T07 cells upon LARS knockdown by shRNA, and RNA-Seq of ribosome-associated RNAs in Lars depleted PyMT tumors

PROVIDER: PRJNA734953 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14722521.fastq.gz	Fastqsanger.gz
	SRR14722522.fastq.gz	Fastqsanger.gz
	SRR14722523.fastq.gz	Fastqsanger.gz
	SRR14722524.fastq.gz	Fastqsanger.gz
	SRR14722525.fastq.gz	Fastqsanger.gz

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Charged tRNA profiling of mcf10a, HCC1806 cells, polysome profiling, RNA-Seq and Ribo-Seq in 4T07 cells upon LARS knockdown by shRNA, and RNA-Seq of ribosome-associated RNAs in Lars depleted PyMT tumors

Project description:In this study, we identify leucyl-tRNA synthetase (LARS) as a breast tumor suppressor. To identify the mechanism underlying LARS-mediated breast tumor suppression, we first conducted charged tRNA profiling to assess charged and total tRNA-Leu expression in cell lines with high and low LARS expression. Expression of select charged and total tRNA-Leu isoacceptors were reduced in cell lines with lower LARS expression. We then conducted RNA-Seq and translation profiling including ribosome profiling (Ribo-Seq), polysome profiling in LARS-depleted cell lines. To test our hypothesis in vivo, we also performed RNA-Seq of ribosome-associated RNAs in Lars depleted PyMT tumors within RiboTag mice. The analyses implicate LARS as a regulator of leucine-rich translation.

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mRNA-seq of HCC1806 cells, treated with siControl or siRNF40 for 48 hours

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