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MicroRNA profiling of different TUT4 and TUT7 deficient mouse tissues/cells against controls

ABSTRACT: MicroRNA profiling of different TUT4 and TUT7 deficient mouse tissues/cells against controls

PROVIDER: PRJEB20501 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1942300.fastq.gz	Fastqsanger.gz
	ERR1942310.fastq.gz	Fastqsanger.gz
	ERR1942320.fastq.gz	Fastqsanger.gz
	ERR1942301.fastq.gz	Fastqsanger.gz
	ERR1942311.fastq.gz	Fastqsanger.gz

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MicroRNA profiling of different TUT4 and TUT7 deficient mouse tissues/cells against controls

Project description:To study the impact of the proteins TUT4 and TUT7 on the miRNome, their genes were conditionally deleted in MEFs, ESCs, liver and bone marrow. Total RNA samples from the TUT4 and TUT7 deficient tissues/cells (together with their control tissues/cells) were used to generate microRNA libraries.

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2014-12-04 | GSE59627 | GEO

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Project description:Terminal uridylation of mRNAs poly(A) tails by Terminal Uridylyl Transferases (TUTs) promote transcript decay. Here, we investigate the role of two functionally redundant mammalian TUTs, TUT4 and TUT7 (TUT4/7), in mouse hepatitis virus (MHV) RNA processing. We generated a TUT4/7 knock-down 17-CL1 cell line using lentivirus encoding shRNAs against Tut4 and Tut7 transcripts (shTUT4/7) and a control 17-CL1 cell line (shCTL) with a non-targeting shRNA. We then infected the shCTL and shTUT4/7 cells with MHV and isolated RNA at 24- and 48-hours post-infection (hpi). We found that viral RNA poly(A) tails of about 20 and 40 nucleotides are highly uridylated and that the uridylation of the 20 nucleotide long tails is dependent on TUT4/7. Depletion of TUT4/7 also resulted in an accumulation of the viral RNA.

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