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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.

2017-08-17 | E-MTAB-5677 | biostudies-arrayexpress

Array 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 transcriptome their genes were conditionally deleted in GV oocytes, MEFs, ECSs, liver and Bone marrow. Total RNA samples from the TUT4 and TUT7 deficient tissues/cells (together with their control tissues/cells) were subjected to array profiling.

2017-08-17 | E-MTAB-5056 | biostudies-arrayexpress

Small RNA profiling of TUT4 and TUT7-deficient mouse pachytene-diplotene cells.

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Uridylation by TUT4 and TUT7 marks mRNA for degradation [TAIL-Seq]

2014-12-04 | GSE59627 | GEO

Uridylation by TUT4 and TUT7 marks mRNA for degradation [RNA-Seq]

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Small RNA profiling of TUT4 and TUT7-deficient mouse pachytene-diplotene cells.

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Uridylation by TUT4 and TUT7 marks mRNA for degradation [RNA-Seq]

Project description:Uridylation occurs pervasively on mRNAs in mammals, yet its mechanism and significance remain unknown. Here we identify TUT4 and TUT7 (also known as ZCCHC11 and ZCCHC6, respectively) as the enzymes that uridylate mRNAs. Uridylation readily occurs on deadenylated mRNAs that are not associated with poly(A) binding protein (PABPC1) in cells. Consistently, purified TUT4 and TUT7 (TUT4/7) selectively uridylate RNAs with short A tails (< ~25 nt) while PABPC1 antagonizes uridylation of polyadenylated mRNAs in vitro. In cells depleted of TUT4/7, the vast majority of mRNAs lose the U tails, and their half-lives are extended. Suppression of mRNA decay factors leads to the accumulation of uridylated mRNAs. In line with this, microRNA induces uridylation of its targets, and TUT4/7 is required for enhanced decay of microRNA targets. Our study explains the mechanism underlying selective uridylation of deadenylated mRNAs, and demonstrates a fundamental role of the U tail as a molecular mark for global mRNA decay. HeLa cells were knocked down of control or TUT4/7, then total RNAs were prepared for RNA-seq on 0, 1, 2, 4h after actinomycin D treatment. The whole processes of experiments were repeated two times.

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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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