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Global RNA stability profiling in HEK293T cells under EGF treatment using TimeLapse-seq

ABSTRACT: Global RNA stability profiling in HEK293T cells under EGF treatment using TimeLapse-seq

PROVIDER: PRJNA609717 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11214813_1.fastq.gz	Fastqsanger.gz
	SRR11214813_2.fastq.gz	Fastqsanger.gz
	SRR11214814_1.fastq.gz	Fastqsanger.gz
	SRR11214814_2.fastq.gz	Fastqsanger.gz
	SRR11214815_1.fastq.gz	Fastqsanger.gz

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Global RNA stability profiling in HEK293T cells under EGF treatment using TimeLapse-seq

Project description:We discovered through LC-MS/MS followed by biochemical assays and immunofluorescence that human microprotein NoBody/NBDY can be phosphorylated during EGF signaling transduction, and that this single post-translational modification of the smallest decapping complex component known to date is necessary to the observed disappearance of P-bodies under EGF treatment. RNA stability measurement of a known hDcp2 substrate, RRP41, showed decreased RNA life-time under EGF treatment. We hence wish to investigate the effect of this phospho-NBDY mediated P-body disassembly on global RNA turnover. Here we present a global profile of RNA stability in human HEK293 cells under EGF treatment via TimeLapse-seq. By comparing this dataset to our previous and current work done in DCP2 KO and in NBDY KO cells, respectively, we demonstrate that P-body dissociation observed during EGF signaling does not cause RNA stability change globally except for a few known EGF regulated transcripts.

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Project description:We previously identified a conserved human microprotein NoBody/NBDY that can interact with the mRNA decapping complex through EDC4 and affects the expression of an NMD (nonsense-mediated decay) substrate. However, it remains unclear the exact mechanism of NBDY-regulated RNA stability change and whether this is the direct cause/consequence of its modulation of P-body structure/numbers. Here we present a global profile of RNA stability in human NBDY knockout cells via TimeLapse-seq. By comparing this dataset to our previous work done in DCP2 KO cells, we demonstrate that NBDY is a specificity factor of the 5'-3' RNA decay. In addition, these data indicate a role of NBDY in cell cycle and other signaling transduction processes as well.

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