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PABP stabilizes select mRNAs populations in human cells

ABSTRACT: PABP stabilizes select mRNAs populations in human cells

PROVIDER: PRJNA777575 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16761900.fastq.gz	Fastqsanger.gz
	SRR16761901.fastq.gz	Fastqsanger.gz
	SRR16761902.fastq.gz	Fastqsanger.gz
	SRR16761903.fastq.gz	Fastqsanger.gz
	SRR16761904.fastq.gz	Fastqsanger.gz

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PABP stabilizes select mRNAs populations in human cells

Project description:Gene expression is tightly regulated at the levels of both mRNA translation and stability. The poly(A) binding protein (PABP) plays a role in regulating these processes by binding the mRNA 3´ poly(A) tail and interfacing with both the translation initiation and mRNA deadenylation machineries. Here we directly investigate the impact of PABP on the translation and stability of endogenous mRNAs in human cell lines. Remarkably, our transcriptome-wide analysis does not generally detect changes to mRNA translation in PABP-depleted cells. In contrast, rapidly depleting PABP alters transcriptome abundance and stability, albeit non-uniformly. Transcripts with long half-lives and short 3’UTRs are preferentially depleted in PABP-depleted cells. PABP depletion induces cell death; however, disrupting the mRNA decapping and 5’-3’ decay machinery can partially suppress this lethality. Finally, we show that disrupting the LSM1-7 complex prevents the premature decay of mRNAs that are destabilized in PABP-depleted cells. Taken together, these findings suggest that PABP plays an important role in preventing the untimely decay of select mRNA populations in human cells.

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m6A and YTHDF proteins control the subcellular localization of select neuronal mRNAs [RIP- and RNA-seq]

Project description:The transport of mRNAs to distal subcellular compartments is an important component of spatial gene expression control in neurons. However, the mechanisms that control mRNA localization in neurons are not completely understood. Here, we identify the abundant base modification, m6A, as a novel regulator of this process. Transcriptome-wide analysis following genetic loss of m6A reveals hundreds of transcripts that exhibit altered subcellular localization in hippocampal neurons. Additionally, using a reporter system, we show that mutation of specific m6A sites in select neuronal transcripts diminishes their localization to neurites. Single molecule fluorescent in situ hybridization experiments further confirm our findings and identify the m6A reader proteins YTHDF2 and YTHDF3 as mediators of this effect. Our findings reveal a novel function for m6A in controlling mRNA localization in neurons and enable a better understanding of the mechanisms through which m6A influences gene expression in the brain.

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