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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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RNA-Seq of WT Flp-In T-REx 293, UPF3A knockout and UPF3A overexpression cell lines in part with additional siRNA-mediated control or UPF3B knockdowns

ABSTRACT: UPF3A and UPF3B are paralogous genes in human cells that are involved in the nonsense-mediated decay (NMD) pathway. NMD is a cellular quality control mechanism that monitors mRNAs during translation. Aberrant translation due to features such as the presence of a premature stop codon downstream on an exon-exon junction activates NMD and leads to the degradation of the mRNA. To investigate the role of UPF3B and UPF3A in NMD, we have generated UPF3A knockout (KO) human Flp-In T-REx 293 cells using CRISPR-Cas9, as well as FLAG-tagged UPF3A overexpressing cells using the PiggyBac transposon system. We generated RNA-Sequencing data for wildtype, UPF3A KO and UPF3A overexpressing (OE) cells, in part with additional siRNA-mediated knockdown of Luciferase (Luc) as control or UPF3B.

INSTRUMENT(S): Illumina NovaSeq 6000

ORGANISM(S): Homo sapiens

SUBMITTER: Volker Böhm

PROVIDER: E-MTAB-10718 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Human UPF3A and UPF3B enable fault-tolerant activation of nonsense-mediated mRNA decay.

Wallmeroth Damaris D Lackmann Jan-Wilm JW Kueckelmann Sabrina S Altmüller Janine J Dieterich Christoph C Boehm Volker V Gehring Niels H NH

The EMBO journal 20220422 10

The paralogous human proteins UPF3A and UPF3B are involved in recognizing mRNAs targeted by nonsense-mediated mRNA decay (NMD). UPF3B has been demonstrated to support NMD, presumably by bridging an exon junction complex (EJC) to the NMD factor UPF2. The role of UPF3A has been described either as a weak NMD activator or an NMD inhibitor. Here, we present a comprehensive functional analysis of UPF3A and UPF3B in human cells using combinatory experimental approaches. Overexpression or knockout of U ...[more]

PMID: 35451084

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