Staufen1-mediated mRNA decay induces Requiem mRNA decay through binding of Staufen1 to the Requiem 3'UTRopen access
- Authors
- Kim, Min Young; Park, Jungyun; Lee, Jong Joo; Ha, Dae Hyun; Kim, Jonghwan; Kim, Chan Gil; Hwang, Jungwook; Kim, Chul Geun
- Issue Date
- Jun-2014
- Publisher
- OXFORD UNIV PRESS
- Citation
- NUCLEIC ACIDS RESEARCH, v.42, no.11, pp.6999 - 7011
- Indexed
- SCIE
SCOPUS
- Journal Title
- NUCLEIC ACIDS RESEARCH
- Volume
- 42
- Number
- 11
- Start Page
- 6999
- End Page
- 7011
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/159817
- DOI
- 10.1093/nar/gku388
- ISSN
- 0305-1048
- Abstract
- Requiem (REQ/DPF2) was originally identified as an apoptosis-inducing protein in mouse myeloid cells and belongs to the novel Kruppel-type zinc finger d4-protein family of proteins, which includes neuro-d4 (DPF1) and cer-d4 (DPF3). Interestingly, when a portion of the REQ messenger ribonucleic acid (mRNA) 3' untranslated region (3'UTR), referred to as G8, was overexpressed in K562 cells, beta-globin expression was induced, suggesting that the 3'UTR of REQ mRNA plays a physiological role. Here, we present evidence that the REQ mRNA 3'UTR, along with its trans-acting factor, Staufen1 (STAU1), is able to reduce the level of REQ mRNA via STAU1-mediated mRNA decay (SMD). By screening a complementary deoxyribonucleic acid (cDNA) expression library with an RNA-ligand binding assay, we identified STAU1 as an interactor of the REQ mRNA 3'UTR. Specifically, we provide evidence that STAU1 binds to putative 30-nucleotide stem-loop-structured RNA sequences within the G8 region, which we term the protein binding site core; this binding triggers the degradation of REQ mRNA and thus regulates translation. Furthermore, we demonstrate that siRNA-mediated silencing of either STAU1 or UPF1 increases the abundance of cellular REQ mRNA and, consequently, the REQ protein, indicating that REQ mRNA is a target of SMD.
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Collections - 서울 자연과학대학 > 서울 생명과학과 > 1. Journal Articles
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