TY  - JOUR
A1  - Kirchhof, Luisa
A1  - Fouani, Youssef
A1  - Knau, Andrea
A1  - Aslan, Galip S.
A1  - Heumüller, Andreas
A1  - Wittig, Ilka
A1  - Müller-McNicoll, Michaela
A1  - Dimmeler, Stefanie
A1  - Jaé, Nicolas Christopher
T1  - The G3BP1-UPF1-associated long non-coding RNA CALA regulates RNA turnover in the cytoplasm
T2  - Non-Coding RNA
N2  - Besides transcription, RNA decay accounts for a large proportion of regulated gene expression and is paramount for cellular functions. Classical RNA surveillance pathways, like nonsense-mediated decay (NMD), are also implicated in the turnover of non-mutant transcripts. Whereas numerous protein factors have been assigned to distinct RNA decay pathways, the contribution of long non-coding RNAs (lncRNAs) to RNA turnover remains unknown. Here we identify the lncRNA CALA as a potent regulator of RNA turnover in endothelial cells. We demonstrate that CALA forms cytoplasmic ribonucleoprotein complexes with G3BP1 and regulates endothelial cell functions. A detailed characterization of these G3BP1-positive complexes by mass spectrometry identifies UPF1 and numerous other NMD factors having cytoplasmic G3BP1-association that is CALA-dependent. Importantly, CALA silencing impairs degradation of NMD target transcripts, establishing CALA as a non-coding regulator of RNA steady-state levels in the endothelium.
KW  - long non-coding RNA
KW  - RNA turnover
KW  - nonsense-mediated mRNA decay
KW  - gene expression
KW  - G3BP1
Y1  - 2022
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/72171
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-721717
SN  - 2311-553X
N1  - This study was supported by the DFG (TRR 267 to I.W., M.M.-M., S.D., N.J.) and the ERC (Advanced Grant Angiolnc to S.D.).
N1  - The mass spectrometry data sets have been deposited with the ProteomeXchange Consortium via the PRIDE partner repository and are publicly available with the data set identifiers PXD033516 and PXD033517.
VL  - 8
IS  - 4, art. 49
SP  - 1
EP  - 15
PB  - MDPI
CY  - Basel
ER  -