Intronic Determinants Coordinate Charme lncRNA Nuclear Activity through the Interaction with MATR3 and PTBP1

0538143 - ÚMG 2021 RIV US eng J - Journal Article
Desideri, F. - Cipriano, A. - Petrezselyova, Silvia - Buonaiuto, G. - Santini, T. - Kašpárek, Petr - Procházka, Jan - Janson, G. - Paiardini, A. - Calicchio, A. - Colantoni, A. - Sedláček, Radislav - Bozzoni, I. - Ballarino, M.
Intronic Determinants Coordinate Charme lncRNA Nuclear Activity through the Interaction with MATR3 and PTBP1.
Cell Reports. Roč. 33, č. 12 (2020), č. článku 108548. ISSN 2211-1247. E-ISSN 2211-1247
R&D Projects: GA MŠMT(CZ) LM2015040; GA MŠMT(CZ) LM2018126; GA MŠMT ED2.1.00/19.0395; GA MŠMT(CZ) ED1.1.00/02.0109; GA MŠMT EF16_013/0001789
Institutional support: RVO:68378050
Keywords : tract binding-protein * noncoding rna * gene-expression * regulatory networks * splicing repressor * phase-separation * distal myopathy * x-chromosome * localization * sequences
OECD category: Developmental biology
Impact factor: 9.423, year: 2020
Method of publishing: Open access
https://www.cell.com/cell-reports/fulltext/S2211-1247(20)31537-0?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2211124720315370%3Fshowall%3Dtrue

Chromatin architect of muscle expression (Charme) is a muscle-restricted long noncoding RNA (lncRNA) that plays an important role in myogenesis. Earlier evidence indicates that the nuclear Charme isoform, named pCharme, acts on the chromatin by assisting the formation of chromatin domains where myogenic transcription occurs. By combining RNA antisense purification (RAP) with mass spectrometry and loss-of-function analyses, we have now identified the proteins that assist these chromatin activities. These proteins-which include a sub-set of splicing regulators, principally PTBP1 and the multifunctional RNA/DNA binding protein MATR3-bind to sequences located within the alternatively spliced intron-1 to form nuclear aggregates. Consistent with the functional importance of pCharme interactome in vivo, a targeted deletion of the intron-1 by a CRISPR-Cas9 approach in mouse causes the release of pCharme from the chromatin and results in cardiac defects similar to what was observed upon knockout of the full-length transcript.
Permanent Link: http://hdl.handle.net/11104/0315964