Exon junction complex dependent mRNA localization is linked to centrosome organization during ciliogenesis

Exon junction complexes (EJCs) mark untranslated spliced mRNAs and are crucial for the mRNA lifecycle. An imbalance in EJC dosage alters mouse neural stem cell (mNSC) division and is linked to human neurodevelopmental disorders. In quiescent mNSC and immortalized human retinal pigment epithelial (RP...

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Veröffentlicht in:Nature communications 2021-03, Vol.12 (1), p.1351-1351, Article 1351
Hauptverfasser: Kwon, Oh Sung, Mishra, Rahul, Safieddine, Adham, Coleno, Emeline, Alasseur, Quentin, Faucourt, Marion, Barbosa, Isabelle, Bertrand, Edouard, Spassky, Nathalie, Le Hir, Hervé
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Sprache:eng
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Zusammenfassung:Exon junction complexes (EJCs) mark untranslated spliced mRNAs and are crucial for the mRNA lifecycle. An imbalance in EJC dosage alters mouse neural stem cell (mNSC) division and is linked to human neurodevelopmental disorders. In quiescent mNSC and immortalized human retinal pigment epithelial (RPE1) cells, centrioles form a basal body for ciliogenesis. Here, we report that EJCs accumulate at basal bodies of mNSC or RPE1 cells and decline when these cells differentiate or resume growth. A high-throughput smFISH screen identifies two transcripts accumulating at centrosomes in quiescent cells, NIN and BICD2 . In contrast to BICD2 , the localization of NIN transcripts is EJC-dependent. NIN mRNA encodes a core component of centrosomes required for microtubule nucleation and anchoring. We find that EJC down-regulation impairs both pericentriolar material organization and ciliogenesis. An EJC-dependent mRNA trafficking towards centrosome and basal bodies might contribute to proper mNSC division and brain development. Exon junction complexes (EJCs) that mark untranslated mRNA are involved in transport, translation and nonsense-mediated mRNA decay. Here the authors show centrosomal localization of EJCs which appears to be required for both the localization of NIN mRNA around centrosomes and ciliogenesis.
ISSN:2041-1723
2041-1723
DOI:10.1038/s41467-021-21590-w