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  Loss of full-length hnRNP R isoform impairs DNA damage response in motoneurons by inhibiting Yb1 recruitment to chromatin

Ghanawi, H., Hennlein, L., Zare, A., Bader, J. M., Salehi, S., Hornburg, D., et al. (2021). Loss of full-length hnRNP R isoform impairs DNA damage response in motoneurons by inhibiting Yb1 recruitment to chromatin. Nucleic Acids Research, 49(21), 12284-12305. doi:10.1093/nar/gkab1120.

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 Urheber:
Ghanawi, Hanaa, Autor
Hennlein, Luisa, Autor
Zare, Abdolhossein, Autor
Bader, Jakob Maximilian1, Autor           
Salehi, Saeede, Autor
Hornburg, Daniel2, Autor           
Ji, Changhe, Autor
Sivadasan, Rajeeve, Autor
Drepper, Carsten, Autor
Meissner, Felix2, Autor           
Mann, Matthias1, Autor           
Jablonka, Sibylle, Autor
Briese, Michael, Autor
Sendtner, Michael, Autor
Affiliations:
1Mann, Matthias / Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, Max Planck Society, ou_1565159              
2Meissner, Felix / Experimental Systems Immunology, Max Planck Institute of Biochemistry, Max Planck Society, ou_2149678              

Inhalt

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Schlagwörter: NUCLEAR RIBONUCLEOPROTEIN-R; DETERMINING GENE-PRODUCT; ACTIN MESSENGER-RNA; COMET ASSAY; GENOME-WIDE; SPINAL-CORD; YB-1; SMN; INTERACTS; ENRICHMENTBiochemistry & Molecular Biology;
 Zusammenfassung: Neurons critically rely on the functions of RNA-binding proteins to maintain their polarity and resistance to neurotoxic stress. HnRNP R has a diverse range of post-transcriptional regulatory functions and is important for neuronal development by regulating axon growth. Hnrnpr pre-mRNA undergoes alternative splicing giving rise to a full-length protein and a shorter isoform lacking its N-terminal acidic domain. To investigate functions selectively associated with the full-length hnRNP R isoform, we generated a Hnrnpr knockout mouse (Hnrnpr(tm1a/tm1a)) in which expression of full-length hnRNP R was abolished while production of the truncated hnRNP R isoform was retained. Motoneurons cultured from Hnrnpr(tm1a/tm1a) mice did not show any axonal growth defects but exhibited enhanced accumulation of double-strand breaks and an impaired DNA damage response upon exposure to genotoxic agents. Proteomic analysis of the hnRNP R interactome revealed the multifunctional protein Yb1 as a top interactor. Yb1-depleted motoneurons were defective in DNA damage repair. We show that Yb1 is recruited to chromatin upon DNA damage where it interacts with gamma-H2AX, a mechanism that is dependent on full-length hnRNP R. Our findings thus suggest a novel role of hnRNP R in maintaining genomic integrity and highlight the function of its N-terminal acidic domain in this context.

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Sprache(n): eng - English
 Datum: 2021
 Publikationsstatus: Erschienen
 Seiten: 22
 Ort, Verlag, Ausgabe: -
 Inhaltsverzeichnis: -
 Art der Begutachtung: -
 Identifikatoren: ISI: 000733312000024
DOI: 10.1093/nar/gkab1120
 Art des Abschluß: -

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Titel: Nucleic Acids Research
  Andere : Nucleic Acids Res
Genre der Quelle: Zeitschrift
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Ort, Verlag, Ausgabe: Oxford : Oxford University Press
Seiten: - Band / Heft: 49 (21) Artikelnummer: - Start- / Endseite: 12284 - 12305 Identifikator: ISSN: 0305-1048
CoNE: https://pure.mpg.de/cone/journals/resource/110992357379342