| First Author | Li X | Year | 2017 |
| Journal | PLoS One | Volume | 12 |
| Issue | 6 | Pages | e0180217 |
| PubMed ID | 28665998 | Mgi Jnum | J:246445 |
| Mgi Id | MGI:5919442 | Doi | 10.1371/journal.pone.0180217 |
| Citation | Li X, et al. (2017) IGFN1_v1 is required for myoblast fusion and differentiation. PLoS One 12(6):e0180217 |
| abstractText | Igfn1 is a complex locus that codes for multiple splicing variants of Immunoglobulin- and Fibronectin-like domain containing proteins predominantly expressed in skeletal muscle. To reveal possible roles for Igfn1, we applied non-selective knock-down by shRNAs as well as specific targeting of Igfn1 exon 13 by CRISPR/Cas9 mutagenesis in C2C12 cells. Decreased expression of Igfn1 variants via shRNAs against the common 3'-UTR region caused a total blunting of myoblast fusion, but did not prevent expression of differentiation markers. Targeting of N-terminal domains by elimination of exon 13 via CRISPR/Cas9 mediated homologous recombination, also resulted in fusion defects as well as large multinucleated cells. Expression of IGFN1_v1 partially rescued fusion and myotube morphology in the Igfn1 exon 13 knock-out cell line, indicating a role for this variant in myoblast fusion and differentiation. However, in vivo overexpression of IGFN1_v1 or the Igfn1 Exon 13 CRISPR/Cas9 targeting vector did not result in significant size changes in transfected fibres. |
