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Stem Cells International
Volume 2017 (2017), Article ID 9210494, 9 pages
Research Article

Myogenic Differentiation from MYOGENIN-Mutated Human iPS Cells by CRISPR/Cas9

1Department of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan
2Department of Biomedical Engineering, Faculty of Life and Medical Sciences, Doshisha University, Kyotanabe, Japan
3Department of Clinical Application, Center for iPS Cell Research and Application, Kyoto University, Kyoto, Japan

Correspondence should be addressed to Takahiko Sato

Received 12 January 2017; Accepted 5 March 2017; Published 4 April 2017

Academic Editor: Yuko Miyagoe-Suzuki

Copyright © 2017 Koki Higashioka et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


It is well known that myogenic regulatory factors encoded by the Myod1 family of genes have pivotal roles in myogenesis, with partially overlapping functions, as demonstrated for the mouse embryo. Myogenin-mutant mice, however, exhibit severe myogenic defects without compensation by other myogenic factors. MYOGENIN might be expected to have an analogous function in human myogenic cells. To verify this hypothesis, we generated MYOGENIN-mutated human iPS cells by using CRISPR/Cas9 genome-editing technology. Our results suggest that MYOD1-independent or MYOD1-dependent mechanisms can compensate for the loss of MYOGENIN and that these mechanisms are likely to be crucial for regulating skeletal muscle differentiation and formation.