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

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 f...

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Main Authors: Koki Higashioka, Noriko Koizumi, Hidetoshi Sakurai, Chie Sotozono, Takahiko Sato
Format: Article
Language:English
Published: Hindawi Limited 2017-01-01
Series:Stem Cells International
Online Access:http://dx.doi.org/10.1155/2017/9210494
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spelling doaj-477317b0aff9441a9db36f2530e474182020-11-24T22:25:53ZengHindawi LimitedStem Cells International1687-966X1687-96782017-01-01201710.1155/2017/92104949210494Myogenic Differentiation from MYOGENIN-Mutated Human iPS Cells by CRISPR/Cas9Koki Higashioka0Noriko Koizumi1Hidetoshi Sakurai2Chie Sotozono3Takahiko Sato4Department of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, JapanDepartment of Biomedical Engineering, Faculty of Life and Medical Sciences, Doshisha University, Kyotanabe, JapanDepartment of Clinical Application, Center for iPS Cell Research and Application, Kyoto University, Kyoto, JapanDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, JapanDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, JapanIt 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.http://dx.doi.org/10.1155/2017/9210494
collection DOAJ
language English
format Article
sources DOAJ
author Koki Higashioka
Noriko Koizumi
Hidetoshi Sakurai
Chie Sotozono
Takahiko Sato
spellingShingle Koki Higashioka
Noriko Koizumi
Hidetoshi Sakurai
Chie Sotozono
Takahiko Sato
Myogenic Differentiation from MYOGENIN-Mutated Human iPS Cells by CRISPR/Cas9
Stem Cells International
author_facet Koki Higashioka
Noriko Koizumi
Hidetoshi Sakurai
Chie Sotozono
Takahiko Sato
author_sort Koki Higashioka
title Myogenic Differentiation from MYOGENIN-Mutated Human iPS Cells by CRISPR/Cas9
title_short Myogenic Differentiation from MYOGENIN-Mutated Human iPS Cells by CRISPR/Cas9
title_full Myogenic Differentiation from MYOGENIN-Mutated Human iPS Cells by CRISPR/Cas9
title_fullStr Myogenic Differentiation from MYOGENIN-Mutated Human iPS Cells by CRISPR/Cas9
title_full_unstemmed Myogenic Differentiation from MYOGENIN-Mutated Human iPS Cells by CRISPR/Cas9
title_sort myogenic differentiation from myogenin-mutated human ips cells by crispr/cas9
publisher Hindawi Limited
series Stem Cells International
issn 1687-966X
1687-9678
publishDate 2017-01-01
description 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.
url http://dx.doi.org/10.1155/2017/9210494
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