Recovery in the Myogenic Program of Congenital Myotonic Dystrophy Myoblasts after Excision of the Expanded (CTG) n Repeat
The congenital form of myotonic dystrophy type 1 (cDM) is caused by the large-scale expansion of a (CTG•CAG) repeat in and . The production of toxic transcripts with long trinucleotide tracts from these genes results in impairment of the myogenic differentiation capacity as cDM's most prominent...
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| Veröffentlicht in: | International journal of molecular sciences 2019-11, Vol.20 (22), p.5685 |
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| creator | André, Laurène M van Cruchten, Remco T P Willemse, Marieke Bezstarosti, Karel Demmers, Jeroen A A van Agtmaal, Ellen L Wansink, Derick G Wieringa, Bé |
| description | The congenital form of myotonic dystrophy type 1 (cDM) is caused by the large-scale expansion of a (CTG•CAG)
repeat in
and
. The production of toxic transcripts with long trinucleotide tracts from these genes results in impairment of the myogenic differentiation capacity as cDM's most prominent morpho-phenotypic hallmark. In the current in vitro study, we compared the early differentiation programs of isogenic cDM myoblasts with and without a (CTG)2600 repeat obtained by gene editing. We found that excision of the repeat restored the ability of cDM myoblasts to engage in myogenic fusion, preventing the ensuing myotubes from remaining immature. Although the cDM-typical epigenetic status of the DM1 locus and the expression of genes therein were not altered upon removal of the repeat, analyses at the transcriptome and proteome level revealed that early abnormalities in the temporal expression of differentiation regulators, myogenic progression markers, and alternative splicing patterns before and immediately after the onset of differentiation became normalized. Our observation that molecular and cellular features of cDM are reversible in vitro and can be corrected by repeat-directed genome editing in muscle progenitors, when already committed and poised for myogenic differentiation, is important information for the future development of gene therapy for different forms of myotonic dystrophy type 1 (DM1). |
| doi_str_mv | 10.3390/ijms20225685 |
| format | Article |
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repeat in
and
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repeat in
and
. The production of toxic transcripts with long trinucleotide tracts from these genes results in impairment of the myogenic differentiation capacity as cDM's most prominent morpho-phenotypic hallmark. In the current in vitro study, we compared the early differentiation programs of isogenic cDM myoblasts with and without a (CTG)2600 repeat obtained by gene editing. We found that excision of the repeat restored the ability of cDM myoblasts to engage in myogenic fusion, preventing the ensuing myotubes from remaining immature. Although the cDM-typical epigenetic status of the DM1 locus and the expression of genes therein were not altered upon removal of the repeat, analyses at the transcriptome and proteome level revealed that early abnormalities in the temporal expression of differentiation regulators, myogenic progression markers, and alternative splicing patterns before and immediately after the onset of differentiation became normalized. Our observation that molecular and cellular features of cDM are reversible in vitro and can be corrected by repeat-directed genome editing in muscle progenitors, when already committed and poised for myogenic differentiation, is important information for the future development of gene therapy for different forms of myotonic dystrophy type 1 (DM1).</description><subject>Cell cycle</subject><subject>Cell Line</subject><subject>Chromatin</subject><subject>CRISPR</subject><subject>Deoxyribonucleic acid</subject><subject>Differentiation</subject><subject>DNA</subject><subject>Dystrophy</subject><subject>Epigenesis, Genetic</subject><subject>Fetuses</subject><subject>Gene Editing</subject><subject>Gene expression</subject><subject>Genetic Therapy</subject><subject>Genomes</subject><subject>Humans</subject><subject>Kinases</subject><subject>Maturation</subject><subject>Morphology</subject><subject>Muscle Development</subject><subject>Muscles</subject><subject>Musculoskeletal system</subject><subject>Mutants</subject><subject>Myoblasts</subject><subject>Myoblasts - 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cytology</topic><topic>Myoblasts - metabolism</topic><topic>Myoblasts - pathology</topic><topic>Myogenesis</topic><topic>Myotonic dystrophy</topic><topic>Myotonic Dystrophy - genetics</topic><topic>Myotonic Dystrophy - pathology</topic><topic>Myotonic Dystrophy - therapy</topic><topic>Myotonin-Protein Kinase - genetics</topic><topic>Myotubes</topic><topic>Protein kinase</topic><topic>Proteins</topic><topic>RNA processing</topic><topic>Skeletal muscle</topic><topic>Transcription factors</topic><topic>Trinucleotide Repeats</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>André, Laurène M</creatorcontrib><creatorcontrib>van Cruchten, Remco T P</creatorcontrib><creatorcontrib>Willemse, Marieke</creatorcontrib><creatorcontrib>Bezstarosti, Karel</creatorcontrib><creatorcontrib>Demmers, Jeroen A A</creatorcontrib><creatorcontrib>van Agtmaal, Ellen L</creatorcontrib><creatorcontrib>Wansink, Derick G</creatorcontrib><creatorcontrib>Wieringa, Bé</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>André, Laurène M</au><au>van Cruchten, Remco T P</au><au>Willemse, Marieke</au><au>Bezstarosti, Karel</au><au>Demmers, Jeroen A A</au><au>van Agtmaal, Ellen L</au><au>Wansink, Derick G</au><au>Wieringa, Bé</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Recovery in the Myogenic Program of Congenital Myotonic Dystrophy Myoblasts after Excision of the Expanded (CTG) n Repeat</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2019-11-13</date><risdate>2019</risdate><volume>20</volume><issue>22</issue><spage>5685</spage><pages>5685-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>The congenital form of myotonic dystrophy type 1 (cDM) is caused by the large-scale expansion of a (CTG•CAG)
repeat in
and
. The production of toxic transcripts with long trinucleotide tracts from these genes results in impairment of the myogenic differentiation capacity as cDM's most prominent morpho-phenotypic hallmark. In the current in vitro study, we compared the early differentiation programs of isogenic cDM myoblasts with and without a (CTG)2600 repeat obtained by gene editing. We found that excision of the repeat restored the ability of cDM myoblasts to engage in myogenic fusion, preventing the ensuing myotubes from remaining immature. Although the cDM-typical epigenetic status of the DM1 locus and the expression of genes therein were not altered upon removal of the repeat, analyses at the transcriptome and proteome level revealed that early abnormalities in the temporal expression of differentiation regulators, myogenic progression markers, and alternative splicing patterns before and immediately after the onset of differentiation became normalized. Our observation that molecular and cellular features of cDM are reversible in vitro and can be corrected by repeat-directed genome editing in muscle progenitors, when already committed and poised for myogenic differentiation, is important information for the future development of gene therapy for different forms of myotonic dystrophy type 1 (DM1).</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>31766224</pmid><doi>10.3390/ijms20225685</doi><orcidid>https://orcid.org/0000-0002-6200-7764</orcidid><orcidid>https://orcid.org/0000-0002-8757-9611</orcidid><orcidid>https://orcid.org/0000-0002-6773-8662</orcidid><orcidid>https://orcid.org/0000-0002-2918-1488</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | International journal of molecular sciences, 2019-11, Vol.20 (22), p.5685 |
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| subjects | Cell cycle Cell Line Chromatin CRISPR Deoxyribonucleic acid Differentiation DNA Dystrophy Epigenesis, Genetic Fetuses Gene Editing Gene expression Genetic Therapy Genomes Humans Kinases Maturation Morphology Muscle Development Muscles Musculoskeletal system Mutants Myoblasts Myoblasts - cytology Myoblasts - metabolism Myoblasts - pathology Myogenesis Myotonic dystrophy Myotonic Dystrophy - genetics Myotonic Dystrophy - pathology Myotonic Dystrophy - therapy Myotonin-Protein Kinase - genetics Myotubes Protein kinase Proteins RNA processing Skeletal muscle Transcription factors Trinucleotide Repeats |
| title | Recovery in the Myogenic Program of Congenital Myotonic Dystrophy Myoblasts after Excision of the Expanded (CTG) n Repeat |
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