Myogenin gene disruption results in perinatal lethality because of severe muscle defect View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1993-08

AUTHORS

Yoko Nabeshima, Kazunori Hanaoka, Michiko Hayasaka, Eisaku Esuml, Shaowei Li, Ikuya Nonaka, Yo-ichi Nabeshima

ABSTRACT

MYOGENIN is a member of the basic helix-loop-helix (bHLH) gene family and converts multipotential mesodermal cells to myoblasts1–4. The four members of the myoD family show unique spatio-temporal expression patterns5 and therefore may have different functions during myogenesis. Here we inactivate the myogenin gene in order to understand its role in myogenesis. Homozygous mutations are lethal perinatally owing to the resulting major defects in skeletal muscle. The extent of disorganization of muscle tissue differs in three regions. In the latero-ventral body wall, most cells, including myogenic cells, disappear and there is rapid accretion of fluid. In the limbs, cells of the myogenic lineage exist, but they are severely disrupted, and some of them are mono-nucleate with properties of myoblasts. In contrast, there are many axial, intercostal and back muscle fibres to be seen, although fibres are mainly disorganized and Z-lines are not present in most myofibrils. These findings are evidence that myogenin is crucial for muscle development in utero and demonstrate that other members of the myogenic gene family cannot compensate for the defect. More... »

PAGES

532-535

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/364532a0

DOI

http://dx.doi.org/10.1038/364532a0

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1053378436

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/8393146


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