Abstract
Differentiation of skeletal muscle involves withdrawal of myoblasts from cell replication, fusion to form multinucleated myotubes, coordinate appearance of a variety of muscle-specific proteins and the disappearance of a set of other proteins responsible for cell growth. The possible activation of the interferon (IFN) system in this process was studied. Thus, the activity of two IFN-induced enzymes known to be part of the system – (2′-5′) oligoadenylate synthetase (2–5A synthetase) and double-stranded RNA-activated protein kinase as well as the expression of 2–5A synthetase coding genes were examined during myogenesis. It is demonstrated that the activity of the enyzmes is transiently increased in cultured myoblasts, reaching a peak activity on the 3rd day in culture and then declining to a basal level. This peak activity precedes both cell fusion and the appearance of muscle-specific proteins – acetylcholine receptors (AChR) and creatine kinase. The same kinetics of 2–5A synthetase activity was evident in myoblasts from chick, rat or mouse origin. The enzymatic product appears to be primarily the trimer form of 2–5A, rather than a set of oligomers observed in enzymatic reactions performed on IFN-treated cells, including muscle cultures. The kinetics of 2–5A synthetase gene expression revealed that the largest amount of specific RNA transcripts appeared on the 1st day after seeding, followed by a reduction thereafter. In addition, a decrease was also observed in expression of c-myc, a cell-growth-associated protooncogene. However, an increase towards the 2nd day of both AChR and myosin light chain gene expression was evident, indicating selective regulation of gene expression during myogenesis.
Original language | English |
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Pages (from-to) | 138-145 |
Number of pages | 8 |
Journal | Differentiation |
Volume | 45 |
Issue number | 2 |
DOIs | |
State | Published - Nov 1990 |
Bibliographical note
Funding Information:Acknowledgements. This study was supported by grants from the Israel Cancer Research Fund (ICRF) and the Mitzi Dobrin Cancer Foundation.
Funding
Acknowledgements. This study was supported by grants from the Israel Cancer Research Fund (ICRF) and the Mitzi Dobrin Cancer Foundation.
Funders | Funder number |
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Mitzi Dobrin Cancer Foundation | |
Israel Cancer Research Fund |