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Sci. Signal., 10 December 2013
Vol. 6, Issue 305, p. ra107
[DOI: 10.1126/scisignal.2004633]

RESEARCH ARTICLES

Editor's Summary

Inhibiting Muscle Repair During Inflammation
When skeletal muscle cells become injured, they secrete the inflammatory cytokine interferon-{gamma} (IFN-{gamma}), which is required for the fusion of myoblasts to form new myofibers that repair the damaged tissue; however, excess IFN-{gamma} represses muscle repair. Londhe and Davie found that IFN-{gamma} inhibited the expression of muscle-specific genes in cultured mouse muscle cells through a mechanism involving the sequential recruitment of the class II transactivator (CIITA) and repressor proteins of the Jumonji and Polycomb families. Mice subjected to muscle injury and a mouse model of muscular dystrophy, which exhibits excess IFN-{gamma} in muscle, had increased amounts of Polycomb proteins in their muscle fibers compared to those of wild-type mice. Together, these data suggest that IFN-{gamma} recruits repressor proteins to muscle-specific genes to inhibit muscle differentiation during inflammation.

Citation: P. Londhe, J. K. Davie, Interferon-{gamma} Resets Muscle Cell Fate by Stimulating the Sequential Recruitment of JARID2 and PRC2 to Promoters to Repress Myogenesis. Sci. Signal. 6, ra107 (2013).

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THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Science Signaling Podcast: 10 December 2013.
J. K. Davie and A. M. VanHook (2013)
Science Signaling 6, pc33
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