Abstract
Skeletal muscle development and regeneration rely on the successive activation of specific transcription factors that engage cellular fate, promote commitment, and drive differentiation. Emerging evidence demonstrates that epigenetic regulation of gene expression is crucial for the maintenance of the cell differentiation status upon division and, therefore, to preserve a specific cellular identity. This depends in part on the regulation of chromatin structure and its level of condensation. Chromatin architecture undergoes remodeling through changes in nucleosome composition, such as alterations in histone post-translational modifications or exchange in the type of histone variants. The mechanisms that link histone post-translational modifications and transcriptional regulation have been extensively evaluated in the context of cell fate and differentiation, whereas histone variants have attracted less attention in the field. In this review, we discuss the studies that have provided insights into the role of histone variants in the regulation of myogenic gene expression, myoblast differentiation, and maintenance of muscle cell identity.
Highlights
Skeletal muscle tissue has a high regenerative potential that relies on tissue-specific stem cells, the satellite cells
Muscle stem cells are established during fetal development where they adopt a satellite position under the basal lamina of the fiber and progressively initiate cell cycle exit into quiescence [2]
The HIRA-ASF1A complex further regulates myogenic differentiation by interacting with the muscle-specific transcription factor MEF2, which is required for the activation of MEF2 target gene expression [27]
Summary
Skeletal muscle tissue has a high regenerative potential that relies on tissue-specific stem cells, the satellite cells. These cells are characterized by the expression of the pairedhomeobox transcription factor PAX7 and, in a subset of muscles, by the co-expression of its paralog PAX3 [1]. Muscle stem cells are established during fetal development where they adopt a satellite position under the basal lamina of the fiber and progressively initiate cell cycle exit into quiescence [2]. A pool of PAX3- and PAX7-double positive muscle stem cells constitutes a reservoir that allows fetal and postnatal muscle growth [3,4,5]. The signaling cascades and the gene regulatory networks that operate to establish the myogenic lineage have been studied thoroughly but the epigenetic regulation of such processes is less understood
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