MYF5 and MYOD regulate rhabdomyosaroma growth and tumor-propagating potential, acting more than as passive markers retained from the target cell-of-origin during transformation.

The epistasis observed in TF-DNA binding preferences can be explained by the presence of two optima of very similar Gibbs energy that are located relatively far from each other in sequence space.

Single myofiber ATAC-Seq provides assessment of chromatin accessibility of a single myofiber without the confounding effects of other cell types present in skeletal muscle.

Combined lineage-tracing strategies, single-cell transcriptomic methods and in situ analyses identified mesodermal bipotent progenitors during craniofacial myogenesis that give rise to myogenic and connective tissues, thus redefining the lineage and evolutionary relationships between muscle and associated stroma.

Genetic mouse models combined with single-cell RNA sequencing reveal the essential role of SRSF2 in directing MyoD progenitors to distinct skeletal muscle domains and controlling their differentiation through the regulation of targeted genes and alternative splicing during skeletal muscle development.

Using multiple genetic reporter system in human pluripotent stem cells, a transcriptional database for human early myogenesis has been established.

While Notch activation dedifferentiates newly differentiated muscle cells; it improves the function of muscle fiber as a niche-supporting cell of muscle stem cells.

The protein Tristetraprolin promotes the decay of MyoD mRNA to maintain satellite cell quiescence.

Genetic lineage tracing reveals the cardiopharyngeal mesoderm as a cellular origin of craniofacial and cardiac lymphatic vessels, which most often affected in lymphatic malformation patients.

Single cell RNA sequencing leads to identification and separation of transcriptionally and functionally heterogeneous, natural human satellite cells, including a subpopulation marked by CAV1 harboring quiescence phenotypes and engraftment potential.