Drosophila DM1 models suggest that elevated cardiac expression of straightjacket/α2δ3, a regulatory subunit of voltage-gated calcium channel, contributes to cardiac conduction defects in DM1.

A novel sequencing-based method to characterize CNBP microsatellite expansions in DM2 patients demonstrates benefits for an improved dissection of DM2 genetic architecture, thus potentially ameliorating patient stratification and genetic counseling.

There is no such thing as a representative skeletal muscle tissue, as each member of this family of tissues expresses a specialized mRNA program.

Senescent cells release an arachidonic acid-derived electrophilic oxylipin that inhibits myoblast differentiation by covalent modification and activation of HRas.

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.

Depending upon the parameters used, neuromuscular stimulation can have beneficial or deleterious impacts on muscle structure and function in an animal model of Duchenne muscular dystrophy.

A decrease of the type 2 myotonic dystrophy gene product CNBP causes an impairment of polyamine metabolism and locomotor dysfunction that can be reverted with polyamine supplementation.

The mechanisms by which non-pathologic short tandem repeats normally influence gene expression and engender rapid genetic variation across phylogeny directly inform how expansions in these same repeats elicit neurological disease.

Expression of the disease gene DUX4 inhibits RNA quality control in skeletal muscle, thereby stabilizing thousands of aberrant RNAs, including its own transcript.

Global transcriptome changes, particularly alternative splicing, are highly dynamic the first 2 weeks after birth, and the example of calcineurin A splicing exemplifies the importance of alternative splicing during skeletal muscle development.