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.

Proteolytic cleavage of the extracellular matrix glycoprotein fibrillin-2 by the secreted metalloprotease ADAMTS6 influences skeletal development by modulating fibrillin microfibril abundance and GDF5/BMP signaling, illustrating the crucial role of extracellular matrix proteostatic mechanisms in growth factor regulation during morphogenesis.

Novel disease pathways underlie disease pathogenesis in Kelch-related nemaline myopathy through proteomic remodeling.

Skeletal muscle organoids differentiated from human pluripotent stem cells offer a system for investigating myogenesis and satellite cell development with translational potential for muscular dystrophy modeling and therapy development.

Hypertrophic chondrocytes of the growth plate undergo a process of dedifferentiation to generate marrow associated skeletal stem and progenitor cells (SSPCs), which ultimately re-differentiate into cells of the osteoblast or adipocyte lineages during skeletal development.

Septin7 is described as a novel component of skeletal muscle cytoskeleton with essential roles in muscle development and the proper organization of the myofilaments and the mitochondrial network while its absence leeds to reduced force and skeletal deformities.

Partial ablation of osteocytes alters lineage cell specifications in bone and bone marrow, resulting in the acceleration of skeletal aging.

Discoidin domain receptor 2 controls craniofacial morphology by acting in skeletal progenitor cells and chondrocytes to control collagen matrix organization, chondrocyte polarity, and growth.

Specification and expansion during rib development is explained by Agent-Based Modeling while respecting the locality of decision-making that occurs as millions of cells coordinate their behavior to form and refine spatial pattern.

A periosteal Bmp2 signaling center couples bone length to bone width during development and must be reactivated by clinical bone anabolic therapies to reduce fracture risk and accelerate fracture repair.