Lipid raft disruption inhibits dorsomedial lip epaxial myotome formation and results in loss of myotome precursor cell specification in the segmental plate mesoderm

Ectoderm secretes important molecular signals that regulate early chicken embryo development and somite myotome formation. The ectoderm also contain membrane microdomains (or lipid rafts) that move from ectoderm‐to‐dermomyotome through dermomyotome filopodia suggesting their role in signaling myotome formation. We investigate lipid raft regulation over somitic myotome formation by in ovo embryo treatment with methyl‐beta‐cyclodextrin (MBC), a molecule that inactivates lipid rafts, and assessed myogenesis by desmin immunolabeling, carbocyanine dye microinjection, and confocal microscopy. In ovo treatment of ectoderm with 2.0mM MBC for 6–10 hours blocked early epaxial myotome, however, myotome formation returned to normal following washout of MBC and overnight embryo growth. Somite arising form the segmental plate mesoderm during MBC treatment were absent for myotome after 12–15 hours of embryo re‐incubation, but showed abnormal myotome after >30 hours. In contrast, somites arising from the segmental plate mesoderm after MBC was removed showed normal myotome development following overnight embryo growth. The absence of epaxial myotome at the dorsomedial lip for somites formed in MBC was confirmed by DiI, DiO and DiD microinjections where no myotome fibers were made following overnight embryo growth. These results suggest that myogenic precursor cell specification for epaxial myotome formation occurs at the cranial end of the segmental plate mesoderm and depends on signals like lipid rafts from the overlying ectoderm. Supported by NIH‐RIMI 1P20MD000544