Misexpression in Xenopus of KCNJ2 carrying ATS-associated mutations causes CFAs in the same structures affected in humans, changes the normal pattern of membrane voltage potential regionalization in the developing face and disrupts expression of important craniofacial patterning genes, revealing the endogenous control of craniofacial patterning by bioelectric cell states.
First-pass extracted concept
bioelectric cell states
Aliases
membrane voltage potential regionalization, resting potential, Vmem
Evidence Snippets
Supporting Sources
Linked Claims
Developmentally patterned potassium flux is required for correct resting-potential regionalization and establishment of early gene expression domains in the anterior ectoderm.
ATS-associated KCNJ2 variants cause craniofacial anomalies in Xenopus and disrupt membrane voltage regionalization in the developing face.
Changing ectodermal resting potential is sufficient to cause craniofacial anomalies and this effect is not tied to a specific ion or channel protein.
Perturbing ectodermal membrane voltage causes craniofacial anomalies only during early neurula stages, whereas late neurulation perturbation does not affect craniofacial development.