Antisense knockdown of the beta1 integrin subunit in the chicken embryo results in abnormal neural crest cell development.
Neural crest cells escape the neural tube by undergoing an epithelial to mesenchymal transition (EMT). This is followed by extensive migration along specific pathways that are lined with extracellular matrix (ECM). In this study, we have examined the roles of matrix receptors containing beta1 integrin subunits in neural crest cell morphogenesis using antisense morpholino oligos electroporated in ovo into avian neural crest cell precursors. Our results show that reduced levels of expression of beta1 integrin subunits in the dorsal neural tube results in an abnormal epithelial to mesenchymal transition. In approximately half of the experimental embryos, however, some neural crest cells filled with beta1 antisense are able to escape the neural tube and migrate ventrally, indicating that grossly normal migration of trunk neural crest cells can take place after beta1 integrin expression is reduced. This study shows the potential of this novel method for investigating the roles of genes that are required for the survival of early mouse embryos in later development events.
Tucker
Richard P
RP
Department of Cell Biology and Human Anatomy, School of Medicine, University of California at Davis, 1 Shields Avenue, Davis, CA 95616, USA. rptucker@ucdavis.edu
D000818:Animals; D002642:Chick Embryo; D019012:Integrin beta1 / Q000032:analysis / Q000235:genetics / Q000502:physiology*; D009432:Neural Crest / Q000002:abnormalities / Q000196:embryology* / Q000648:ultrastructure; D034622:RNA Interference; D016372:RNA, Antisense / Q000235:genetics
D019012:Integrin beta1; D016372:RNA, Antisense