Scientist have reported the creation of a strong loss-of-function phenotype for the normal prion protein (PrP) in zebrafish embryos. This phenotype is characterized by the loss of embryonic cell adhesion and arrested gastrulation. The results of additional experiments indicate that the normal prion protein (1) mediates Ca+2-independent homophilic cell adhesion and signaling; and (2) modulates Ca+2-dependent cell adhesion by regulating the delivery of E-cadherin to the plasma membrane. The authors stated that their data uncover evolutionarily conserved roles of PrP in cell communication, which ultimately impinge on the stability of adherens cell junctions during embryonic development. The results were published in PLoS Biology, and an accompanying paper comments on the results. [PLoS Biology article] [PLoS Biology commentary]Login Or Register To Read Full Story