Semaphorin3d mediates Cx43-dependent phenotypes during fin regeneration.

ABSTRACT: Gap junctions are proteinaceous channels that reside at the plasma membrane and permit the exchange of ions, metabolites, and second messengers between neighboring cells. Connexin proteins are the subunits of gap junction channels. Mutations in zebrafish cx43 cause the short fin (sof(b123)) phenotype which is characterized by short fins due to defects in length of the bony fin rays. Previous findings from our lab demonstrate that Cx43 is required for both cell proliferation and joint formation during fin regeneration. Here we demonstrate that semaphorin3d (sema3d) functions downstream of Cx43. Semas are secreted signaling molecules that have been implicated in diverse cellular functions such as axon guidance, cell migration, cell proliferation, and gene expression. We suggest that Sema3d m

SUBMITTER: Ton QV 

PROVIDER: S-EPMC3358573 | biostudies-literature | 2012 Jun

REPOSITORIES: biostudies-literature