Meeting Abstract
One of the key events in early vertebrate evolution was the transition from a sessile, filter-feeding lifestyle to one of active predation that was characterized by innovations in morphology, physiology, and behavior, and exploitation of ecological opportunity. The evolutionary success of early vertebrates is linked to the acquisition of the neural crest, a migratory, multipotent cell population that arises along the vertebrate embryonic central nervous system. One of the hallmarks of neural crest cells is the initiation of an epithelial-mesenchymal transition (EMT), a mechanism that promotes the migration of neural crest cells along stereotypical pathways in the early vertebrate embryo. Although a conserved gene regulatory network orchestrates neural crest EMT among gnathostome vertebrates, the evolutionary origins of this network among basal vertebrates are relatively unknown. Using the sea lamprey as an experimental model, we show that a lamprey orthologue of Snail, a master regulatory factor controlling EMT in gnathostomes, is not expressed in pre-migratory or migratory neural crest. By contrast, morpholino-mediated gene knockdown of lamprey SoxD abrogated EMT in neural crest cells, as indicated by persistent expression of EMT markers such as Id and SoxE2 within the dorsal neural tube, and lack of neural crest-derived structures in the pharynx. Together, these preliminary results suggest that SoxD is master regulatory switch controlling EMT in lamprey, and indicate that the mechanism of neural crest EMT in agnathan vertebrates is highly divergent relative to gnathostomes. To further test this notion, we used CRISPR/Cas to generate deletion mutants of SoxD, and subsequently analyzed expression of key EMT regulatory factors, including Sox E2, Twist(s), Sip1 and RhoB.
