The protein Sip1 enables restless neural crest cells to leave home, Rogers et al. report.
From their birthplace in the embryonic neural tube, neural crest cells scatter throughout the body, giving rise to such diverse structures as the core of the adrenal gland and pigment cells in the skin. Neural crest cells share some similarities with metastatic cancer cells. Before they make a move, both types of cells undergo an epithelial-to-mesenchymal transition (EMT) in which they lose polarity, dramatically change morphology, and detach from their neighbors. The transcription factor Sip1 might help promote EMT in tumor cells, but its role in neural crest cells is uncertain.
Rogers et al. found that neural crest cells in chick embryos also manufacture Sip1. After reducing Sip1 production in neural crest precursors, the researchers discovered that the cells left the neural tube but didn’t travel far from it. They often remained stuck to other cells and showed reduced levels of the transcription factor SOX10, which marks migrating neural crest cells.
As cancer cells go through EMT, they replace E-cadherin molecules on their surface with N-cadherin molecules. Rogers et al. found that Sip1 regulates the expression and localization of both adhesion molecules. Reducing Sip1 levels, the researchers determined, hiked the amount of E-cadherin in neural crest cells and reduced the amount of N-cadherin in the neural tube. The study shows that the migration of neural crest cells entails two separate steps—exit from the neural tube and dispersal. Sip1 is only necessary for the second step, which the protein might encourage by spurring the cells to decrease E-cadherin levels.
Text by Mitch Leslie