The neural crest is an embryonic cell population whose migratory behavior has been likened to cancer invasion during metastasis. Neural crests differentiate into a wide array of cell types, including muscle, cartilage, bones, melanocytes, neurons, and glia. Although the role of mechanical cues has been demonstrated in the migration and differentiation of neural crest cells, little is known about whether mechanics play any role in their early formation.

Neural crest cells are formed through a process called 'embryonic induction,' which involves an interaction between signaling and responding tissues, leading to a change in the direction of differentiation in the responding tissue. Considerable progress has been made in identifying inductive signals, yet how tissues control their responsiveness to these signals, known as competence, remains poorly understood. While the role of molecular signals in competence has been studied, the influence of tissue mechanics on competence remains unexplored.

In this seminar, I will present our recent results showing that neural crest competence decreases concomitantly with an increase in the hydrostatic pressure of the blastocoel, an embryonic cavity in contact with the prospective neural crest. By manipulating hydrostatic pressure in vivo, we demonstrate that this increase leads to the inhibition of YAP signaling and impairs Wnt activation in the responding tissue, which is required for neural crest induction. Furthermore, we show that hydrostatic pressure controls neural crest induction in amphibian and mouse embryos and in human cells, suggesting a conserved mechanism across vertebrates. Our work elucidates how tissue mechanics can interact with signaling pathways to regulate embryonic competence.

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