Abstract
The vertebrate neural crest is a population of migratory cells that originates in the dorsal aspect of the embryonic neural tube. These cells undergo an epithelial-to-mesencyhmal transition (EMT), delaminate from the neural tube and migrate extensively to generate an array of differentiated cell types. Elucidating the gene regulatory networks involved in neural crest cell induction, migration and differentiation are thus crucial to understanding vertebrate development. To this end, we have identified Annexin A6 as an important regulator of chick midbrain neural crest cell emigration. Annexin proteins comprise a family of calcium-dependent, membrane-binding molecules that mediate a variety of cellular and physiological processes including cell adhesion, migration and invasion. Our data indicate that Annexin A6 is expressed in the proper spatio-temporal pattern in the chick midbrain to play a potential role in neural crest cell ontogeny. To investigate Annexin A6 function, we have depleted or overexpressed Annexin A6 in the developing midbrain neural crest cell population. Our results show that knock-down or overexpression of Annexin A6 reduces or expands the migratory neural crest cell domain, respectively. Importantly, this phenotype is not due to any change in cell proliferation or cell death but can be correlated with changes in the size of the premigratory neural crest cell population and with markers associated with EMT. Taken together, our data indicate that Annexin A6 plays a pivotal role in modulating the formation of cranial migratory neural crest cells during vertebrate development.
Highlights
Neural crest cells are a population of migratory cells in the developing vertebrate embryo
In order to ascertain a potential role for Annexin A6 in chick midbrain neural crest cell development, we performed wholemount in situ hybridization, in conjunction with transverse sectioning, to document the expression profile of Annexin A6 in the developing embryo
In order to investigate whether Annexin A6 knock-down reduced neural crest cell emigration by altering the process of epithelial-to-mesencyhmal transition (EMT), we examined the distribution of several adherens and tight junction proteins whose down-regulation has been previously correlated with neural crest cell EMT/migration [19,20,21,22, our unpublished data] (Fig. 5)
Summary
Neural crest cells are a population of migratory cells in the developing vertebrate embryo. These cells initially reside in the most dorsal region of the neural tube as premigratory neural crest cells that subsequently undergo an epithelial-to-mesencyhmal transition (EMT) to become motile These migratory cells traverse stereotypical pathways in both the head and trunk and later differentiate to form a wide variety of structures in the embryo, including the craniofacial skeleton, components of the peripheral nervous system and heart, and skin pigment cells [1]. Because of the contributions of neural crest cells to multiple derivatives, it is critical to study how these cells arise in the developing embryo, including the role of various genes in controlling the induction, migration, and differentiation of the neural crest To this end, we explored a potential role for Annexin A6 in neural crest cell development and find that Annexin A6 functions in controlling neural crest cell emigration in the developing chick midbrain. Our studies reveal a novel function for an annexin family member in controlling midbrain neural crest cell emigration in the developing chick embryo
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