Abstract
I show in my study that the chick transcription factor cSox3, (a member of sub-group B1 of Sox gene family), is expressed in four lateral patches at the rostral edge of the epibranchial arches and that these mark the epibranchial placodes. These patches of cSox3 expression arise by gradual thinning from broader areas of cSox3 expression with concomitant loss of cSox3 in non-placodal regions. Cells leaving the epithelial placodes as they initiate neurogenesis lose cSox3 expression and sequentially express Ngn1, NeuroD, NeuroM and Phox2a but do not express Ngn2. This is in contrast to studies in the mouse where it is Ngn2, rather than Ngn1 that is predominantly expressed in epibranchial derived neuroblasts. Double labelling analyses show that cSox3, Ngn1, NeuroD, NeuroM and Phox2a overlap with the expression of neuronal markers NF (neurofilament) and Hu. Overexpression of cSox3 interferes with normal neuroblast migration and results in changes in ectodermal morphology. These include induction of a thick ectoderm and placodal like structures. Thus, cSox3 provides a useful tool for the study of placode formation, and loss of cSox3 expression appears to be a necessary event in normal neurogenesis from the epibranchial placodes. Overexpression of Ngn2 results in loss of cSox3 expression and in activation of cNeuroD. This activation is varied and dependent on the region of transfection. Triggering neurogenesis ectopically outside the branchial region by Ngn2 initiates inwards cellular migration and leads to cellular aggregation. Thus, Ngn2 provides a useful tool to examine the regions of competency of the ectoderm to undergo specific steps in neurogenesis.