Role of Gli2 transcription factor in the development of Xenopus laevis neural crest

SANTIAGO CERRIZUELA; MARÍA BELÉN PALACIO; MANUEL J. AYBAR

Santiago

Simposio; International Symposium Visualisation and manipulation of signals and forces in developing tissues; 2014

Biomedical Neuroscience Institute, ICM, Chile

The neural crest is a transient multipotent and migratory cell population that is unique to vertebrate embryos. These cells differentiate and give rise to a diverse variety of cellular types and tissues such as cartilages, bone, connective tissue, endocrine and pigmentary cells, neurons and glia. This differentiation potential combined with a remarkable capacity of self-renewal support the fact that these cells have stem-cell properties. Indian Hedgehog signaling pathway plays a key role in Xenopus laevis neural crest formation, maintenance and migration. The transcription factor Gli2 is an effector of this pathway, and acts as a transcriptional activator in different systems. In this work we established a detailed expression pattern of this gene at neurula stages. We show that it is expressed in the lateral neural plate border, which subsequently forms the neural crest. It is also expressed in the anterior neural plate border, the prospective forebrain. Overexpression of gli2 mRNA in segmenting embryos produced an increase in the expression of neural crest specific markers. The specific knock-out of gli2 function using an antisense morpholino oligonucleotide produced a decrease in these specific gene markers foxd3 and snail2 along with a decreased expression of the neural crest inducer pax3. Loss of gli2 function also affected neural crest cells migration. Changes in the size of neural crest population were accompanied by compensatory changes in the specification of contiguous territories (neural plate and prospective epidermis). The abrogation of gli2 strongly affected the formation of cartilages derived from the neural crest. Taken together our results suggest a key participation of gli2 in the genetic network that controls the specification of the neural crest cells.