Hisato Kondoh

TL;DR: In transgenic mouse embryos, N-terminally truncated Gli2, unlike the full length protein, activates a Shh target gene, HNF3beta, in the dorsal neural tube, thus mimicking the effect of Shh signal, which suggests that unmasking of the strong activation potential of Gli 2 through modulation of the N-Terminal repression domain is one of the key mechanisms of the Shh signaling.

TL;DR: It is demonstrated that Pax6 initiates lens development by forming a molecular complex with SOX2 on the lens-specific enhancer elements, e.g., the delta-crystallin minimal enhancer DC5, providing the molecular basis of synergistic activation by Pax6 and SoX2.

TL;DR: Activating (B1) and repressing (B2) subgroups of Group B Sox genes display interesting overlaps of expression domains in developing tissues, suggesting that target genes of Group A SOX proteins are finely regulated by the counterbalance of activating and repressed SOXprotein.

TL;DR: The results argue that the proximal portion of the C-terminal domain of SOX1/2 specifically interacts with the partner factor, and this interaction determines the specificity of the SOX3/2 action, and the highly selective SOX-partner factor interactions presumably stabilize the DNA binding of theSOX proteins and provide the mechanism for regulatory target selection.

TL;DR: High N-myc expression provoked massive ventral migration of the neural crest population and those cells that migrated to the ganglion-forming areas underwent neuronal differentiation with the cell type determined by the nature of the Ganglion.