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. 2006 Feb 27;103(10):3651–3656. doi: 10.1073/pnas.0508238103

Fig. 4.

Fig. 4.

Proposed mechanisms underlying the control of Mesp2 expression. Tbx6 and NICD (colored ovals) interact with the conserved upstream sites in the Mesp2 gene, sites A–D (represented by boxes). Tbx6 binds to site B (two molecules) and site D (single molecule). Site A and site C interact with RBPJκ to achieve a significant increase in Mesp2 expression levels in the presence of Notch signals (A). This activation fully depends on the binding of Tbx6 to site B or site D (B). Tbx6 may activate Mesp2 expression without site A and site C, presumably through an RBPJκ-independent Notch signaling pathway and via other signals (C). (D) Schematic representation of a proposed model that may explain developmentally regulated Mesp2 expression in the anterior PSM. (a) NICD is highly accumulated in the anterior PSM and less in the posterior (1, 2) to activate Mesp2 expression (red arrows). There may be a threshold level of NICD accumulation to initiate Mesp2 activation (broken line). (b) Tbx6 protein is distributed in the tailbud and PSM (20) and facilitates Mesp2 activation by NICD. (c) It is possible that the activation of Mesp2 expression in the tailbud and posterior PSM, if any, is repressed by other factor(s), such as Fgf8 (36), via an unknown mechanism. (d) As a result, Mesp2 expression is restricted in the anterior PSM (red box).