TY - JOUR
T1 - Modulation of the ligand-independent traffic of Notch by Axin and Apc contributes to the activation of Armadillo in Drosophila
AU - Muñoz-Descalzo, Silvia
AU - Tkocz, Katarzyna
AU - Balayo, Tina
AU - Martinez-Arias, Alfonso
PY - 2011/4/15
Y1 - 2011/4/15
N2 - There is increasing evidence for close functional interactions between Wnt and Notch signalling. In many instances, these are mediated by convergence of the signalling events on common transcriptional targets, but there are other instances that cannot be accounted for in this manner. Studies in Drosophila have revealed that an activated form of Armadillo, the effector of Wnt signalling, interacts with, and is modulated by, the Notch receptor. Specifically, the ligand-independent traffic of Notch serves to set up a threshold for the amount of this form of Armadillo and therefore for Wnt signalling. In the current model of Wnt signalling, a complex assembled around Axin and Apc allows GSK3 (Shaggy) to phosphorylate Armadillo and target it for degradation. However, genetic experiments suggest that the loss of function of any of these three elements does not have the same effect as elevating the activity of β-catenin. Here, we show that Axin and Apc, but not GSK3, modulate the ligandindependent traffic of Notch. This finding helps to explain unexpected differences in the phenotypes obtained by different ways of activating Armadillo function and provides further support for the notion that Wnt and Notch signalling form a single functional module.
AB - There is increasing evidence for close functional interactions between Wnt and Notch signalling. In many instances, these are mediated by convergence of the signalling events on common transcriptional targets, but there are other instances that cannot be accounted for in this manner. Studies in Drosophila have revealed that an activated form of Armadillo, the effector of Wnt signalling, interacts with, and is modulated by, the Notch receptor. Specifically, the ligand-independent traffic of Notch serves to set up a threshold for the amount of this form of Armadillo and therefore for Wnt signalling. In the current model of Wnt signalling, a complex assembled around Axin and Apc allows GSK3 (Shaggy) to phosphorylate Armadillo and target it for degradation. However, genetic experiments suggest that the loss of function of any of these three elements does not have the same effect as elevating the activity of β-catenin. Here, we show that Axin and Apc, but not GSK3, modulate the ligandindependent traffic of Notch. This finding helps to explain unexpected differences in the phenotypes obtained by different ways of activating Armadillo function and provides further support for the notion that Wnt and Notch signalling form a single functional module.
UR - http://www.scopus.com/inward/record.url?scp=79955398515&partnerID=8YFLogxK
UR - http://dx.doi.org/10.1242/dev.061309
U2 - 10.1242/dev.061309
DO - 10.1242/dev.061309
M3 - Article
AN - SCOPUS:79955398515
VL - 138
SP - 1501
EP - 1506
JO - Development
JF - Development
SN - 0950-1991
IS - 8
ER -