Apical constriction and invagination downstream of the canonical Wnt signaling pathway require Rho1 and Myosin II.

ABSTRACT: The tumor suppressor Adenomatous polyposis coli (APC) is a negative regulator of Wnt signaling and functions in cytoskeletal organization. Disruption of human APC in colonic epithelia initiates benign polyps that progress to carcinoma following additional mutations. The early events of polyposis are poorly understood, as is the role of canonical Wnt signaling in normal epithelial architecture and morphogenesis. To determine the consequences of complete loss of APC in a model epithelium, we generated APC2 APC1 double null clones in the Drosophila wing imaginal disc. APC loss leads to segregation, apical constriction, and invagination that result from transcriptional activation of canonical Wnt signaling. Further, we show that Wnt-dependent changes in cell fate can be decoupled from Wnt-depe

SUBMITTER: Zimmerman SG 

PROVIDER: S-EPMC4056678 | biostudies-literature | 2010 Apr

REPOSITORIES: biostudies-literature