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Dev Biol
2010[Apr]; 340
(1
): 54-66
PMID20102708
show ga
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-dependent changes in cell shape. Wnt activation is reported to
upregulate DE-cadherin in wing discs, and elevated DE-cadherin is thought to
promote apical constriction. We find that apical constriction and invagination of
APC null tissue are independent of DE-cadherin elevation, but are dependent on
Myosin II activity. Further, we show that disruption of Rho1 suppresses apical
constriction and invagination in APC null cells. Our data suggest a novel link
between canonical Wnt signaling and epithelial structure that requires activation
of the Rho1 pathway and Myosin II.
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