Loss of Apc in vivo immediately perturbs Wnt signaling, differentiation, and migration

AUTOR(ES)

Sansom, Owen J.

FONTE

Cold Spring Harbor Laboratory Press

RESUMO

Although Apc is well characterized as a tumor-suppressor gene in the intestine, the precise mechanism of this suppression remains to be defined. Using a novel inducible Ahcre transgenic line in conjunction with a loxP-flanked Apc allele we, show that loss of Apc acutely activates Wnt signaling through the nuclear accumulation of β-catenin. Coincidentally, it perturbs differentiation, migration, proliferation, and apoptosis, such that Apc-deficient cells maintain a “crypt progenitor-like” phenotype. Critically, for the first time we confirm a series of Wnt target molecules in an in vivo setting and also identify a series of new candidate targets within the same setting.

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