β-Catenin is essential for pancreatic acinar but not islet development
Acinar cell
Beta-catenin
Enteroendocrine cell
DOI:
10.1242/dev.02063
Publication Date:
2005-09-29T00:24:26Z
AUTHORS (4)
ABSTRACT
Despite our increasingly sophisticated understanding of transcriptional regulation in pancreas development, we know relatively little about the extrinsic signaling pathways involved this process. We show here that early pancreatic epithelium exhibits a specific enrichment unphosphorylated beta-catenin protein, hallmark activation canonical Wnt pathway. To determine if pathway is functionally required for normal have specifically deleted gene these cells. Pancreata developing without are hypoplastic, although their progenitors appear and exhibit no premature differentiation or death. Surprisingly, marked contrast to its role intestine, loss does not significantly perturb islet endocrine cell mass function. The major defect beta-catenin-deficient an almost complete lack acinar cells, which normally comprise majority organ. beta-Catenin appears be cell-autonomously specification rather than survival maintenance, as deletion differentiated cells has effect. Thus, data consistent with crucial signals lineage differentiation.
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