Affiliation:
1. Department of Genetics and Development, Columbia University Medical Center, 701 W. 168th Street, New York, New York 10032
Abstract
ABSTRACT
Axin is a central component of the canonical Wnt signal transduction machinery, serving as a scaffold for the β-catenin destruction complex. The related protein Axin2/Conductin, although less extensively studied, is thought to perform similar functions. Loss of
Axin
causes early embryonic lethality, while
Axin2
-null mice are viable but have craniofacial defects. Mutations in either gene contribute to cancer in humans. The lack of redundancy between
Axin
and
Axin2
could be due to their different modes of expression: while Axin is expressed ubiquitously, Axin2 is expressed in tissue- and developmental-stage-specific patterns, and its transcription is induced by canonical Wnt signaling. Alternatively, the two proteins might have partially different functions, a hypothesis supported by the observation that they differ in their subcellular localizations in colon epithelial cells. To test the functional equivalence of Axin and Axin2 in vivo, we generated knockin mice in which the
Axin
gene was replaced with Myc-tagged Axin or Axin2 cDNA. Mice homozygous for the resulting alleles,
Axin
Ax
or
Axin
Ax2
, express no endogenous Axin but express either Myc-Axin or Myc-Axin2 under the control of the
Axin
locus. Both
Axin
Ax/Ax
and
Axin
Ax2/Ax2
homozygotes are apparently normal and fertile, demonstrating that the Axin and Axin2 proteins are functionally equivalent.
Publisher
American Society for Microbiology
Subject
Cell Biology,Molecular Biology
Cited by
106 articles.
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