Abstract

Canonical Wnt-signalling is well understood and has been extensively described in many developmental processes. The regulation of this signalling pathway is of outstanding relevance for proper development of the vertebrate and invertebrate embryo. Axin2 provides a negative-feedback-loop in the canonical Wnt-pathway, being a target gene and a negative regulator. Here we provide a detailed analysis of the expression pattern in the development of the chicken embryo. By performing in-situ hybridization on chicken embryos from stage HH 04+ to HH 32 we detected a temporally and spatially restricted dynamic expression of Axin2. In particular, data about the expression of Axin2 mRNA in early embryogenesis, somites, neural tube, limbs, kidney and eyes was obtained.

Highlights

  • Axin2 is a homologue of Axin protein

  • The N-terminal RGS-domain has been found to interact with the tumour suppressor gene adenomatous polyposis coli (APC) [1, 6]

  • As this study aims to emphasize the relevance of Axin2 in regulating the Wnt-signalling pathway, it is important to mention the state of the art regarding the role of canonical Wnt-pathway in development and in disease

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Summary

Introduction

Axin ( called Axil or Conductin) is a homologue of Axin protein. It shares approximately 45% of amino acids with Axin [1, 2]. Being responsible for the degradation of the downstream canonical Wnt-signalling pathway molecule β-catenin, Axin and Axin function as negative regulators of the canonical Wnt-signalling pathway [5, 10,11,12]. The canonical Wnt-pathway was described, followed by at least two non-canonical pathways. The pathway of planar cell polarity (PCP) and the Wnt/Ca2+-pathway are referred to as non-canonical pathways [13,14,15]. These are described to establish orientation in epithelia (PCP) and to play a role in early embryonic ventral patterning (Wnt/Ca2+-pathway) ([16] for review). In this study, only the canonical pathway is of relevance, constituting a venue for the PLOS ONE | DOI:10.1371/journal.pone.0163610 September 28, 2016

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