Axin2L regulates planar cell polarity in Xenopus embryos

Abstract

Axin proteins function as central scaffolds of the {beta}-catenin destruction complex in the Wnt/{beta}-catenin pathway that has been considered distinct from the planar cell polarity (PCP) pathway. Here, we show that dorsal expression of mutated Axin2L, a predominant Axin homolog in Xenopus early embryos, disrupts convergent extension movements and neural tube closure in a manner reminiscent of the mutations in vertebrate PCP genes. GFP-Axin2L becomes planar polarized in the epidermal cells adjacent to the folding neural plate and those surrounding a wound. Axin2L associated and colocalized with ADIP, a similarly polarized protein that is essential for neural tube morphogenesis and embryonic wound healing. Interference with Axin2L function abrogated Vangl2 accumulation at the anterior sides of neuroepithelial cells and impaired ciliogenesis in the gastrocoel roof plate. We propose that, in addition to the canonical Wnt pathway, Axin2L controls PCP signaling during vertebrate morphogenesis.