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First published online April 10, 2009

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Vangl2 keeps on trac(t)

Female reproductive tract (FRT) development in vertebrates is controlled by Wnts, but little is known about the different intracellular pathways involved. Now, Alysia vandenBerg and David Sassoon describe how non-canonical Wnt signalling through a core member of the planar cell polarity (PCP) signalling pathway, vang-like 2 (Vangl2), is involved in this process (p. 1559). They report that loop-tail mice, which carry a Vangl2 mutation (Vangl2^Lp), have FRT defects at birth that resemble those of Wnt7a mutants. Their findings show that the polarity of uterine epithelial cells in Vangl2^Lp mice is abnormal, with defective cytoskeletal actin polarisation and mislocalised scribble 1 - an apicobasal polarity protein. As Vangl2^Lp mutants die at birth, the researchers grafted FRTs from mutants into normal mice to study the later effects of this mutation. They found that the initial defects worsen over two weeks and that Wnt7a levels are reduced in both homozygous and heterozygous grafted Vangl2^Lp FRTs, indicating that Vangl2 acts dominantly in the FRT. From their findings, the authors conclude that both canonical and non-canonical Wnt signalling participate in FRT development.

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Related articles in Development:

Non-canonical Wnt signaling regulates cell polarity in female reproductive tract development via van gogh-like 2

Alysia L. vandenBerg and David A. Sassoon
Development 2009 136: 1559-1570. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in Development Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?