Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pgen.1000427
Title: Sfrp controls apicobasal polarity and oriented cell division in developing gut epithelium
Authors: Matsuyama, M.
Aizawa, S.
Shimono, A. 
Issue Date: Mar-2009
Citation: Matsuyama, M., Aizawa, S., Shimono, A. (2009-03). Sfrp controls apicobasal polarity and oriented cell division in developing gut epithelium. PLoS Genetics 5 (3) : -. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pgen.1000427
Abstract: Epithelial tubular morphogenesis leading to alteration of organ shape has important physiological consequences. However, little is known regarding the mechanisms that govern epithelial tube morphogenesis. Here, we show that inactivation of Sfrp1 and Sfrp2 leads to reduction in fore-stomach length in mouse embryos, which is enhanced in the presence of the Sfrp5 mutation. In the mono-cell layer of fore-stomach epithelium, cell division is normally oriented along the cephalocaudal axis; in contrast, orientation diverges in the Sfrps-deficient fore-stomach. Cell growth and apoptosis are not affected in the Sfrps- deficient fore-stomach epithelium. Similarly, cell division orientation in fore-stomach epithelium diverges as a result of inactivation of either Stbm/Vangl2, an Fz/PCP component, or Wnt5a. These observations indicate that the oriented cell division, which is controlled by the Fz/PCP pathway, is one of essential components in fore-stomach morphogenesis. Additionally, the small intestine epithelium of Sfrps compound mutants fails to maintain proper apicobasal polarity the defect was also observed in Wnt5a-inactivated small intestine. In relation to these findings, Sfrp1 physically interacts with Wnt5a and inhibits Wnt5a signaling. We propose that Sfrp regulation of Wnt5a signaling controls oriented cell division and apicobasal polarity in the epithelium of developing gut. Copyright: ©2009 Matsuyama et al.
Source Title: PLoS Genetics
URI: http://scholarbank.nus.edu.sg/handle/10635/117155
ISSN: 15537390
DOI: 10.1371/journal.pgen.1000427
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