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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.

Sfrp Controls Apicobasal Polarity and Oriented Cell Division in Developing Gut Epithelium