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First published online 8 February 2006
doi: 10.1242/dev.02274

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Sfrp1 and Sfrp2 regulate anteroposterior axis elongation and somite segmentation during mouse embryogenesis

¹ Vertebrate Body Plan, Center for Developmental Biology, RIKEN Kobe, Minatojima-Minami, Chuou-ku, Kobe 650-0047, Japan.
² The Graduate School of Biological Sciences, Nara Institute of Science and Technology, 8916-5 Takayama, Ikoma, Nara, 630-0101, Japan.
³ Applied Biological Science, Faculty of Science and Technology, Tokyo University of Science, 641 Yamazaki, Noda-shi, Chiba 278-8510, Japan.
⁴ Kuju Agricultural Research Center, Kyushu University Graduate School of Agriculture, Naoiri-gun Kuju-cho 878-0201, Japan.

^* Author for correspondence (e-mail: ashimono{at}cdb.riken.jp)

Accepted 4 January 2006

Regulation of Wnt signaling is essential for embryonic patterning. Sfrps are secreted Wnt antagonists that directly interact with the Wnt ligand to inhibit signaling. Here, we show that Sfrp1 and Sfrp2 are required for anteroposterior (AP) axis elongation and somitogenesis in the thoracic region during mouse embryogenesis. Double homozygous mutations in Sfrp1 and Sfrp2 lead to severe shortening of the thoracic region. By contrast, a homozygous mutation in one or the other exerts no effect on embryogenesis, indicating that Sfrp1 and Sfrp2 are functionally redundant. The defect of a shortened thoracic region appears to be the consequence of AP axis reduction and incomplete somite segmentation. The reduction in the AP axis is partially due to abnormalities in cell migration of pre-somitic mesoderm from the end of gastrulation. Aberrant somite segmentation is associated with altered oscillations of Notch signaling, as evidenced by abnormal Lfng and Hes7 expression during somitogenesis in the thoracic region. This study suggests that Wnt regulation by Sfrp1 and Sfrp2 is required for embryonic patterning.

Key words: Sfrp1, Sfrp2, Wnt signaling, Wnt antagonists, Embryonic patterning, Somitogenesis

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