Evidence for crucial role of hindgut expansion in directing proper migration of primordial germ cells in mouse early embryogenesis

Kenshiro Hara, Masami Kanai-Azuma, Mami Uemura, Hiroshi Shitara, Choji Taya, Hiromichi Yonekawa, Hayato Kawakami, Naoki Tsunekawa, Masamichi Kurohmaru, Yoshiakira Kanai

研究成果: Article査読

51 被引用数 (Scopus)

抄録

During mouse gastrulation, primordial germ cells (PGCs) become clustered at the base of the allantois and move caudally into the hindgut endoderm before entering the genital ridges. The precise roles of endoderm tissues in PGC migration, however, remain unclear. By using Sox17 mutants with a specific endoderm deficiency, we provide direct evidence for the crucial role of hindgut expansion in directing proper PGC migration. In Sox17-null embryos, PGCs normally colonize in the allantois and then a small front-row population of PGCs moves properly into the most posterior gut endoderm. Defective hindgut expansion, however, causes the failure of further lateral PGC movement, resulting in the immobilization of PGCs in the hindgut entrance at the later stages. In contrast, the majority of the remaining PGCs moves into the visceral endoderm layer, but relocate outside of the embryonic gut domain. This leads to a scattering of PGCs in the extraembryonic yolk sac endoderm. This aberrant migration of Sox17-null PGCs can be rescued by the supply of wildtype hindgut cells in chimeric embryos. Therefore, these data indicate that hindgut morphogenic movement is crucial for directing PGC movement toward the embryonic gut side, but not for their relocation from the mesoderm into the endoderm.

本文言語English
ページ(範囲)427-439
ページ数13
ジャーナルDevelopmental Biology
330
2
DOI
出版ステータスPublished - 2009 6 15

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology
  • Cell Biology

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