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Role of TSC-22 during early embryogenesis in Xenopus laevis

  1. Akiko Hashiguchi1,
  2. Koji Okabayashi2,
  3. Makoto Asashima2,3,*

Article first published online: 6 JAN 2005

DOI: 10.1111/j.1440-169x.2004.00770.x

Issue

Development, Growth & Differentiation

Development, Growth & Differentiation

Volume 46, Issue 6, pages 535–544, December 2004

Additional Information

How to Cite

Hashiguchi, A., Okabayashi, K. and Asashima, M. (2004), Role of TSC-22 during early embryogenesis in Xenopus laevis. Development, Growth & Differentiation, 46: 535–544. doi: 10.1111/j.1440-169x.2004.00770.x

Author Information

  1. 1

    Department of Biological Sciences, Graduate School of Science, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8654,

  2. 2

    International Cooperative Research Project (ICORP), Japan Science and Technology Corporation (JST) and

  3. 3

    Department of Life Sciences (Biology), Graduate School of Arts and Sciences, The University of Tokyo, 3-8-1 Komaba, Meguro-ku, Tokyo 153-8902, Japan.

* *Author to whom all Correspondence should be addressed. Email: asashi@bio.c.u-tokyo.ac.jp.

Publication History

  1. Issue published online: 6 JAN 2005
  2. Article first published online: 6 JAN 2005
  3. Received 16 September 2004; revised 18 October 2004; accepted 21 October 2004.

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Keywords:

  • cell cycle;
  • cell migration;
  • gastrulation;
  • TSC-22;
  • Xenopus laevis

Transforming growth factor-β1-stimulated clone 22 (TSC-22) encodes a leucine zipper-containing protein that is highly conserved. During mouse embryogenesis, TSC-22 is expressed at the site of epithelial–mesenchymal interaction. Here, we isolated Xenopus laevis TSC-22 (XTSC-22) and analyzed its function in early development. XTSC-22 mRNA was first detected in the ectoderm of late blastulae. Translational knockdown using XTSC-22 antisense morpholino oligonucleotides (XTSC-22-MO) caused a severe delay in blastopore closure in gastrulating embryos. This was not due to mesoderm induction or convergent-extension, as confirmed by whole-mount in situ hybridization and animal cap assay. Cell lineage tracing revealed that migration of ectoderm cells toward blastopore was disrupted in XTSC-22-depleted embryos, and these embryos had a marked increase in the number of dividing cells. In contrast, cell division was suppressed in XTSC-22 mRNA-injected embryos. Co-injection of XTSC-22-MO and mRNA encoding p27Xic1, which inhibits cell cycle promotion by binding cyclin/Cdk complexes, reversed aberrant cell division. This was accompanied by rescue of the delay in blastopore closure and cell migration. These results indicate that XTSC-22 is required for cell movement during gastrulation though cell cycle regulation.

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