β-Catenin asymmetry is regulated by PLA1 and retrograde traffic in C. elegans stem cell divisions

Takahiro Kanamori, Takao Inoue, Taro Sakamoto, Keiko Gengyo-Ando, Masafumi Tsujimoto, Shohei Mitani, Hitoshi Sawa, Junken Aoki, Hiroyuki Arai

Research output: Contribution to journalArticlepeer-review

33 Citations (Scopus)

Abstract

Asymmetric division is an important property of stem cells. In Caenorhabditis elegans, the Wnt/β-catenin asymmetry pathway determines the polarity of most asymmetric divisions. The Wnt signalling components such as β-catenin localize asymmetrically to the cortex of mother cells to produce two distinct daughter cells. However, the molecular mechanism to polarize them remains to be elucidated. Here, we demonstrate that intracellular phospholipase A1 (PLA1), a poorly characterized lipid-metabolizing enzyme, controls the subcellular localizations of β-catenin in the terminal asymmetric divisions of epithelial stem cells (seam cells). In mutants of ipla-1, a single C. elegans PLA1 gene, cortical β-catenin is delocalized and the asymmetry of cell-fate specification is disrupted in the asymmetric divisions. ipla-1 mutant phenotypes are rescued by expression of ipla-1 in seam cells in a catalytic activity-dependent manner. Furthermore, our genetic screen utilizing ipla-1 mutants reveals that reduction of endosome-to-Golgi retrograde transport in seam cells restores normal subcellular localization of β-catenin to ipla-1 mutants. We propose that membrane trafficking regulated by ipla-1 provides a mechanism to control the cortical asymmetry of β-catenin.

Original languageEnglish
Pages (from-to)1647-1657
Number of pages11
JournalEMBO Journal
Volume27
Issue number12
DOIs
Publication statusPublished - 2008 Jun 18

Keywords

  • Asymmetric divisions
  • C. elegans
  • Phospholipase
  • Retrograde trafficking
  • The Wnt/β-catenin asymmetry pathway

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)

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