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β‐Catenin asymmetry is regulated by PLA 1 and retrograde traffic in C. elegans stem cell divisions
Author(s) -
Kanamori Takahiro,
Inoue Takao,
Sakamoto Taro,
GengyoAndo Keiko,
Tsujimoto Masafumi,
Mitani Shohei,
Sawa Hitoshi,
Aoki Junken,
Arai Hiroyuki
Publication year - 2008
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/emboj.2008.102
Subject(s) - biology , microbiology and biotechnology , caenorhabditis elegans , mutant , wnt signaling pathway , beta catenin , cell fate determination , asymmetric cell division , cell division , cell , signal transduction , genetics , gene , transcription factor
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 A 1 (PLA 1 ), 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 PLA 1 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.