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Regulation of asymmetric positioning of nuclei by Wnt and Src signaling and its roles in POP‐1/TCF nuclear asymmetry in Caenorhabditis elegans
Author(s) -
Sugioka Kenji,
Sawa Hitoshi
Publication year - 2010
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/j.1365-2443.2010.01388.x
Subject(s) - wnt signaling pathway , biology , microbiology and biotechnology , caenorhabditis elegans , asymmetric cell division , cell cortex , cell polarity , cell division , cell fate determination , polarity (international relations) , centrosome , anchoring , signal transduction , mutant , nuclear localization sequence , cell , nucleus , genetics , cell cycle , cytoskeleton , gene , structural engineering , transcription factor , engineering
In various polarized cells, positions of nuclei are often off‐center. However, extrinsic signals regulating nuclear off‐centering and its biologic roles remain to be elucidated. In Caenorhabditis elegans , polarity of the EMS cell undergoing asymmetric division is regulated by the MOM‐2/Wnt and MES‐1 signals from its posterior neighbor P2 cell. We show that after divisions of different cells including EMS, the nuclei of the posterior but not anterior daughter cells are anchored to the posterior cell cortex via centrosomes. We also show that this nuclear anchoring is regulated by components of the Wnt pathway and SRC‐1 that functions in MES‐1 signaling. To understand the biologic roles of nuclear anchoring, we analyzed its effects on asymmetric nuclear localization of POP‐1/TCF that is also regulated by Wnt and Src signaling. We found that in mom‐2 mutants where the nuclear anchoring and POP‐1 asymmetry is partially inhibited, the proximity of the nucleus to the cell cortex correlated with POP‐1 asymmetry. Furthermore, in mutants of mom‐2 , the defect in the anchoring is clearly correlated with that of asymmetric fate determination. These results suggest that the asymmetric nuclear anchoring functions in asymmetric division by enhancing POP‐1 asymmetry.