Involvement of Girdin in the Determination of Cell Polarity during Cell Migration

Cell migration is a critical cellular process that determines embryonic development and the progression of human diseases. Therefore, cell- or context-specific mechanisms by which multiple promigratory proteins differentially regulate cell migration must be analyzed in detail. Girdin (girders of act...

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Main Authors:	Ohara, Kei, Enomoto, Atsushi, Kato, Takuya, Hashimoto, Takahiko, Isotani-Sakakibara, Mayu, Asai, Naoya, Ishida-Takagishi, Maki, Weng, Liang, Nakayama, Masanori, Watanabe, Takashi, Kato, Katsuhiro, Kaibuchi, Kozo, Murakumo, Yoshiki, Hirooka, Yoshiki, Goto, Hidemi, Takahashi, Masahide
Format:	Online
Language:	English
Published:	Public Library of Science 2012
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3344933/

id	pubmed-3344933
recordtype	oai_dc
spelling	pubmed-33449332012-05-09 Involvement of Girdin in the Determination of Cell Polarity during Cell Migration Ohara, Kei Enomoto, Atsushi Kato, Takuya Hashimoto, Takahiko Isotani-Sakakibara, Mayu Asai, Naoya Ishida-Takagishi, Maki Weng, Liang Nakayama, Masanori Watanabe, Takashi Kato, Katsuhiro Kaibuchi, Kozo Murakumo, Yoshiki Hirooka, Yoshiki Goto, Hidemi Takahashi, Masahide Research Article Cell migration is a critical cellular process that determines embryonic development and the progression of human diseases. Therefore, cell- or context-specific mechanisms by which multiple promigratory proteins differentially regulate cell migration must be analyzed in detail. Girdin (girders of actin filaments) (also termed GIV, Gα-interacting vesicle associated protein) is an actin-binding protein that regulates migration of various cells such as endothelial cells, smooth muscle cells, neuroblasts, and cancer cells. Here we show that Girdin regulates the establishment of cell polarity, the deregulation of which may result in the disruption of directional cell migration. We found that Girdin interacts with Par-3, a scaffolding protein that is a component of the Par protein complex that has an established role in determining cell polarity. RNA interference-mediated depletion of Girdin leads to impaired polarization of fibroblasts and mammary epithelial cells in a way similar to that observed in Par-3-depleted cells. Accordingly, the expression of Par-3 mutants unable to interact with Girdin abrogates cell polarization in fibroblasts. Further biochemical analysis suggests that Girdin is present in the Par protein complex that includes Par-3, Par-6, and atypical protein kinase C. Considering previous reports showing the role of Girdin in the directional migration of neuroblasts, network formation of endothelial cells, and cancer invasion, these data may provide a specific mechanism by which Girdin regulates cell movement in biological contexts that require directional cell movement. Public Library of Science 2012-05-04 /pmc/articles/PMC3344933/ /pubmed/22574214 http://dx.doi.org/10.1371/journal.pone.0036681 Text en Ohara et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Ohara, Kei Enomoto, Atsushi Kato, Takuya Hashimoto, Takahiko Isotani-Sakakibara, Mayu Asai, Naoya Ishida-Takagishi, Maki Weng, Liang Nakayama, Masanori Watanabe, Takashi Kato, Katsuhiro Kaibuchi, Kozo Murakumo, Yoshiki Hirooka, Yoshiki Goto, Hidemi Takahashi, Masahide
spellingShingle	Ohara, Kei Enomoto, Atsushi Kato, Takuya Hashimoto, Takahiko Isotani-Sakakibara, Mayu Asai, Naoya Ishida-Takagishi, Maki Weng, Liang Nakayama, Masanori Watanabe, Takashi Kato, Katsuhiro Kaibuchi, Kozo Murakumo, Yoshiki Hirooka, Yoshiki Goto, Hidemi Takahashi, Masahide Involvement of Girdin in the Determination of Cell Polarity during Cell Migration
author_facet	Ohara, Kei Enomoto, Atsushi Kato, Takuya Hashimoto, Takahiko Isotani-Sakakibara, Mayu Asai, Naoya Ishida-Takagishi, Maki Weng, Liang Nakayama, Masanori Watanabe, Takashi Kato, Katsuhiro Kaibuchi, Kozo Murakumo, Yoshiki Hirooka, Yoshiki Goto, Hidemi Takahashi, Masahide
author_sort	Ohara, Kei
title	Involvement of Girdin in the Determination of Cell Polarity during Cell Migration
title_short	Involvement of Girdin in the Determination of Cell Polarity during Cell Migration
title_full	Involvement of Girdin in the Determination of Cell Polarity during Cell Migration
title_fullStr	Involvement of Girdin in the Determination of Cell Polarity during Cell Migration
title_full_unstemmed	Involvement of Girdin in the Determination of Cell Polarity during Cell Migration
title_sort	involvement of girdin in the determination of cell polarity during cell migration
description	Cell migration is a critical cellular process that determines embryonic development and the progression of human diseases. Therefore, cell- or context-specific mechanisms by which multiple promigratory proteins differentially regulate cell migration must be analyzed in detail. Girdin (girders of actin filaments) (also termed GIV, Gα-interacting vesicle associated protein) is an actin-binding protein that regulates migration of various cells such as endothelial cells, smooth muscle cells, neuroblasts, and cancer cells. Here we show that Girdin regulates the establishment of cell polarity, the deregulation of which may result in the disruption of directional cell migration. We found that Girdin interacts with Par-3, a scaffolding protein that is a component of the Par protein complex that has an established role in determining cell polarity. RNA interference-mediated depletion of Girdin leads to impaired polarization of fibroblasts and mammary epithelial cells in a way similar to that observed in Par-3-depleted cells. Accordingly, the expression of Par-3 mutants unable to interact with Girdin abrogates cell polarization in fibroblasts. Further biochemical analysis suggests that Girdin is present in the Par protein complex that includes Par-3, Par-6, and atypical protein kinase C. Considering previous reports showing the role of Girdin in the directional migration of neuroblasts, network formation of endothelial cells, and cancer invasion, these data may provide a specific mechanism by which Girdin regulates cell movement in biological contexts that require directional cell movement.
publisher	Public Library of Science
publishDate	2012
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3344933/
_version_	1611527657098313728

Involvement of Girdin in the Determination of Cell Polarity during Cell Migration

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