PAR-6–PAR-3 mediates Cdc42-induced Rac activation through the Rac GEFs STEF/Tiam1

Nishimura, Takashi; Yamaguchi, Tomoya; Kato, Katsuhiro; Yoshizawa, Masato; Nabeshima, Yo Ichi; Ohno, Shigeo; Hoshino, Mikio; Kaibuchi, Kozo

doi:10.1038/ncb1227

Cited by 346 publications

(425 citation statements)

References 30 publications

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“…Examination of the potential target list for miR302/367 revealed Tiam1 and Lis1 as predicted targets of miR302/367 (see Table S2 in the supplementary material). The Rac activator Tiam1, a T-lymphoma invasion and metastasis-inducing protein, acts as a crucial component of the Par complex in regulating neuronal and epithelial apical-basal polarity (Chen and Macara, 2005;Mertens et al, 2005;Nishimura et al, 2005). Lis1 (-subunit of plateletactivating factor acetylhydrolase) is essential for proliferation and the precise control of mitotic spindle orientation in both neuroepithelial stem cells and radial glial progenitor cells (Yingling et al, 2008;Yamada et al, 2010).…”

Section: Regulation Of Endoderm Progenitor Apical-basal Polarity By Mmentioning

confidence: 99%

Regulation of lung endoderm progenitor cell behavior by miR302/367

et al. 2011

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SUMMARYThe temporal and spatial control of organ-specific endoderm progenitor development is poorly understood. miRNAs affect cell function by regulating programmatic changes in protein expression levels. We show that the miR302/367 cluster is a target of the transcription factor Gata6 in mouse lung endoderm and regulates multiple aspects of early lung endoderm progenitor development. miR302/367 is expressed at early stages of lung development, but its levels decline rapidly as development proceeds. Gain-and loss-of-function studies show that altering miR302/367 expression disrupts the balance of lung endoderm progenitor proliferation and differentiation, as well as apical-basal polarity. Increased miR302/367 expression results in the formation of an undifferentiated multi-layered lung endoderm, whereas loss of miR302/367 activity results in decreased proliferation and enhanced lung endoderm differentiation. miR302/367 coordinates the balance between proliferation and differentiation, in part, through direct regulation of Rbl2 and Cdkn1a, whereas apical-basal polarity is controlled by regulation of Tiam1 and Lis1. Thus, miR302/367 directs lung endoderm development by coordinating multiple aspects of progenitor cell behavior, including proliferation, differentiation and apical-basal polarity.

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Section: Regulation Of Endoderm Progenitor Apical-basal Polarity By Mmentioning

confidence: 99%

Regulation of lung endoderm progenitor cell behavior by miR302/367

et al. 2011

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“…PAR polarity proteins are essential for appropriate control of cytoskeletal, and thus cellular, polarity in a wide variety of polarized cell types (Mertens et al 2005;Nishimura et al 2005;Macara 2006, 2008;Pegtel et al 2007;Nakayama et al 2008;St Johnston and Ahringer 2010). Baz/Par interaction with the Rac-GEF, TIAM, regulates actin dynamics in a number of different systems (Nishimura et al 2005;Zhang and Macara 2006;Heasman and Ridley 2008), and contributes to TJ formation in epithelia (Chen and Macara 2005;Mertens et al 2005;Gopalakrishnan et al 2007).…”

Section: Branched Actin Networkmentioning

confidence: 99%

Phosphoinositides in Cell Architecture

Shewan

Eastburn²,

Mostov

2011

Cold Spring Harbor Perspectives in Biology

173

159

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Inositol phospholipids have been implicated in almost all aspects of cellular physiology including spatiotemporal regulation of cellular signaling, acquisition of cellular polarity, specification of membrane identity, cytoskeletal dynamics, and regulation of cellular adhesion, motility, and cytokinesis. In this review, we examine the critical role phosphoinositides play in these processes to execute the establishment and maintenance of cellular architecture. Epithelial tissues perform essential barrier and transport functions in almost all major organs. Key to their development and function is the establishment of epithelial cell polarity. We place a special emphasis on highlighting recent studies demonstrating phosphoinositide regulation of epithelial cell polarity and how individual cells use phosphoinositides to further organize into epithelial tissues.P hosphoinositides (PIs) are essential components of cellular membranes in eukaryotes. Though these specialized lipids comprise less than 1% of the cellular lipid cohort, they play key roles in many fundamental biological processes (Di Paolo and De Camilli 2006;Saarikangas et al. 2010). PIs possess such far ranging roles by serving as specialized membrane docking sites for effectors of numerous cellular signal transduction cascades. PIs also serve as precursors of lipid second messengers. They are concentrated on the cytosolic face of cellular membranes (Fig. 1A) and rapidly diffuse within the plane of the membrane. Reversible phosphorylation of the myo-inositol head group of phosphatidylinositol (PtdIns) at positions 3, 4, and 5 (Fig. 1B) gives rise to the seven PI isoforms identified in eukaryotic cells. PtdIns(4)P and PtdIns(4,5)P 2 are constitutively present in membranes and comprise the largest pool of cellular PIs, whereas PtdIns(3,4,5)P 3 is essentially undetectable in most types of unstimulated cells (Lemmon and Ferguson 2000;Saarikangas et al. 2010).The spatiotemporally regulated production and turnover of phosphoinositides is crucial for localized PI signaling and function. Numerous phosphatidylinositol kinases and phosphatases are involved in regulating the metabolism of the various PI isoforms (Fig. 1)

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“…Neuroepithelial radial glia target the PAR3/6 complex in their apical domain along the ventricular wall (Manabe et al 2002;Costa et al 2008). Proteins reported to exist in a complex with PAR3/ 6 include atypical forms of protein kinase C (aPKC: PKCl and z) (Joberty et al 2000;Lin et al 2000;Qiu et al 2000), the small GTPase cdc42 (Joberty et al 2000;Lin et al 2000;Qiu et al 2000), the kinesin motor protein KIF3A (Nishimura et al 2004), the guanine exchange factor Tiam1/STEF (Chen and Macara 2005;Nishimura et al 2005), the lipid and protein phosphatase PTEN (von Stein et al 2005;Feng et al 2008), the GTPase activating protein (GAP) p190RhoGAP (Zhang and Macara 2008), the tumor suppressor lethal giant larvae (lgl) (Plant etal. 2003), the scaffold protein inscuteable (Schoberet al 1999), the ubiquitin ligases Smurf1 (Ozdamar et al 2005) and Smurf2 (Schwamborn et al 2007b), and the transforming growth factor receptor1 (TGFbR1) (Ozdamaret al 2005).…”

Section: Par3-par6-apkcmentioning

confidence: 99%

Initiating and Growing an Axon

Polleux¹,

Snider²

2010

Cold Spring Harbor Perspectives in Biology

163

127

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The ability of neurons to form a single axon and multiple dendrites underlies the directional flow of information transfer in the central nervous system. Dendrites and axons are molecularly and functionally distinct domains. Dendrites integrate synaptic inputs, triggering the generation of action potentials at the level of the soma. Action potentials then propagate along the axon, which makes presynaptic contacts onto target cells. This article reviews what is known about the cellular and molecular mechanisms underlying the ability of neurons to initiate and extend a single axon during development. Remarkably, neurons can polarize to form a single axon, multiple dendrites, and later establish functional synaptic contacts in reductionist in vitro conditions. This approach became, and remains, the dominant model to study axon initiation and growth and has yielded the identification of many molecules that regulate axon formation in vitro (Dotti et al. 1988). At present, only a few of the genes identified using in vitro approaches have been shown to be required for axon initiation and outgrowth in vivo. In vitro, axon initiation and elongation are largely intrinsic properties of neurons that are established in the absence of relevant extracellular cues. However, the importance of extracellular cues to axon initiation and outgrowth in vivo is emerging as a major theme in neural development (Barnes and Polleux 2009). In this article, we focus our attention on the extracellular cues and signaling pathways required in vivo for axon initiation and axon extension.

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PAR-6–PAR-3 mediates Cdc42-induced Rac activation through the Rac GEFs STEF/Tiam1

Cited by 346 publications

References 30 publications

Regulation of lung endoderm progenitor cell behavior by miR302/367

Regulation of lung endoderm progenitor cell behavior by miR302/367

Phosphoinositides in Cell Architecture

Initiating and Growing an Axon

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