Cdc42 and Cellular Polarity: Emerging Roles at the Golgi

Farhan, Hesso; Hsu, Victor

doi:10.1016/j.tcb.2015.11.003

Cited by 74 publications

(57 citation statements)

References 45 publications

(67 reference statements)

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“…S6F). This provides in vivo evidence that CDC42 is involved in the trafficking of receptors from the Golgi to the membrane, and is consistent with a report that the Golgi complex represents a predominant location for CDC42 in mammalian cells (Farhan and Hsu, 2016). The current study is consistent with the finding that CDC42 regulates bidirectional Golgi transport by targeting the dual functions of Coat protein complex I in cargo sorting and carrier formation (Park et al, 2015).…”

Section: Cdc42 Might Regulate Cellular Component Trafficking During Psupporting

confidence: 92%

CDC42 is required for epicardial and pro-epicardial development by mediating FGF receptor trafficking to the plasma membrane

Zhao

Qureshi

et al. 2017

Journal of Cell Science

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The epicardium contributes to multiple cardiac lineages and is essential for cardiac development and regeneration. However, the mechanism of epicardium formation is unclear. This study aimed to establish the cellular and molecular mechanisms underlying the dissociation of pro-epicardial cells (PECs) from the pro-epicardium (PE) and their subsequent translocation to the heart to form the epicardium. We used lineage tracing, conditional deletion, mosaic analysis and ligand stimulation in mice to determine that both villous protrusions and floating cysts contribute to PEC translocation to myocardium in a CDC42-dependent manner. We resolved a controversy by demonstrating that physical contact of the PE with the myocardium constitutes a third mechanism for PEC translocation to myocardium, and observed a fourth mechanism in which PECs migrate along the surface of the inflow tract to reach the ventricles. Epicardial-specific Cdc42 deletion disrupted epicardium formation, and Cdc42 null PECs proliferated less, lost polarity and failed to form villous protrusions and floating cysts. FGF signaling promotes epicardium formation in vivo, and biochemical studies demonstrated that CDC42 is involved in the trafficking of FGF receptors to the cell membrane to regulate epicardium formation.

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Section: Cdc42 Might Regulate Cellular Component Trafficking During Psupporting

confidence: 92%

CDC42 is required for epicardial and pro-epicardial development by mediating FGF receptor trafficking to the plasma membrane

Zhao

Qureshi

et al. 2017

Journal of Cell Science

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“…PKCζ phosphorylates PARD3 of the PAR complex. CDC42, an important small G protein in the apicobasal polarity signaling network, may be involved in Golgi vesicular transport [23][24][25][26][27] . Interestingly, the binding of atypical PKCζ with polar lipids such as ceramide can regulate cell polarity 28,29 .…”

mentioning

confidence: 99%

Primary cilia control cell alignment and patterning in bone development via ceramide-PKCζ-β-catenin signaling

Lim

Yuan

et al. 2020

Commun Biol

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Intraflagellar transport (IFT) proteins are essential for cilia assembly and function. IFT protein mutations lead to ciliopathies, which manifest as variable skeletal abnormalities. However, how IFT proteins regulate cell alignment during bone development is unknown. Here, we show that the deletion of IFT20 in osteoblast lineage using Osterix-Cre and inducible type I Collagen-CreERT cause a compromised cell alignment and a reduced bone mass. This finding was validated by the disorganized collagen fibrils and decreased bone strength and stiffness in IFT20-deficient femurs. IFT20 maintains cilia and cell alignment in osteoblasts, as the concentric organization of three-dimensional spheroids was disrupted by IFT20 deletion. Mechanistically, IFT20 interacts with the ceramide-PKCζ complex to promote PKCζ phosphorylation in cilia and induce the apical localization of β-catenin in osteoblasts, both of which were disrupted in the absence of IFT20. These results reveal that IFT20 regulates polarity and cell alignment via ceramide-pPKCζ-β-catenin signaling during bone development.

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“…Cdc42 controls multiple steps in these processes, including the exit of basolateral proteins from the TGN and the targeting of exocytic vesicles . Therefore, activation of Cdc42 at AJ may aid the exocytosis of claudins.…”

Section: Aj Provide a Platform For Traffickingmentioning

confidence: 99%

Cell Adhesion Structures in Epithelial Cells Are Formed in Dynamic and Cooperative Ways

Shigetomi

Ikenouchi

2019

BioEssays

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There are many morphologically distinct membrane structures with different functions at the surface of epithelial cells. Among these, adherens junctions (AJ) and tight junctions (TJ) are responsible for the mechanical linkage of epithelial cells and epithelial barrier function, respectively. In the process of new cell-cell adhesion formation between two epithelial cells, such as after wounding, AJ form first and then TJ form on the apical side of AJ. This process is very complicated because AJ formation triggers drastic changes in the organization of actin cytoskeleton, the activity of Rho family of small GTPases, and the lipid composition of the plasma membrane, all of which are required for subsequent TJ formation. In this review, the authors focus on the relationship between AJ and TJ as a representative example of specialization of plasma membrane regions and introduce recent findings on how AJ formation promotes the subsequent formation of TJ. Figure 6. Addition of cholesterol restores the formation of TJ in α-catenin KO cells. Time-lapse imaging of α-catenin KO epithelial cells expressing GFP-claudin-3. Cholesterol-saturated MβCD (75 mM) was added to the medium to restore the level of cholesterol in the plasma membrane at time 0. GFP-claudin-3 gradually accumulate at the cell-cell interface and TJ is formed even in the absence of AJ. Scale bar, 20 µm. Adapted with permission. [72]

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Cdc42 and Cellular Polarity: Emerging Roles at the Golgi

Cited by 74 publications

References 45 publications

CDC42 is required for epicardial and pro-epicardial development by mediating FGF receptor trafficking to the plasma membrane

CDC42 is required for epicardial and pro-epicardial development by mediating FGF receptor trafficking to the plasma membrane

Primary cilia control cell alignment and patterning in bone development via ceramide-PKCζ-β-catenin signaling

Cell Adhesion Structures in Epithelial Cells Are Formed in Dynamic and Cooperative Ways

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