Polarity and endocytosis: reciprocal regulation

Shivas, Jessica M.; Morrison, Holly A.; Bilder, David; Skop, Ahna R.

doi:10.1016/j.tcb.2010.04.003

Cited by 99 publications

(100 citation statements)

References 63 publications

(74 reference statements)

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“…It might function in regulating vesicle trafficking or protein targeting, as reported in yeasts (Efe et al, 2005;Gillingham et al, 2006;Jochum et al, 2002;Singer-Krüger et al, 2008;Wicky et al, 2004). As vesicle trafficking is often linked with establishing and maintaining cell polarity (Gould and Lippincott-Schwartz, 2009;Shivas et al, 2010), it is an attractive idea that Mon2 might regulate the polarity protein localization and/or mediate the signal transduction for cell polarization in somatic cells, as well as in germ cells. Supporting this idea, a Mon2 homolog in C. elegans has been implicated in the asymmetric division of epithelial stem cells (Kanamori et al, 2008).…”

Section: Mon2 Couples Endocytic Activity With Cortical Actin Remodelingmentioning

confidence: 96%

DrosophilaMon2 couples Oskar-induced endocytosis with actin remodeling for cortical anchorage of the germ plasm

Tanaka¹,

Kato²,

Matsuda³

et al. 2011

Development

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SUMMARYDrosophila pole (germ) plasm contains germline and abdominal determinants. Its assembly begins with the localization and translation of oskar (osk) RNA at the oocyte posterior, to which the pole plasm must be restricted for proper embryonic development. Osk stimulates endocytosis, which in turn promotes actin remodeling to form long F-actin projections at the oocyte posterior pole. Although the endocytosis-coupled actin remodeling appears to be crucial for the pole plasm anchoring, the mechanism linking Osk-induced endocytic activity and actin remodeling is unknown. Here, we report that a Golgi-endosomal protein, Mon2, acts downstream of Osk to remodel cortical actin and to anchor the pole plasm. Mon2 interacts with two actin nucleators known to be involved in osk RNA localization in the oocyte, Cappuccino (Capu) and Spire (Spir), and promotes the accumulation of the small GTPase Rho1 at the oocyte posterior. We also found that these actin regulators are required for Oskdependent formation of long F-actin projections and cortical anchoring of pole plasm components. We propose that, in response to the Osk-mediated endocytic activation, vesicle-localized Mon2 acts as a scaffold that instructs the actin-remodeling complex to form long F-actin projections. This Mon2-mediated coupling event is crucial to restrict the pole plasm to the oocyte posterior cortex.

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Section: Mon2 Couples Endocytic Activity With Cortical Actin Remodelingmentioning

confidence: 96%

DrosophilaMon2 couples Oskar-induced endocytosis with actin remodeling for cortical anchorage of the germ plasm

Tanaka¹,

Kato²,

Matsuda³

et al. 2011

Development

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“…Much of the connection between cell competition and tumour development comes from studies on a group of Drosophila tumour suppressor genes. Some of them (lethal giant larvae (lgl), scribble (scrib) and disc large (dlg)) affect the apico-basal polarity of epithelial cells (Assemat et al, 2008, Tepass et al, 2001, while others like Vps25, Rab5 or avalanche are components of the endosomal trafficking machinery (Shivas et al, 2010).…”

Section: Cell Competition As a Tumour Suppressor Mechanism In Drosophilamentioning

confidence: 99%

Cell competition, apoptosis and tumour development

Morata

Ballesteros-Arias²

2015

Int. J. Dev. Biol.

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The phenomenon of cell competition is an interactive process originally discovered in the imaginal discs of Drosophila; it is a developmental mechanism that identifies and eliminates cells that are weaker than their neighbours or have features that make them different or not well adapted to their surroundings. It appears to be an important homeostatic mechanism to contribute to the general fitness of developing tissues. Here we discuss some of the basic features of cell competition and then focus on results indicating that cell competition is responsible for the removal of malignant or aberrant cells that may appear during development, although in certain circumstances it can revert its role to promote tumour growth. We also consider several recent studies that indicate that cell competition also occurs in vertebrates where it performs similar functions.

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“…PAR1 (negatively regulated by aPKC) acts on the E3 ubiquitin ligase Mindbomb to regulate Notch ligands in the signal-sending cells. Polarity proteins are key regulators of endocytic trafficking [28,41], and can function to segregate proteins to the apical or basal side through regulation of intracellular trafficking [42].…”

Section: Introductionmentioning

confidence: 99%

PKCζ regulates Notch receptor routing and activity in a Notch signaling-dependent manner

et al. 2014

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Activation of Notch signaling requires intracellular routing of the receptor, but the mechanisms controlling the distinct steps in the routing process is poorly understood. We identify PKCζ as a key regulator of Notch receptor intracellular routing. When PKCζ was inhibited in the developing chick central nervous system and in cultured myoblasts, Notch-stimulated cells were allowed to undergo differentiation. PKCζ phosphorylates membrane-tethered forms of Notch and regulates two distinct routing steps, depending on the Notch activation state. When Notch is activated, PKCζ promotes re-localization of Notch from late endosomes to the nucleus and enhances production of the Notch intracellular domain, which leads to increased Notch activity. In the non-activated state, PKCζ instead facilitates Notch receptor internalization, accompanied with increased ubiquitylation and interaction with the endosomal sorting protein Hrs. Collectively, these data identify PKCζ as a key regulator of Notch trafficking and demonstrate that distinct steps in intracellular routing are differentially modulated depending on Notch signaling status.

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Polarity and endocytosis: reciprocal regulation

Cited by 99 publications

References 63 publications

DrosophilaMon2 couples Oskar-induced endocytosis with actin remodeling for cortical anchorage of the germ plasm

DrosophilaMon2 couples Oskar-induced endocytosis with actin remodeling for cortical anchorage of the germ plasm

Cell competition, apoptosis and tumour development

PKCζ regulates Notch receptor routing and activity in a Notch signaling-dependent manner

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