The cell biology of planar cell polarity

Devenport, Danelle

doi:10.1083/jcb.201408039

Cited by 273 publications

(319 citation statements)

References 94 publications

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“…The exact reason is not known currently, but one possibility is that MEF migration is less dependent on Prickle1 than MKN1 cell migration, and that Prickle1 haploinsufficiency results in the inhibition of migration to a similar level to Prickle1 homozygous knockout. Although Prickle1 is considered to be one of the proteins that regulates the PCP pathway (Devenport, 2014;Gray et al, 2011;Singh and Mlodzik, 2012;Veeman et al, 2003a), our results show that Prickle1 localization close to focal adhesions does not depend on Dvls, Wnt or Vangl1 and Vangl2. Therefore, the regulation of focal adhesion turnover would be a new function of Prickle1, independent of the Wnt and PCP pathway.…”

Section: Discussionsupporting

confidence: 51%

“…Loss of Prickle results in phenotypes affecting the stereotypical arrangement of sensory bristles and cellular hairs on the wing, abdomen and thorax, as well as ommatidia in the eye. These are similar to phenotypes resulting from loss of dishevelled (Dsh) and frizzled (fz), which are also known to encode core PCP proteins (Devenport, 2014;Veeman et al, 2003a;Yang and Mlodzik, 2015). In addition to these genes, flamingo (Fmi), Strabismus (Stbm) and Diego (Dgo) are required for acquisition of epithelial polarity in the Drosophila eye, wing and epidermis.…”

Section: Introductionmentioning

confidence: 77%

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Prickle1 promotes focal adhesion disassembly in cooperation with CLASP-LL5β complex in migrating cells

Lim

Matsumoto

Yamamoto

et al. 2016

Journal of Cell Science

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Prickle is known to be involved in planar cell polarity, including convergent extension and cell migration; however, the detailed mechanism by which Prickle regulates cellular functions is not well understood. Here, we show that Prickle1 regulates front-rear polarization and migration of gastric cancer MKN1 cells. Prickle1 preferentially accumulated at the cell retraction site in close proximity to paxillin at focal adhesions. Prickle1 dynamics correlated with those of paxillin during focal adhesion disassembly. Furthermore, Prickle1 was required for focal adhesion disassembly. CLASPs (of which there are two isoforms, CLASP1 and CLASP2, in mammals) and LL5β (also known as PHLDB2) have been reported to form a complex at cell edges and to control microtubule-dependent focal adhesion disassembly. Prickle1 was associated with CLASPs and LL5β, and was required for the LL5β-dependent accumulation of CLASPs at the cell edge. Knockdown of CLASPs and LL5β suppressed Prickle1-dependent cell polarization and migration. Prickle1 localized to the membrane through its farnesyl moiety, and the membrane localization was necessary for Prickle1 to regulate migration, to bind to CLASPs and LL5β, and to promote microtubule targeting of focal adhesions. Taken together, these results suggest that Prickle1 promotes focal adhesion disassembly during the retraction processes of cell polarization and migration.

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Section: Discussionsupporting

confidence: 51%

Section: Introductionmentioning

confidence: 77%

Prickle1 promotes focal adhesion disassembly in cooperation with CLASP-LL5β complex in migrating cells

Lim

Matsumoto

Yamamoto

et al. 2016

Journal of Cell Science

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“…This type of organization is typified in the fly wing, where bristles point in a common direction (Devenport, 2014). Two systems for planar polarity have been described: the core planar cell polarity (PCP) pathway and the Fat/Dachsous system (Sopko and McNeill, 2009).…”

Section: Introductionmentioning

confidence: 99%

Fat3 and Ena/VASP proteins influence the emergence of asymmetric cell morphology in the developing retina

2016

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Neurons exhibit asymmetric morphologies throughout developmentfrom migration to the elaboration of axons and dendrites -that are correctly oriented for the flow of information. For instance, retinal amacrine cells migrate towards the inner plexiform layer (IPL) and then retract their trailing processes, thereby acquiring a unipolar morphology with a single dendritic arbor restricted to the IPL. Here, we provide evidence that the Fat-like cadherin Fat3 acts during multiple stages of amacrine cell development in mice to orient overall changes in cell shape towards the IPL. Using a time-lapse imaging assay, we found that developing amacrine cells are less directed towards the IPL in the absence of Fat3, during both migration and retraction. Consistent with its predicted role as a cell-surface receptor, Fat3 functions cell-autonomously and is able to influence the cytoskeleton directly through its intracellular domain, which can bind and localize Ena/VASP family actin regulators. Indeed, a change in Ena/VASP protein distribution is sufficient to recapitulate the Fat3 mutant amacrine cell phenotype. Thus, Fat-like proteins might control the polarized development of tissues by sculpting the cytoskeleton of individual cells.

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“…Another well-characterized example of a polarized epithelium is the mammalian intestine, which has a specialized apical surface with microvilli that maximize the absorptive functions of this organ (Saotome et al 2004). Since the PCP pathway is well described in other reviews, yet few studies address its role in pancreas development (Barrow 2006;Cortijo et al 2012;Devenport 2014;Karner et al 2006), we will focus here on the establishment of apical-basal polarity in the pre-pancreatic epithelium.…”

Section: Epithelial Cell Polaritymentioning

confidence: 99%

“…PCP refers to the orientation of cells along the axis of the tissue (perpendicular to the apical-basal axis) and has been shown to direct various cellular processes, including directed migration, convergent extension and oriented cell division (Devenport 2014;Karner et al 2009). Apical-basal polarity involves the establishment of different 'sides' of an epithelial sheet, each domain displaying a distinct molecular composition-as the plasma membrane has a different set of proteins targeted towards each domain-and functionality.…”

Section: Epithelial Cell Polaritymentioning

confidence: 99%

Progenitor Epithelium

Marty-Santos

Cleaver

2015

J Histochem Cytochem.

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SummaryInsulin-producing β cells within the vertebrate fetal pancreas acquire their fate in a step-wise manner. Whereas the intrinsic factors dictating the transcriptional or epigenetic status of pancreatic lineages have been intensely examined, less is known about cell-cell interactions that might constitute a niche for the developing β cell lineage. It is becoming increasingly clear that understanding and recapitulating these steps may instruct in vitro differentiation of embryonic stem cells and/or therapeutic regeneration. Indeed, directed differentiation techniques have improved since transitioning from 2D to 3D cultures, suggesting that the 3D microenvironment in which β cells are born is critical. However, to date, it remains unknown whether the changing architecture of the pancreatic epithelium impacts the fate of cells therein. An emerging challenge in the field is to elucidate how progenitors are allocated during key events, such as the stratification and subsequent resolution of the pre-pancreatic epithelium, as well as the formation of lumens and branches. Here, we assess the progenitor epithelium and examine how it might influence the emergence of pancreatic multipotent progenitors (MPCs), which give rise to β cells and other pancreatic lineages. (J Histochem Cytochem 63:559-574, 2015)

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The cell biology of planar cell polarity

Cited by 273 publications

References 94 publications

Prickle1 promotes focal adhesion disassembly in cooperation with CLASP-LL5β complex in migrating cells

Prickle1 promotes focal adhesion disassembly in cooperation with CLASP-LL5β complex in migrating cells

Fat3 and Ena/VASP proteins influence the emergence of asymmetric cell morphology in the developing retina

Progenitor Epithelium

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