Par3 interacts with Prickle3 to generate apical PCP complexes in the vertebrate neural plate

Chuykin, Ilya; Ossipova, Olga; Sokol, Sergei Y.

doi:10.7554/elife.37881

Cited by 35 publications

(28 citation statements)

References 91 publications

(150 reference statements)

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“…In addition, assessment for specificity by a rescue strategy of the Par3MO is not possible because expression of Par3 alone also leads to apicobasal defects (Afonso and Henrique, 2006). The mild effects observed after Par3MO electroporation are in line with Par3 lossof-function data published elsewhere (Chuykin et al, 2018), suggesting that the knockdown is efficient; however, readers may decide to ignore these data due to the lack of formal validation of Par3MO.…”

Section: Overexpression Of Mmp14 Is Sufficient To Promote Basal Mitosmentioning

confidence: 81%

MMP14 is required for delamination of chick neural crest cells independently of its catalytic activity

et al. 2020

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Matrix metalloproteinases have a broad spectrum of substrates ranging from extracellular matrix components and adhesion molecules to chemokines and growth factors. Despite being mostly secreted, MMPs have been detected in the cytosol, the mitochondria or the nucleus. Although most of the attention is focused on their role in matrix remodeling, the diversity of their substrates and their complex trafficking open the possibility for non-canonical functions. Yet in vivo examples and experimental demonstration of the physiological relevance of such activities are rare. Here, we have used chick neural crest (NC) cells, a highly migratory stem cell population likened to invasive cancer cells, as a model for physiological epithelialmesenchymal transition (EMT). We demonstrate that MMP14 is required for NC delamination. Interestingly, this role is independent of its cytoplasmic tail and of its catalytic activity. Our in vivo data indicate that, in addition to being a late pro-invasive factor, MMP14 is also likely to be an early player, owing to its role in EMT.

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Section: Overexpression Of Mmp14 Is Sufficient To Promote Basal Mitosmentioning

confidence: 81%

MMP14 is required for delamination of chick neural crest cells independently of its catalytic activity

et al. 2020

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“…During mouse inner ear development, Par3 is asymmetrically localized in dependence on canonical PCP and Rac signaling but independently of Par6 and aPKC, moreover, it does not control spindle positioning through LGN/Gαi (Landin Malt et al, 2019). Interestingly, it has also been recently shown that Par3 might have an instructive role in PCP by direct binding to the core canonical PCP component Prickle3 during establishment of PCP in the Xenopus neural plate (Chuykin et al, 2018). On the other hand, Par3-dependent apicobasal polarity seems to be required to set up PCP in avian embryos (Lin and Yue, 2018).…”

Section: Discussionmentioning

confidence: 99%

Planar Asymmetries in the C. elegans Embryo Emerge by Differential Retention of aPARs at Cell-Cell Contacts

Dutta

Odedra

Pohl

2019

Front. Cell Dev. Biol.

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Formation of the anteroposterior and dorsoventral body axis in Caenorhabditis elegans depends on cortical flows and advection of polarity determinants. The role of this patterning mechanism in tissue polarization after formation of cell-cell contacts is not fully understood. Here, we demonstrate that planar asymmetries are established during left-right symmetry breaking: Centripetal cortical flows asymmetrically and differentially advect anterior polarity determinants (aPARs) from contacts to the medial cortex, resulting in their unmixing from apical myosin. Contact localization and advection of PAR-6 requires balanced CDC-42 activation, while asymmetric retention and advection of PAR-3 can occur independently of PAR-6. Concurrent asymmetric retention of PAR-3, E-cadherin/HMR-1 and opposing retention of antagonistic CDC-42 and Wnt pathway components leads to planar asymmetries. The most obvious mark of planar asymmetry, retention of PAR-3 at a single cell-cell contact, is required for proper cytokinetic cell intercalation. Hence, our data uncover how planar polarity is established in a system without the canonical planar cell polarity pathway through planar asymmetric retention of aPARs.

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“…Phosphorylated, "active" myosin-II is primarily localised to these cell borders. A large body of work in Xenopus demonstrates that the apical determinant Par3 physically associates with PCP components to localise them at the apical surface 80 where they reside preferentially at contractile cell-cell junctions 81 .…”

Section: Discussionmentioning

confidence: 99%

Cell non-autonomy amplifies disruption of neurulation by mosaic Vangl2 deletion

Galea

Maniou

Marshall

et al. 2020

Preprint

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Post-zygotic mutations that generate tissue mosaicism are increasingly associated with severe congenital defects, including those arising from failed neural tube closure. We observed that elevation of the neural folds during mouse spinal neurulation is vulnerable to deletion of the planar cell polarity core component Van Gogh-like (Vangl)2 in as few as 16% of neuroepithelial cells. Vangl2-deleted cells are typically dispersed throughout the neuroepithelium, and each non-autonomously prevents apical constriction by an average of five Vangl2-replete neighbours. This inhibition of apical constriction involves reduced myosin-II recruitment to neighbour cell borders and shortening of basally-extending microtubule tails, which are known to facilitate apical constriction. Vangl2-deleted cells themselves continue to apically constrict and preferentially recruit myosin-II to their apical cell cortex rather than to apical cap sarcomere-like organisations. Such non-autonomous effects can explain how post-zygotic mutations affecting a minority of cells can cause catastrophic failure of morphogenesis leading to clinically important birth defects.

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Par3 interacts with Prickle3 to generate apical PCP complexes in the vertebrate neural plate

Cited by 35 publications

References 91 publications

MMP14 is required for delamination of chick neural crest cells independently of its catalytic activity

MMP14 is required for delamination of chick neural crest cells independently of its catalytic activity

Planar Asymmetries in the C. elegans Embryo Emerge by Differential Retention of aPARs at Cell-Cell Contacts

Cell non-autonomy amplifies disruption of neurulation by mosaic Vangl2 deletion

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