Microtubules are required for the maintenance of planar cell polarity in monociliated floorplate cells

Mathewson, Andrew W.; Berman, Daniel; Moens, Cecilia B.

doi:10.1016/j.ydbio.2019.04.007

Cited by 10 publications

(19 citation statements)

References 84 publications

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“…However, whereas the primary function of microtubule tails in the bi-layered Xenopus neuroepithelium is believed to be cell elongation 90 , shortened tails in the pseudostrati ed epithelium of Cre;Fl/-embryos were not associated with apical-basal shortening. Our ndings are also in contrast to previous studies which implicate microtubule polymerisation in the establishment and maintenance of PCP component polarisation 50,91 . Molecular mechanisms underlying this seemingly bi-directional interaction are a matter for future work, but our ndings reveal a dynamic interplay between PCP, microtubules and actomyosin in the mammalian neuroepithelium.…”

Section: Resulting Apical Constriction Of Neuroepithelial Cells Requicontrasting

confidence: 99%

“…Stopping myosin activation, through expression of dominant negative Rock or constitutively active myosin phosphatase, prevents anterior localisation of Vangl2 in the apical surface of the Xenopus neuroepithelium 24 . Apical localisation of PCP components occurs through tra cking in vesicles along apicobasally-oriented microtubules in the zebra sh neuroepithelium 50 .…”

Section: Resulting Apical Constriction Of Neuroepithelial Cells Requimentioning

confidence: 99%

“…Cytoskeletal regulation by Vangl2/PCP signalling is well established in other contexts, and both actomyosin and microtubule changes may underlie differential apical constriction in the neuroepithelium following mosaic Vangl2 deletion [22][23][24]36,49,50 . Neuroepithelial cells assemble apical phosphorylated, active non-muscle myosin light chain-II around their cell cortex ( Figure 5A).…”

Section: Mosaic Vangl2 Deletion Alters the Actomyosin And Microtubulementioning

confidence: 99%

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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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Section: Resulting Apical Constriction Of Neuroepithelial Cells Requicontrasting

confidence: 99%

Section: Resulting Apical Constriction Of Neuroepithelial Cells Requimentioning

confidence: 99%

Section: Mosaic Vangl2 Deletion Alters the Actomyosin And Microtubulementioning

confidence: 99%

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

Galea

Maniou

Marshall

et al. 2020

Preprint

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“…Floor-plate polarization shows temporal progression but no spatial synchronization Posterior positioning of the BB in the zebrafish FP is visible as soon as 18 hours post-fertilization (hpf) ( 17 ) and is maintained at least until 72 hpf ( 21 ). From 24 hpf onward, coupled to posterior tilting of cilia, it is instrumental in propelling the cerebrospinal fluid in the spinal cord central canal ( 5 , 22 ).…”

Section: Resultsmentioning

confidence: 99%

Planar polarization of cilia in the zebrafish floor-plate involves Par3-mediated posterior localization of highly motile basal bodies

Donati

Schneider‐Maunoury

Vesque

2019

Preprint

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To produce a directional flow, ciliated epithelia display a uniform orientation of ciliary beating. Oriented beating requires planar cell polarity (PCP), which leads to planar orientation and asymmetric positioning of the ciliary basal body (BB) along the polarity axis. We took advantage of the polarized mono-ciliated epithelium of the embryonic zebrafish floor plate (FP) to investigate by live-imaging the dynamics and mechanisms of BB polarization. We showed that BBs, although bearing a cilium, were highly motile along the polarity axis, contacting either the anterior or posterior membranes, exclusively at the level of apical junctions positive for Par3. Par3 was posteriorly enriched before BB posterior positioning and FP polarization was disrupted upon Par3 overexpression. In the PCP mutant Vangl2, BBs showed poorly oriented movements correlated with Par3 mislocalization. Our data lead us to propose a conserved function for Par3 in controlling BB asymmetric positioning downstream of the PCP pathway.

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“…This signaling is performed by the Frizzled/Dishevelled/Flamingo/Diego and the Vang/Prickle/Flamingo complexes, with their Drosophila Planar Polarity Effector (PPE) and vertebrate Ciliogenesis and PLANar polarity Effector (CPLANE) [ 111 ]. The components of the signaling pathways are delivered to the cell edges via microtubules [ 112 , 113 ], which suggests a connection with the centrosome position [ 24 ]. Both signaling pathways affect the dynamics of actin and its location in cells and are mainly studied in relation to the polarized arrangement of hairs on the Drosophila wing cells [ 111 ].…”

Section: Molecular Mechanisms That Determine the Location Of Centrmentioning

confidence: 99%

Centering and Shifting of Centrosomes in Cells

Burakov

Nadezhdina

2020

Cells

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Centrosomes have a nonrandom localization in the cells: either they occupy the centroid of the zone free of the actomyosin cortex or they are shifted to the edge of the cell, where their presence is justified from a functional point of view, for example, to organize additional microtubules or primary cilia. This review discusses centrosome placement options in cultured and in situ cells. It has been proven that the central arrangement of centrosomes is due mainly to the pulling microtubules forces developed by dynein located on the cell cortex and intracellular vesicles. The pushing forces from dynamic microtubules and actomyosin also contribute, although the molecular mechanisms of their action have not yet been elucidated. Centrosomal displacement is caused by external cues, depending on signaling, and is drawn through the redistribution of dynein, the asymmetrization of microtubules through the capture of their plus ends, and the redistribution of actomyosin, which, in turn, is associated with basal-apical cell polarization.

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Microtubules are required for the maintenance of planar cell polarity in monociliated floorplate cells

Cited by 10 publications

References 84 publications

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

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

Planar polarization of cilia in the zebrafish floor-plate involves Par3-mediated posterior localization of highly motile basal bodies

Centering and Shifting of Centrosomes in Cells

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