Dynamic trafficking and turnover of JAM-C is essential for endothelial cell migration
Identifieur interne : 000C68 ( Ncbi/Checkpoint ); précédent : 000C67; suivant : 000C69Dynamic trafficking and turnover of JAM-C is essential for endothelial cell migration
Auteurs : Katja B. Kostelnik [Royaume-Uni] ; Amy Barker [Royaume-Uni] ; Christopher Schultz [Royaume-Uni] ; Tom P. Mitchell [Royaume-Uni] ; Vinothini Rajeeve [Royaume-Uni] ; Ian J. White [Royaume-Uni] ; Michel Aurrand-Lions [France] ; Sussan Nourshargh [Royaume-Uni] ; Pedro Cutillas [Royaume-Uni] ; Thomas D. Nightingale [Royaume-Uni]Source :
- PLoS Biology [ 1544-9173 ] ; 2019.
Abstract
Junctional complexes between endothelial cells form a dynamic barrier that hinders passive diffusion of blood constituents into interstitial tissues. Remodelling of junctions is an essential process during leukocyte trafficking, vascular permeability, and angiogenesis. However, for many junctional proteins, the mechanisms of junctional remodelling have yet to be determined. Here, we used receptor mutagenesis, horseradish peroxidase (HRP), and ascorbate peroxidase 2 (APEX-2) proximity labelling, alongside light and electron microscopy (EM), to map the intracellular trafficking routes of junctional adhesion molecule-C (JAM-C). We found that JAM-C cotraffics with receptors associated with changes in permeability such as vascular endothelial cadherin (VE-Cadherin) and neuropilin (NRP)-1 and 2, but not with junctional proteins associated with the transmigration of leukocytes. Dynamic JAM-C trafficking and degradation are necessary for junctional remodelling during cell migration and angiogenesis. By identifying new potential trafficking machinery, we show that a key point of regulation is the ubiquitylation of JAM-C by the E3 ligase Casitas B-lineage lymphoma (CBL), which controls the rate of trafficking versus lysosomal degradation.
Url:
DOI: 10.1371/journal.pbio.3000554
PubMed: 31790392
PubMed Central: 6907879
Affiliations:
- France, Royaume-Uni
- Angleterre, Grand Londres, Provence-Alpes-Côte d'Azur
- Londres, Marseille
- University College de Londres, Université de Londres
Links toward previous steps (curation, corpus...)
- to stream Pmc, to step Corpus: 000767
- to stream Pmc, to step Curation: 000767
- to stream Pmc, to step Checkpoint: 000808
- to stream Ncbi, to step Merge: 000C68
- to stream Ncbi, to step Curation: 000C68
Links to Exploration step
PMC:6907879Le document en format XML
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<front><div type="abstract" xml:lang="en"><p>Junctional complexes between endothelial cells form a dynamic barrier that hinders passive diffusion of blood constituents into interstitial tissues. Remodelling of junctions is an essential process during leukocyte trafficking, vascular permeability, and angiogenesis. However, for many junctional proteins, the mechanisms of junctional remodelling have yet to be determined. Here, we used receptor mutagenesis, horseradish peroxidase (HRP), and ascorbate peroxidase 2 (APEX-2) proximity labelling, alongside light and electron microscopy (EM), to map the intracellular trafficking routes of junctional adhesion molecule-C (JAM-C). We found that JAM-C cotraffics with receptors associated with changes in permeability such as vascular endothelial cadherin (VE-Cadherin) and neuropilin (NRP)-1 and 2, but not with junctional proteins associated with the transmigration of leukocytes. Dynamic JAM-C trafficking and degradation are necessary for junctional remodelling during cell migration and angiogenesis. By identifying new potential trafficking machinery, we show that a key point of regulation is the ubiquitylation of JAM-C by the E3 ligase Casitas B-lineage lymphoma (CBL), which controls the rate of trafficking versus lysosomal degradation.</p>
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</TEI>
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<li>Royaume-Uni</li>
</country>
<region><li>Angleterre</li>
<li>Grand Londres</li>
<li>Provence-Alpes-Côte d'Azur</li>
</region>
<settlement><li>Londres</li>
<li>Marseille</li>
</settlement>
<orgName><li>University College de Londres</li>
<li>Université de Londres</li>
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