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ZO-1 controls endothelial adherens junctions, cell-cell tension, angiogenesis, and barrier formation.

Tornavaca O, Chia M, Dufton N, Almagro LO, Conway DE, Randi AM, Schwartz MA, Matter K, Balda MS - J. Cell Biol. (2015)

Bottom Line: ZO-1 depletion led to tight junction disruption, redistribution of active myosin II from junctions to stress fibers, reduced tension on VE-cadherin and loss of junctional mechanotransducers such as vinculin and PAK2, and induced vinculin dissociation from the α-catenin-VE-cadherin complex.Claudin-5 depletion only mimicked ZO-1 effects on barrier formation, whereas the effects on mechanotransducers were rescued by inhibition of ROCK and phenocopied by JAM-A, JACOP, or p114RhoGEF down-regulation.ZO-1 was required for junctional recruitment of JACOP, which, in turn, recruited p114RhoGEF.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Cell Biology, UCL Institute of Ophthalmology, University College London, London EC1V 9EL, England, UK.

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JAM-A down-regulation redistributes ZO-1 and claudin-5, and induces focal adhesions. (A and C) Cells transfected with control or JAM-A siRNAs were analyzed by immunofluorescence for the indicated proteins. (B) Equivalent samples were analyzed by expression of the indicated proteins by immunoblotting. Results shown are representative from three duplicate experiments performed. Bars, 30 µm.
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fig5: JAM-A down-regulation redistributes ZO-1 and claudin-5, and induces focal adhesions. (A and C) Cells transfected with control or JAM-A siRNAs were analyzed by immunofluorescence for the indicated proteins. (B) Equivalent samples were analyzed by expression of the indicated proteins by immunoblotting. Results shown are representative from three duplicate experiments performed. Bars, 30 µm.

Mentions: JAM-A was efficiently depleted by two siRNAs and affected the localization of claudin-5 and ZO-1, but not VE-cadherin (Fig. 5). Hence, JAM-A and ZO-1 appear to be linked in a bidirectional, cooperative manner, as each influenced the other’s distribution and both were required for claudin-5 localization at tight junctions. Reduced expression of JAM-A induced redistribution of PAK2 and vinculin from cell contacts to focal adhesions and induction of stress fibers (Fig. 5 C). ZO-1 and JAM-A therefore form a functional unit that regulates tight junction assembly and cytoskeletal organization.


ZO-1 controls endothelial adherens junctions, cell-cell tension, angiogenesis, and barrier formation.

Tornavaca O, Chia M, Dufton N, Almagro LO, Conway DE, Randi AM, Schwartz MA, Matter K, Balda MS - J. Cell Biol. (2015)

JAM-A down-regulation redistributes ZO-1 and claudin-5, and induces focal adhesions. (A and C) Cells transfected with control or JAM-A siRNAs were analyzed by immunofluorescence for the indicated proteins. (B) Equivalent samples were analyzed by expression of the indicated proteins by immunoblotting. Results shown are representative from three duplicate experiments performed. Bars, 30 µm.
© Copyright Policy - openaccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4362456&req=5

fig5: JAM-A down-regulation redistributes ZO-1 and claudin-5, and induces focal adhesions. (A and C) Cells transfected with control or JAM-A siRNAs were analyzed by immunofluorescence for the indicated proteins. (B) Equivalent samples were analyzed by expression of the indicated proteins by immunoblotting. Results shown are representative from three duplicate experiments performed. Bars, 30 µm.
Mentions: JAM-A was efficiently depleted by two siRNAs and affected the localization of claudin-5 and ZO-1, but not VE-cadherin (Fig. 5). Hence, JAM-A and ZO-1 appear to be linked in a bidirectional, cooperative manner, as each influenced the other’s distribution and both were required for claudin-5 localization at tight junctions. Reduced expression of JAM-A induced redistribution of PAK2 and vinculin from cell contacts to focal adhesions and induction of stress fibers (Fig. 5 C). ZO-1 and JAM-A therefore form a functional unit that regulates tight junction assembly and cytoskeletal organization.

Bottom Line: ZO-1 depletion led to tight junction disruption, redistribution of active myosin II from junctions to stress fibers, reduced tension on VE-cadherin and loss of junctional mechanotransducers such as vinculin and PAK2, and induced vinculin dissociation from the α-catenin-VE-cadherin complex.Claudin-5 depletion only mimicked ZO-1 effects on barrier formation, whereas the effects on mechanotransducers were rescued by inhibition of ROCK and phenocopied by JAM-A, JACOP, or p114RhoGEF down-regulation.ZO-1 was required for junctional recruitment of JACOP, which, in turn, recruited p114RhoGEF.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Cell Biology, UCL Institute of Ophthalmology, University College London, London EC1V 9EL, England, UK.

Show MeSH
Related in: MedlinePlus