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ExlA induces disruption of cell-cell junctions

Published on 19 February 2020
ExlA+ strains induce a disruption of cell-cell junctions. Furthermore, E-cadherin at epithelial junctions and VE-cadherin at endothelial junctions, were missing after incubation with bacteria. We found that ADAM10, an eukaryotic transmembrane protease, whose natural substrates are the cadherins, is activated by ExlA. ExlA pore formation induces a calcium influx that triggers ADAM10 activation and export to the plasma membrane, where it cleaves the cadherins. 

Furthermore, our work demonstrates that ADAM10 is not the cellular receptor for ExlA and that calcium influx is also responsible for the cell death program induced by ExlA. In addition, we showed that the mechanism of ADAM10 activation/cadherin cleavage was similarly induced by ShlA, a pore-forming toxin secreted by Serratia marcescens, suggesting that this mechanism might be induced by several pore-forming toxins [13]

Reboud E. et al (2017) PLOS Pathogens

[13] Reboud et al (2017) PLoS pathogens 13(8):e1006579.,