In contrast, the E-cadherin patterns were still widely intact during infection with the HtrAHp double mutant H46A/D47A/K50A/D51A or HtrA/HtrAHpΔN2 deletion variant, respectively, suggesting an important role of amino-terminal HtrAHp cleavage at both sites on protease activity, and thus, on damaging cell-to-cell junctions (Figures 4G,H). Here, CDH1 is linked to infection.