Figure 5. ExoS ADP‐ribosyltransferase activity inhibited autophagy and mTOR signaling pathway.

• A, F
  A549 cells were infected for 4 h with ExoS‐deficient P. aeruginosa (ΔS), ExoS‐containing P. aeruginosa (S^WT), P. aeruginosa containing ExoS with loss‐of‐function mutations in the GTPase‐activating domain (S^G−A+), in the ADP ribosylation domain (S^G+A−), or in both domains (S^G−A−). Cell lysates were evaluated by immunoblotting.
• B
  A549 cells were transfected, for 24 h, with a plasmid expressing empty vector (EV), WT GFP‐ExoS, a GFP‐ExoS mutant for ADPRT domain (S^G+A−) or a GFP‐ExoS mutant deficient in both GAP and ADPRT domains (S^G−A−). Cell lysates were evaluated by immunoblotting.
• C
  A549 cells were treated for 24 h with 100 µM of the ADPRT activity inhibitor MIBG and then left uninfected (NI) or infected with P. aeruginosa containing ExoS with ADPRT activity only (S^G−A+). Cell lysates were evaluated by immunoblotting.
• D, E
  A549 cells were infected for 4 h with WT or P. aeruginosa mutants (ΔpscD, ΔSTY, ΔS, and ΔTY). Cell lysates were evaluated by immunoblotting.

Source data are available online for this figure.