Supplementary Materials

The PDF file includes:

• Fig. S1. ACD-induced activation of Rac1 is abolished when delivered with RID on the wild-type toxin.
• Fig. S2. ACD-induced phosphorylation of ERK, p38, and JNK is suppressed when codelivered with RID and ABH.
• Fig. S3. Schematic of single and double catalytically active MARTX_Vc toxin effector strains and triple inactive MARTX_Vc toxin effector strain.
• Fig. S4. Actin laddering in HeLa cells treated with V. cholerae.
• Fig. S5. ABH-mediated inhibition of host response to ACD varies across independent experiments.
• Fig. S6. Both RID and ABH suppress ACD-induced phosphorylation of ERK, p38, and JNK MAPK pathways.
• Fig. S7. Actin cross-linking in cells harvested in Triton X-100 lysis buffer.
• Fig. S8. MAPK activation in response to the Triple* MARTX_Vc toxin effector strain.
• Fig. S9. RID and ABH block MAPK signaling without modulating ACD activity.
• Legends for tables S1 and S2
• Table S3. Bacterial strains and plasmids used in this study.
• Table S4. Sequences of gBlocks used in this study.
• Table S5. Primers used in this study.

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Other Supplementary Material for this manuscript includes the following:

• Table S1 (Microsoft Excel format). MARTX effector–dependent transcriptional responses in V. cholerae–infected T84 cells.
• Table S2 (Microsoft Excel format). ACD-dependent transcriptional responses in V. cholerae–infected T84 cells.