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 MARTXVc toxin effector strains and triple inactive MARTXVc 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* MARTXVc 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.
Other Supplementary Material for this manuscript includes the following: