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. 2017 Dec 12;6:e27444. doi: 10.7554/eLife.27444

Figure 7. Endogenous RhoGDIα and SUMO are localized at Shigella-induced actin foci.

(A) SUMO1 accumulates at Shigella (M90T) entry sites. Representative ApoTome-generated micrographs of Shigella-infected Ubc9 WT or Ubc9 KO MEFs after 10 min infection. Samples were fixed and processed for immunostaining using anti-SUMO1 antibody (green) and staining of actin (red) and nuclei (blue) (white square, inset). (B) The Pearson’s coefficient (Rr) was used to measure the signal intensity correlation between SUMO1 and Shigella-induced actin foci stainings. Data are means ±SEM (at least 40 foci analyzed per condition). p value calculated as described in Materials and Methods. (C) SUMO2/3 accumulates at Shigella (M90T) entry sites. Same as in A using a SUMO2/3 antibody. (D) Same as in B with SUMO2/3 signal. (E) Recruitment of RhoGDIα is at Shigella (M90T) entry sites. Same as in A using a RhoGDIα antibody. (F) Same as in B with RhoGDIα signal. NS: non significant.

Figure 7—source data 1. Source data files relative to Figure 7B, D and F.
DOI: 10.7554/eLife.27444.020

Figure 7.

Figure 7—figure supplement 1. SUMO1 and SUMO2/3 accumulate at Shigella (M90T) entry site in Hela cells.

Figure 7—figure supplement 1.

Cells were infected with Shigella strain M90T for 10 min at 37°C. Samples were fixed and processed for immunostaining using anti-SUMO1 (green, upper panel) or anti-SUMO2/3 antibody (green, lower panel) and staining of actin (red) and nuclei (blue) (white square, inset). Representative ApoTome-generated micrographs are presented (white square, inset).