Figure 1.

Differential activation of Cdc42 and Rac1 by Salmonella effector proteins in vivo. (A) COS-2 cells were infected with wild-type (WT) S. typhimurium or its isogenic type III secretion-defective invA mutant (defective in its ability to induce actin cytoskeleton rearrangements and bacterial uptake; Galán et al., 1992) for the indicated times (in minutes), and the relative levels of activated Rac1 or Cdc42 were determined by the amount bound to GST-PAK-CRIB. Activated GTPase levels were normalized to the amount of total Rac1 or Cdc42 in cell lysates as analyzed by Western blotting. The intensity of the bands was quantified using ImageJ software. Values are the mean ± SD (error bars) of three independent experiments normalized to the response of cells infected with the invA mutant. (B) COS-2 cells were infected with different mutant strains of S. typhimurium (as indicated), and, 20 min after infection, the relative levels of activated Rac1 or Cdc42 were determined as indicated in A. Values are the mean ± SD of three independent experiments.