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First published online February 18, 2009


Journal of Cell Science 122, 503e (2009)
© The Company of Biologists Limited
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In this issue

Virulence via fine-tuning of RhoG


Figure 1

Yersinia bacteria, which cause various human illnesses, use many different mechanisms to subvert host-cell responses and propagate disease. The Rho family of GTPases is commonly targeted by invading pathogens, as these proteins mediate many essential cellular functions (such as cytoskeletal organisation). For example, Yersinia outer proteins (Yops) have been shown to modulate the Rho GTPases RhoA, Rac1 and Cdc42. Martin Aepfelbacher and colleagues (p. 696) now show that RhoG (which acts upstream of Rac1) is differentially activated in host cells over the course of an infection with Yersinia enterocolitica. During invasion, before Yops are translocated into host cells, the triggering of host-cell β1-integrin activation by the Yersinia protein invasin causes RhoG activation, which facilitates bacterial entry. Thereafter, YopE specifically inhibits the activity of RhoG, which leads to downstream inhibition of Rac1 activity. The authors go on to show that YopE can also inhibit Rac1 and Cdc42 directly, and that its substrate specificity is determined by its localisation in the Golgi and ER. This work reveals that RhoG is targeted by Yersinia virulence mechanisms, and that its activity is modulated by the bacteria and depends on the stage of infection.


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Related articles in JCS:

Yersinia enterocolitica differentially modulates RhoG activity in host cells
Bernhard Roppenser, Anja Röder, Moritz Hentschke, Klaus Ruckdeschel, and Martin Aepfelbacher
JCS 2009 122: 696-705. [Abstract] [Full Text]  




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