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Maintaining Virulence
Agrobacterium tumefaciens is a bacterial pathogen that genetically transforms its hosts, which include several commercially important plants such as grapevines and roses, and induces neoplastic growths termed crown galls (tumors). Agrobacterium-induced genetic transformation and tumorigenesis require the integration of a bacterial DNA molecule into the host genome, a process that involves the virulence factor VirF, an F-box protein that is incorporated into the host cell machinery that targets proteins for degradation. Many F-box proteins, including VirF, are themselves unstable and become degraded, leading Magori and Citovsky to investigate how Agrobacterium stabilizes VirF. They found that VirD5, another effector protein produced by Agrobacterium, associated with VirF and prevented its degradation. Indeed, a strain of Agrobacterium lacking VirD5 formed fewer tumors on tomato plants than did a wild-type strain with VirD5. These findings suggest a general strategy by which other pathogens may stabilize their F-box effector proteins in infected cells.
Abstract
The SCF (Skp1–Cul1–F-box protein) ubiquitin ligase complex plays a pivotal role in various biological processes, including host-pathogen interactions. Many pathogens exploit the host SCF machinery to promote efficient infection by translocating pathogen-encoded F-box proteins into the host cell. How pathogens ensure sufficient amounts of the F-box effectors in the host cell despite the intrinsically unstable nature of F-box proteins, however, remains unclear. We found that the Agrobacterium F-box protein VirF, an important virulence factor, undergoes rapid degradation through the host proteasome pathway. This destabilization of VirF was counteracted by VirD5, another bacterial effector that physically associated with VirF. These observations reveal a previously unknown counterdefense strategy used by pathogens against potential host antimicrobial responses.
