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• W2000313986 abstract "During infection the food-borne pathogen Listeria monocytogenes exploits a large number of the host cell's functions including post-translational modifications involving ubiquitinylation and phosphorylation, which specifically modify the activity of key proteins. The effects of pathogenic bacteria on the ubiquitin-like modification known as SUMOylation, an essential process in eukaryotic cells, remain largely unknown. Now a study in L. monocytogenes-infected human cells and in a mouse model shows that its virulence factor, listeriolysin O (LLO), induces a decrease in the levels of cellular SUMOylated proteins by triggering degradation of Ubc9, an essential enzyme of the SUMOylation machinery. This work suggests that Listeria — and probably other pathogens too — dampens the host response to infection by decreasing the SUMOylation level of key regulatory proteins. SUMOylation is a post-translational protein modification that affects many eukaryotic cellular processes. It is shown here that cellular infection with Listeria monocytogenes induces degradation of one of the essential SUMOylation enzymes, Ubc9, through a mechanism that involves a bacterial toxin, listeriolysin O. This effect on SUMOylation may support efficient infection by Listeria. During infection, pathogenic bacteria manipulate the host cell in various ways to allow their own replication, propagation and escape from host immune responses. Post-translational modifications are unique mechanisms that allow cells to rapidly, locally and specifically modify activity or interactions of key proteins. Some of these modifications, including phosphorylation and ubiquitylation1,2, can be induced by pathogens. However, the effects of pathogenic bacteria on SUMOylation, an essential post-translational modification in eukaryotic cells3, remain largely unknown. Here we show that infection with Listeria monocytogenes leads to a decrease in the levels of cellular SUMO-conjugated proteins. This event is triggered by the bacterial virulence factor listeriolysin O (LLO), which induces a proteasome-independent degradation of Ubc9, an essential enzyme of the SUMOylation machinery, and a proteasome-dependent degradation of some SUMOylated proteins. The effect of LLO on Ubc9 is dependent on the pore-forming capacity of the toxin and is shared by other bacterial pore-forming toxins like perfringolysin O (PFO) and pneumolysin (PLY). Ubc9 degradation was also observed in vivo in infected mice. Furthermore, we show that SUMO overexpression impairs bacterial infection. Together, our results reveal that Listeria, and probably other pathogens, dampen the host response by decreasing the SUMOylation level of proteins critical for infection." @default.
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• W2000313986 date "2010-04-01" @default.
• W2000313986 modified "2023-10-18" @default.
• W2000313986 title "Listeria monocytogenes impairs SUMOylation for efficient infection" @default.
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• W2000313986 doi "https://doi.org/10.1038/nature08963" @default.
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