Phosphoinositide lipids and the Legionella pathogen vacuole.

Subversion of vesicle trafficking is vital for intracellular survival of Legionella pneumophila within host cells. L. pneumophila produces several type IV-translocated effector proteins that modify components of the phagosomal membrane, in particular the phosphoinositide (PI) lipids. Within eukaryotic cells PIs co-define subcellular compartments and membrane dynamics. The generation, half-life, and localization of PI lipids are not only tightly regulated by the host cell, but also targeted and modulated by a number of L. pneumophila effectors. These effectors either anchor to PIs, directly modify the lipids, or recruit PI-metabolizing enzymes to the LCV membrane. Together, PI-subverting L. pneumophila effectors act jointly to promote the formation of a replication-permissive niche inside the host.