Evidence for Acquisition ofLegionellaType IV Secretion Substrates via Interdomain Horizontal Gene Transfer

Top Cited Papers
Open Access
Publisher Website
Google Scholar
Abstract
Intracellular pathogens exploit host cell functions to create a replication niche inside eukaryotic cells. The causative agent of Legionnaires' disease, the γ-proteobacteriumLegionella pneumophila, resides and replicates within a modified vacuole of protozoan and mammalian cells.L. pneumophilatranslocates effector proteins into host cells through the Icm-Dot complex, a specialized type IVB secretion system that is required for intracellular growth. To find out if some effector proteins may have been acquired through interdomain horizontal gene transfer (HGT), we performed a bioinformatic screen that searched for eukaryotic motifs in all open reading frames of theL. pneumophilaPhiladelphia-1 genome. We found 44 uncharacterized genes with many distinct eukaryotic motifs. Most of these genes contain G+C biases compared to otherL. pneumophilagenes, supporting the theory that they were acquired through HGT. Furthermore, we found that several of them are expressed and up-regulated in stationary phase in an RpoS-dependent manner. In addition, at least seven of these gene products are translocated into host cells via the Icm-Dot complex, confirming their role in the intracellular environment. Reminiscent of the case with most Icm-Dot substrates, most of the strains containing mutations in these genes grew comparably to the parent strain intracellularly. Our findings suggest that inL. pneumophila, interdomain HGT may have been a major mechanism for the acquisition of determinants of infection.