The role of FTL_1684 during Erythrocyte Invasion by Francisella tularensis.

Lisa Marie Nachtwey, Joseph Horzempa

Abstract


Francisella tularensis is a highly virulent Gram-negative bacterium, which infects numerous cell types of its mammalian host causing the disease tularemia. In addition to invading phagocytes of the human immune system as well as other non-phagocytic cells, F. tularensis is also capable of invading non-endocytic erythrocytes, a feature of tularemia that enhances tick colonization and thereby bacterial transmission. The mechanism by which F. tularensis manipulates erythrocytes for entry is still fairly unknown. Among several genes induced in the presence of erythrocytes was FTL_1684 encoding for a homologue of PrmC found in several distantly related bacterial species. PrmC encodes for a methyltransferase catalyzing the methylation of class I release factors RF1 and RF2 which facilitates effective translational termination of selective genes, many of which are required for pathogenesis.  The effects of the deletion of FTL_1684 on pathogenesis and erythrocyte invasion are currently investigated. Based on potential gene function, it was hypothesized that the ΔFTL_1684 mutant of F. tularensis LVS will be attenuated in its pathogenesis as well as its ability to invade erythrocytes; ineffective translational termination may reduce expression of functional F. tularensis-associated virulence and invasion factors. PrmC homologues were furthermore suggested as novel universal drug targets and drug-mediated inactivation of PrmC as an effective way to not only aid curing tularemia but also prevent further transmission via a tick vector.

Keywords


Francisella tularensis; erythrocyte invasion; pathogenesis; PrmC; FTL_1684

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