Chlamydia trachomatis alters phosphoinositides distribution in infected host cell

DAMIANI MT; ALONSO BIVOU M; LUJÁN A; GAMBARTE TUDELA J; GOUD B; PICAS L

BUENOS AIRES

Congreso; SOCIEDAD CONJUNTA DE BIOCIENCIAS; 2017

ABSTRACT (ID:1358) Chlamydia trachomatis (CT) is an obligate intracellular pathogen which resides and multiplies in a vacuole called inclusion. This pathogen establishes complex interactions with host cells to facilitate the acquisition of host-derived molecules that are essential for its survival. Phosphoinositides (PtdIns) regulate key cellular processes such as vesicular trafficking and cellular signalling, by controlling the subcellular localisation and activation of effector PtdIns-binding proteins. However, little is known about the role of PtdIns during chlamydial infection. In this study, we proposed that CT targets PtdIns metabolism to promote the biogenesis of its replicative compartment. First, we analysed the subcellular distribution of different PtdIns in both, uninfected and CT infected cells by indirect immunofluorescence. Particularly, we assessed modifications in the level of the different PtdIns species at the plasma membrane (PM) and the chlamydial inclusion membrane. In addition, we quantified the amount of PtdIns(4)P, PtdIns(4,5)P2, and PtdIns(3,4,5)P3 at the PM in CT-infected cells by using a novel micro-pattern technique. Furthermore, by spinning disk microscopy (SDM), we observed PtdIns dynamics at different post-infection times. By these approaches, we demonstrated that this intracellular bacterium alters PtdIns subcellular distribution and metabolism. Mainly, CT infection produced a decrease on PtdIns(4,5)P2 production at the PM while promoted the recruitment and accumulation of this particular PtdIns at the chlamydial inclusion membrane. Collectively, our results suggest a novel host-pathogen interaction that may be important for understanding CT pathogenesis.