Reduced expression of the lipid transfer protein StarD7 promotes chlamydial replication

PANZETTA ME; SAKA HA; FLORES MARTIN J; GENTI RAIMONDI S

Charlotte, NC

Congreso; Chlamydia Basic Research Society Biennial Meeting; 2017

Chlamydia Basic Research Society

Chlamydia trachomatis (Ct) is the leading bacterial cause of sexually transmitted infections and infectious blindness globally. Ct survives intracellularly in a vacuole or "inclusion", from where it manipulates cellular machinery to acquire nutrients. StarD7 is a protein of the START family that participates in the transport of phosphatidylcholine (PC) in the host cell. Although Ct lacks the machinery for de novo synthesis of PC, it constitutes ~ 40% of its membrane phospholipids. Therefore, Ct acquires PC from the host. We hypothesized that Ct uses StarD7 to acquire PC. Localization and expression levels of StarD7 in Ct-infected HeLa cells were analyzed by immunofluorescence (IF) microscopy and western blot assays, respectively. The impact of StarD7 RNAi silencing on the generation of infectious progeny was evaluated. Non-infected, untreated or non-silenced cells, as appropriate, were used as controls. The results were analyzed statistically by ANOVA-Tukey.A redistribution of StarD7 was observed around the inclusion. Expression levels of StarD7 were not modified during infection. The silencing of StarD7 was associated with an increase in the generation of infectious progeny.StarD7 was relocated around the inclusion, suggesting that this protein may have a role in Ct infection. However, the silencing of StarD7 did not negatively impact Ct multiplication, indicating that this protein is not required for PC essential nutrient acquisition. On the contrary, and surprisingly, the silencing of StarD7 led to greater generation of infectious progeny. This suggests that the StarD7 deficit triggers changes in the host cell that promote Ct replication.