MYO1C, MYO6 and MYO18A are necessary for Chlamydia trachomatis development.

CUERVO BUSTAMANTE ME; DEL BALZO D; DAMIANI MT; CAPMANY A

Salta

Congreso; LV Annual SAIB XIV PABMB 2019; 2019

SAIB y PABMB

Chlamydia trachomatis (CT) is an obligate intracellular bacterium and the most frequent bacterial agent of sexually transmitted infections. Latest research has placed CT as a risk factor of cellular transformation, which could lead to cervical or ovarian cancer development. This bacterium induces several alteration in the host cell such as inhibition of apoptosis and cytokinesis, decrease in molecules involved in cell adhesion and loss of front?rear polarity in migrating cells. The cytoskeleton and the associated proteins are the main factors that ensure polarized trafficking and a correct cell division. Particularly, myosins stand out, not only because of their role in actin cytoskeleton arrangement but also because of their implication in vesicular transport. By confocal microscopy we observed that MYO1C is recruited to the chlamydial inclusion at 24h post-infection. We recently published that MYO1C stabilizes actin at the Golgi apparatus facilitating the arrival of incoming transport carriers at this organelle. Strikingly, CT establishes a close relationship with the Golgi apparatus, receiving from this organelle a continuous supply of vesicles loaded with essential nutrients. Thus, CT could recruit this myosin as a strategy to ensure the arrival of post-Golgi vesicles. Interestingly, the knock down of MYO1C impairs the CT development, assessed by flow cytometry and confocal microscopy. Moreover, this function could be shared with MYO6 and MYO18A that are also necessary for a normal chlamydial development and function of the Golgi apparatus. Our results suggest that MYO1C, MYO6 and MYO18A are manipulated by CT to ensure its development.