MYO1C PARTICIPATES IN CHLAMYDIAL INVASION AND DEVELOPMENT

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

Congreso; IV Reunión Conjunta de Sociedades de Biología de la República Argentina; 2020

Sociedad de Biología de Cuyo

The obligate intracellular pathogen Chlamydia trachomatis cause sexually transmitted diseases. This bacterium, in women, can lead to several complications such as pelvic inflammatory disease, ectopic pregnancy, and infertility. C. trachomatis provoke an extensive remodeling in the host cell, including Golgi fragmentation, actin cytoskeleton reshaping, and cytokinesis inhibition. Additionally, C. trachomatis intercepts different intracellular trafficking pathways of the host cell to acquire essential nutrients for its survival and replication. We recently published that Myo1C stabilizes actin at the Golgi apparatus facilitating the arrival of incoming transport carriers at this organelle. Strikingly, C. trachomatis establishes a close relationship with the Golgi apparatus, receiving from this organelle a continuous supply of vesicles loaded with essential lipids. Our objective was to determine if C. trachomatis manipulated Myo1C as a strategy to ensure its development. We observed, by confocal microscopy, that endogenous and over-express Myo1C was recruited to the chlamydial inclusion. The knockdown of Myo1C impaired the C. trachomatis development and caused the destabilization of the actin belt that surrounds the inclusion. Moreover, we determined that Myo1C depletion provoked a decrease of C. trachomatis infection rate, assessed by flow cytometry and confocal microscopy. Our findings indicate that Myo1C is involved in both invasion and development of C. trachomatis.