IHEM   20887
INSTITUTO DE HISTOLOGIA Y EMBRIOLOGIA DE MENDOZA DR. MARIO H. BURGOS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Chlamydia trachomatis uses host AKT/AS160 pathway to ensure its development
Autor/es:
CAPMANY A; LEIVA N; GAMBARTE J
Lugar:
Potrero de los Funes, San Luis
Reunión:
Congreso; XLVII Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular.; 2011
Institución organizadora:
SAIB
Resumen:
Chlamydia trachomatis is a Gram negative obligate intracellular bacterium that causes genital and ocular infections in humans. This bacterium replicates in a vacuole named inclusion. We demonstrated that Rab14, a key regulator of vesicular transport between the Golgi apparatus and early endosomes, is recruited to the inclusion and is involved on sphingolipids delivery from theGolgi to the inclusion. Furthermore, new results show that infection with C. trachomatis causes an increase in Rab14 expression and activates AKT. On the other hand, it has been described that active AKT causes the inhibition of AS160, a GAP (GTPase Activating Protein) for Rab14. We postulate that C. trachomatis manipulates PI3K/Akt/AS160 pathway to ensure the arrival of sphingolipids departed from the Golgi through Rab14-positive vesicles. We analyzed the effect of a specific AKT inhibitor (iAkt) on Chlamydia-infected cells. Treatment with iAkt decreases chlamydial inclusion size and reduces Rab14 recruitment to the inclusion in a doses-dependent manner. Moreover, iAKT treatment of infected cells generates abnormal bacterial forms assessed by electron microscopy. Likewise, inclusion forming unit analysis shows that iAKT treatment significantly decreases bacterial multiplication and infectivity. These data suggest that Chlamydia trachomatis usurps PI3K/Akt/AS160 pathway to ensure its survival.