INVESTIGADORES
LEIVA Natalia Lorena
congresos y reuniones científicas
Título:
Chlamydia trachomatis uses host AKT/AS160 pathway to ensure its development
Autor/es:
CAPMANY A; LEIVA N; GAMBARTE J; DAMIANI MT
Lugar:
Potrero de los Funes. San Luis
Reunión:
Congreso; XLVII Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular (SAIB); 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 the
Golgi 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.