AUTHOR=Ferreira Éden R. , Bonfim-Melo Alexis , Cordero Esteban M. , Mortara Renato A. 

TITLE=ERM Proteins Play Distinct Roles in Cell Invasion by Extracellular Amastigotes of Trypanosoma cruzi

JOURNAL=Frontiers in Microbiology

VOLUME=8

YEAR=2017

URL=https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2017.02230

DOI=10.3389/fmicb.2017.02230

ISSN=1664-302X

ABSTRACT=<p>The protozoan parasite <italic>Trypanosoma cruzi</italic> is the causative agent of Chagas' disease. In mammalian hosts, <italic>T. cruzi</italic> alternates between trypomastigote and amastigote forms. Additionally, trypomastigotes can differentiate into amastigotes in the extracellular environment generating infective extracellular amastigotes (EAs). Ezrin-radixin-moesin (ERM) are key proteins linking plasma membrane to actin filaments, the major host cell component responsible for EA internalization. Our results revealed that depletion of host ezrin and radixin but not moesin inhibited EAs invasion in HeLa cells. ERM are recruited and colocalize with F-actin at EA invasion sites as shown by confocal microscopy. Invasion assays performed with cells overexpressing ERM showed increased EAs invasion in ezrin and radixin but not moesin overexpressing cells. Finally, time-lapse experiments have shown altered actin dynamics leading to delayed EA internalization in ezrin and radixin depleted cells when compared to control or moesin depleted cells. Altogether, these findings show distinct roles of ERM during EAs invasion, possibly regulating F-actin dynamics and plasma membrane interplay.</p>