Open AccessT rypanosoma cruzi extracellular amastigotes trigger the protein kinase D 1‐cortactin‐actin pathway during cell invasion
Author(s) -
BonfimMelo Alexis,
Zanetti Bianca Ferrarini,
Ferreira Éden Ramalho,
Vandoninck Sandy,
Han Sang Won,
Van Lint Johan,
Mortara Renato Arruda,
Bahia Diana
Publication year - 2015
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.12472
Subject(s) - cortactin , biology , microbiology and biotechnology , invadopodia , actin , internalization , extracellular , kinase , podosome , cell , cytoskeleton , biochemistry , genetics , cancer , cancer cell
Summary T rypanosoma cruzi extracellular amastigotes ( EAs ) display unique mechanisms for cell invasion that are highly dependent on host actin filaments. Protein kinase D 1 ( PKD 1) phosphorylates and modulates the activity of cortactin, a key regulator of actin dynamics. We evaluated the role of host cortactin and PKD1 in actin filament dynamics during H e L a cell invasion by EAs . Host cortactin, PKD1 and actin are recruited by EAs based on experiments in fixed and live cells by time lapse confocal microscopy. EAs trigger PKD1 and extracellular signal‐regulated kinase 1/2 activation, but not Src family kinases, and selectively phosphorylate cortactin. Heat‐killed EAs and non‐infective epimastigotes both triggered distinct host responses and did not recruit the molecules studied herein. EA invasion was influenced by depletion or overexpression of host cortactin and PKD1 , respectively, suggesting the involvement of both proteins in this event. Collectively, these results show new host cell mechanisms subverted during EA internalization into non‐phagocytic cells.