
LYT1 Protein Is Required for Efficient In Vitro Infection by Trypanosoma cruzi
Author(s) -
Rebeca ManningCela,
Anna Carollina Alves de Melo Côrtes,
Elena GonzálezRey,
Wesley C. Van Voorhis,
John Swindle,
A. Gustavo González
Publication year - 2001
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.69.6.3916-3923.2001
Subject(s) - infectivity , biology , trypanosoma cruzi , amastigote , in vitro , internalization , microbiology and biotechnology , mutant , vacuole , extracellular , virology , parasite hosting , gene , cell , virus , leishmania , genetics , cytoplasm , world wide web , computer science
Trypanosoma cruzi invasion of host cells involves several discrete steps: attachment, parasite internalization mediated by recruitment and fusion of host cell lysosomes, and escape from the parasitophorous vacuole to liberate amastigotes to multiply freely in the cytosol. This report describes the initial characterization of the LYT1 gene and the demonstration that the gene product is involved in cell lysis and infectivity. Mutational analysis demonstrated that deletion of LYT1 resulted in attenuation of infection, which was associated with diminished hemolytic activity. Reintroduction of LYT1 restored infectivity in null mutants, confirming the critical role of LYT1 in infection. Additionally, in vitro stage transition experiments with LYT1-deficient lines showed that these parasites converted to extracellular amastigote-like cells and metacyclic trypomastigotes more rapidly than wild-type parasites, suggesting that the diminished infectivity was not a result of the LYT1 deficiency that affected the parasite's ability to complete the life cycle.