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Infection and Immunity, June 2001, p. 3916-3923, Vol. 69, No. 6
Seattle Biomedical Research
Institute,1 Departments of Pathobiology
and Medicine, University of Washington,4 and
Infection Disease Research Institute,5
Seattle, Washington; Departamento de Biomedicina Molecular,
Centro de Investigación y de Estudios Avanzados del IPN, Mexico
City, D.F., Mexico2; and Instituto de
Parasitología y Biomedicina, CSIC, Granada,
Spain3
Received 11 January 2001/Returned for modification 28 February
2001/Accepted 22 March 2001
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.
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.6.3916-3923.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
LYT1 Protein Is Required for Efficient In Vitro
Infection by Trypanosoma cruzi
*
Corresponding author. Mailing address: Infection
Disease Research Institute, 1124 Columbia St., Suite 600, Seattle, WA
98104. Phone: (206)381-0883. Fax: (206) 381-3678. E-mail:
jswindle{at}idri.org.
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