Impairment of cell division of Trypanosoma cruzi epimastigotes

Abstract

The mechanisms that facilitate the adaptation of Trypanosoma cruzi to two distinct hosts, insect and vertebrate, are poorly understood, in part Fig. 1) and PCR amplification of the 1.3 kilobase GAPDH-IR-neo r fragment from gDNA of the transfectants (data not shown). However, GAPDHIR-neo r did not integrate into the TcGPI8 gene and the 3' and 5' ends of TcGPI8 were absent (data not shown). Genome walking and PCR-cloning identified the site of insertion of the GAPDHIR/neo r cassette ( Fig. 2A-B) as adjacent to

Trypanocidal Activity of Aziridinyl Nitrobenzamide Prodrugs

“…Initial constructs designed to target and replace one of the gGAPDH loci produced luminescent epimastigotes. However, these cells failed to develop into invasive parasites, consistent with a previous report suggesting gGAPDH levels are critical for T. cruzi differentiation (56). To circumvent this problem, we integrated the luciferase construct into the parasite's ribosomal array.…”