Impairment of cell division of Trypanosoma cruzi epimastigotes.
The mechanisms that facilitate the adaptation of Trypanosoma cruzi to two distinct hosts, insect and vertebrate, are poorly understood, in part due to the limited ability to perform gene disruption studies by homologous recombination. This report describes a developmentally-defective phenotype that resulted from integration of a drug marker adjacent to the GAPDH gene in T. cruzi.
Zacks
Michele A
MA
Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555-0609, USA. mazacks@utmb.edu
D000818:Animals; D002455:Cell Division / Q000235:genetics / Q000502:physiology*; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000235:genetics*; D006790:Host-Parasite Interactions; D008018:Life Cycle Stages; D010641:Phenotype; D014162:Transfection; D014349:Trypanosoma cruzi / Q000166:cytology* / Q000201:enzymology / Q000235:genetics
D005987:Glyceraldehyde-3-Phosphate Dehydrogenases