James D. Hilley

TL;DR: It is shown that pseudogene formation and gene loss are the principal forces shaping the different genomes of Leishmania, and genes that are differentially distributed between the species encode proteins implicated in host-pathogen interactions and parasite survival in the macrophage.

TL;DR: It is demonstrated that there is little variation in unique gene content across Leishmania species, but large-scale genetic heterogeneity can result through gene amplification on disomic chromosomes and variation in chromosome number.

TL;DR: It is shown that whole-genome sequence data reveals genetic structure within these lines not shown by multilocus typing, and suggests that drug resistance has emerged multiple times in this closely related set of lines, providing additional power to track the drug resistance and epidemiology of an important human pathogen.

TL;DR: The cloned L. mexicana GPI8 gene that encodes the catalytic component of the GPI:protein transamidase complex that adds GPI anchors to nascent cell surface proteins in the endoplasmic reticulum is cloned and suggests that GPI-anchored surface proteins are not essential to L.mexicANA for its entry into and survival within mammalian host cells in vitro or in vivo.

TL;DR: A major cysteine proteinase of Leishmania mexicana, that is predominantly expressed in the form of the parasite that causes disease in mammals, has been overexpressed in Escherichia coli and purified from inclusion bodies to apparent homogeneity.