Figures
GCN5-mediated histone modifications in the protozoan parasite Toxoplasma gondii.
Toxoplasma tachyzoites proliferating within human fibroblast cells were stained for an immunofluorescence assay using an antibody that recognizes acetylated lysine 18 of histone H3, a primary substrate of histone acetyltransferase TgGCN5-A, and a nuclear co-stain (red). The antibody illuminates chromatin within parasite nuclei (smaller, yellow) and the larger host cell nucleus. Toxoplasma, which causes congenital birth defects and opportunistic infection, is incurable because it can develop into a tissue cyst. Parasites lacking TgGCN5-A are no longer capable of activating genes induced during cyst formation triggered by alkaline stress (see Naguleswaran et al., doi:10.1371/journal.ppat.1001232).
Image Credit: William J. Sullivan Jr., Indiana University School of Medicine
Citation: (2010) PLoS Pathogens Issue Image | Vol. 6(12) December 2010. PLoS Pathog 6(12): ev06.i12. https://doi.org/10.1371/image.ppat.v06.i12
Published: December 23, 2010
Copyright: © 2010 William J. Sullivan Jr. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Toxoplasma tachyzoites proliferating within human fibroblast cells were stained for an immunofluorescence assay using an antibody that recognizes acetylated lysine 18 of histone H3, a primary substrate of histone acetyltransferase TgGCN5-A, and a nuclear co-stain (red). The antibody illuminates chromatin within parasite nuclei (smaller, yellow) and the larger host cell nucleus. Toxoplasma, which causes congenital birth defects and opportunistic infection, is incurable because it can develop into a tissue cyst. Parasites lacking TgGCN5-A are no longer capable of activating genes induced during cyst formation triggered by alkaline stress (see Naguleswaran et al., doi:10.1371/journal.ppat.1001232).
Image Credit: William J. Sullivan Jr., Indiana University School of Medicine