Fig. 2: T. gondii infection induces several hallmarks of genome instability in primary human endothelial cells. | Communications Biology

Fig. 2: T. gondii infection induces several hallmarks of genome instability in primary human endothelial cells.

From: Toxoplasma gondii infection induces early host cell cycle arrest and DNA damage in primary human host cells by a MYR1-dependent mechanism

Fig. 2

HUVEC (n = 3) were infected with tachyzoites (MOI 0.5:1) of TgΔhce1, TgΔmyr1 mutants and control parasites (TgΔku80) (A) Comet assay was used to detect parasite-driven general DNA strand breaks induction (at 12 h p. i.) and showed that T. gondii infection induced DNA damage in a MYR1- and HCE1-independent fashion. Scale bar: 100 µm. B, C Host cell genome instability was evaluated by cell binucleation (indicating cytokinesis failure) and micronuclei formation. Current data show an increased percentage of binucleated cells and micronuclei in HUVEC infected with all, TgΔhce1, TgΔmyr1 mutants and control parasites (TgΔku80). D Exemplary illustrations of a T. gondii-infected host cell experiencing binucleated phenotype, and cells with micronuclei and simultaneous staining of γH2AX-based DNA damage foci. The results show that most of the binucleated cells were positive for DNA damage in contrast to micronuclei. Micronuclei are indicated by white arrowheads. On average, 1400 cells were counted in each non-infected and T. gondii strain infection in (A−C). The scale bar represents 5 µm. Graph bars represent the median ± SD of three biological donors. The p values were calculated using a one-way ANOVA followed by a Kruskal Wallis multiple comparison test of variance, using the non-infected condition (n. i.) as control. A p < 0.05 was considered as significant.

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