Figure 1 | Scientific Reports

Figure 1

From: Toxoplasma-induced changes in host risk behaviour are independent of parasite-derived AaaH2 tyrosine hydroxylase

Figure 1

Host infection dynamics remain unaffected after deletion of the AaaH2 gene from the Toxoplasma genome. (A) The full AaaH2 gene sequence (white boxes) was substituted by the coding sequence for the dihydrofolate reductase protein (DHFR). Arrows indicate primer identification and orientation and red sequences represent homology region. (B) PCR analysis of purified genomes from mutant parasites (∆AaaH2) confirmed deletion of the AaaH2 gene (left panel), and the presence of the DHFR marker (right panel). The primer pairs used and sizes of the amplification products are indicated. Relevant cropped regions of the gels are shown and full-length gels are presented in Supplementary Figure S3. (C) No differences in relative AaaH1 expression levels were observed in TgWT and TgAaaH2KO bradyzoites (left panel). When compared with control expression levels (TgWT, value of 1), no significant AaaH1 expression fold change was detected in mutant bradyzoites (right panel). (D) No changes in infection efficiency or parasite viability were found between TgAaaH2KO and the parental strain TgWT. (E) Weight analysis throughout infection showed that acute infection resulted in marked weight loss over the first 2 weeks. As chronic infection is established, infected animals (independent of infective parasite strain) recover to initial weight values (dotted line), which are always inferior to weight values in control animals (F). Mouse saline group, n = 28; TgWT group, n = 15; TgAaaH2KO group, n = 25. (G) The number of cysts formed in brains infected with the TgAaaH2KO strain was increased relative to the parental strain (TgWT). Mouse TgWT group, n = 14; TgAaaH2KO group, n = 14. *p < 0.05. The data are presented as the mean ± SEM.