1998 年 8 巻 4 号 p. 227-232
We have induced the loss of kinetoplast DNA in Trypanosoma evansi by successive treatment of infected mice with a basic fuchsin dye, pararosaniline.
The “akinetoplastic” clones induced from a “kinetoplastic” strain were propagated by single cell inoculation into mice. In the course of assessing akinetoplastidy by DAPI staining after pararosaniline treatment, various fragmentation patterns and smaller–sized kDNA were detected. Semi-quantitative measurement of kDNA fluorescence indicated that pararosaniline causes a gradual decrease of the minicircle DNA. We attempted to obtain the parasites with intermediate kDNA, however these were unstable and tending to become akinetoplastic.
We then compared the growth rate of the akinetoplastic parasites with the original kinetoplastic strain. The growth of the kinetoplastics was relatively constant in the presence or absence of pararosaniline. On the other hand, the kDNA-deficient mutants showed a delayed growth rate and it was retarded when they were subjected to increasing dosage of the dye. According to these results we speculate that minicircle DNA of Trypanosoma evansi is not essential for the parasite growth, however it may facilitate the division and segregation of the mitochondrion and the genome during cell division.