Absence of detectable alteration in the kinetoplast DNA of a Trypanosoma brucei clone following loss of ability to infect the insect vector (Glossina morsitans).
A monomorphic bloodstream population of Trypanosoma brucei EATRO 1244 was derived from a cloned pleomorphic parental population by 77 rapid passages through mice. Loss of pleomorphism was accompanied by increased virulence of trypanosomes towards the mammal, by loss of ability to infect the tsetse fly, Glossina morsitans, loss of ability to transform to the procyclic stage in vitro at 26 degrees C, and by loss of oligomycin-sensitive ATPase activity in trypanosome homogenates. No differences in the maxicircle component of the kinetoplast DNAs (kDNA) of the two populations were detected by electron microscopy of kDNA network spreads or by electrophoretic analysis of restriction endonuclease digests. It appears, therefore, that loss of transmissibility and associated ability of the trypanosomes to activate the mitochondrion need not necessarily be the result of deletions in the mitochondrial (maxicircle) genome. We suggest that point mutations in critical mitochondrial genes, undetectable using out methods, or mutations of nuclear genes coding for important mitochondrial enzymes, may account for the observed changes in phenotype.[1]References
- Absence of detectable alteration in the kinetoplast DNA of a Trypanosoma brucei clone following loss of ability to infect the insect vector (Glossina morsitans). Hajduk, S.L., Vickerman, K. Mol. Biochem. Parasitol. (1981) [Pubmed]
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