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Journal of Cell Science, Vol 35, Issue 1 185-202, Copyright © 1979 by Company of Biologists

JOURNAL ARTICLES

Dyskinetoplasty in two species of trypanosomatids

SL Hajduk

Dyskinetoplastic cells from both Crithidia fasciculata and Trypanosoma equiperdum lack detectable kinetoplast DNA (kDNA) by conventional staining techniques. Two dyskinetoplastic strains of T. equiperdum, either acriflavine-induced or spontaneously occurring, show normal amounts of kDNA (p = 1.692 g/cm3) in analytical caesium chloride, ultracentrifugation. Electron and fluorescence microscopy of the dyskinetoplastic strains of T. equiperdum suggest that the kDNA network is fragmented and dispersed throughout the mitochondrion. The fragmentation and dispersion of the kDNA, rather than a reduction in the amount of kDNA, is the cause of the lack of kinetoplast staining in the dyskinetoplastic strains of T. equiperdum. Acriflavine-treated cultures of C. fasciculata show a decrease in the amount of kDNA (p = 1.703 g/cm3) corresponding to the percentage of dyskinetoplastic cells in the cultures. Electron and fluorescence microscopy of acriflavine-treated cultures of C. fasciculata show the loss of the kDNA network in cells which lack Giemsa and Feulgen staining, confirming the hypothesis that the kDNA is lost in dyskinetoplastic trypanosomatids from insects. Possible modes of acriflavine action are considered and a proposed mechanism for acriflavine action in trypanosomes from mammals is presented.


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M. W. Timms, F. J. van Deursen, E. F. Hendriks, and K. R. Matthews
Mitochondrial Development during Life Cycle Differentiation of African Trypanosomes: Evidence for a Kinetoplast-dependent Differentiation Control Point
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© The Company of Biologists Ltd 1979