Mitochondrial DNA modulation of the anchorage-independent phenotype of transformed avian cells.
The progressive loss of mitochondrial DNA in the presence of ethidium bromide in immortal avian cell lines correlates with a decrease in their potential for anchorage-independent growth in soft agar. In short-term treated cells, this effect is reversible and the recovery of cloning potential parallels the recovery of control levels of mitochondrial DNA. Long-term ethidium-bromide-treated cells are permanently respiration-deficient and display anchorage-dependent growth. Anchorage-independent revertants can be selected, suggesting that the lack of a respiratory chain per se might not be responsible for the inability of mitochondrial DNA-depleted cells to grow in soft agar. Cybrids formed from the fusion of mitochondrial DNA-depleted, anchorage-dependent cells to cytoplasts from parental cells are capable of growth in soft agar. The mitochondria-specific inhibitor, rhodamine 6G, prevents the recovery of the anchorage-independent phenotype in similar hybrids. These results suggest that mitochondrial DNA is required to maintain the transformed phenotype of avian cells.
Zinkewich-Péotti
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Département de Biochimie, Faculté de Médecine, Université de Montréal, Québec, Canada.
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Morais
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D000818:Animals; D002455:Cell Division / Q000187:drug effects; D002461:Cell Line, Transformed; D002471:Cell Transformation, Neoplastic; D004272:DNA, Mitochondrial / Q000032:analysis / Q000502:physiology*; D004996:Ethidium / Q000494:pharmacology; D010641:Phenotype; D011784:Quail; D012235:Rhodamines / Q000494:pharmacology
D004272:DNA, Mitochondrial; D012235:Rhodamines; C026188:rhodamine 6G; D004996:Ethidium