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.
Département de Biochimie, Faculté de Médecine, Université de Montréal, Québec, Canada.
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Zinkewich-Péotti
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Parent
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Morais
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