From :
Cybrid Models of mtDNA Disease and Transmission, from Cells to Mice

Ian A. Trounce and Carl A. Pinkert

Current Topics in Developmental Biology, Volume 77, 2007, Pages 157-183

Cybrids, or “cytoplasmic hybrids,” are cultured cells manipulated to contain introduced mitochondrial DNA (mtDNA). The cybrids are produced by first treating mitochondrial donor cells with cytochalasin B to weaken the cytoskeleton, before subjecting the cells to a centrifugal force, either as attached cells or in suspension. The dense nuclei are extruded, leaving plasma membrane-bound “cytoplasts” containing cell cytoplasm and organelles, including mitochondria. These cytoplasts are then fused with a nuclear donor cell line (originally using Sendai virus, but now using either polyethylene glycol or electrofusion), and transformant clones (cybrids) selected either with drug-resistance markers or by selecting for respiratory competence with ρ0 cell fusions as discussed below.

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B. The First Mammalian Cell Cybrids: CAPR and Other Selectable Markers

The first mammalian cultured cell phenotype identified to segregate with mtDNA was in human (HeLa) cells, where mtDNA imparted resistance to the antibiotic chloramphenicol (Spolsky and Eisenstadt, 1972). This group coined the term cybrid when they were the first to demonstrate cosegregation of this phenotype with mtDNA markers, implying mtDNA mutation(s) as the cause of the phenotype (Bunn 1974 and Wallace 1975). Several other mtDNA-linked drug-resistant phenotypes were identified in mammalian cells in the 1970s and 1980s, including resistance to the complex III inhibitors antimycin and myxothiazol (Howell and Gilbert, 1988) and later, to the complex I inhibitor rotenone (Bai 1998 and Bai 2000).

The development of robust DNA-sequencing methods in the late 1970s led to the identification of single-base substitutions in the 16S rRNA gene of the mtDNA of independently derived yeast, mouse, and human chloramphenicol-resistant (CAPR) cell lines (Blanc 1981a, Blanc 1981b, Dujon 1980 and Kearsey 1981). The field of mammalian mitochondrial genetics was thus born. These pioneering studies were in turn followed by identification of the first cytochrome b mutants (Howell and Gilbert, 1988) and more recently ND5, ND6, and COI mutants.