NDLI: Teratocarcinoma cells as vehicles for introducing specific mutant mitochondrial genes into mice.

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Teratocarcinoma cells as vehicles for introducing specific mutant mitochondrial genes into mice.

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Teratocarcinoma cells as vehicles for introducing specific mutant mitochondrial genes into mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Mintz, B. Dewey, M. J. Watanabe, T.
Abstract	The immediate purpose of the experiment was to establish a means of introducing specific mitochondrially encoded mutant genes into mice. Mouse teratocarcinoma stem cells were used as vehicles for the cytoplasmic markers because of their known capacity for normal somatic and germinal differentiation after injection into blastocysts. The mutation of choice, chloramphenicol resistance (CAP(R)), was first produced in a melanoma cell line by mutagenesis and selection. The CAP(R) trait was then transferred from a resistant melanoma cell to a sensitive (CAP(S)) teratocarcinoma cell by fusing to the latter only the cytoplasmic portion of the CAP(R) donor. This indirect route demonstrated the cytoplasmic provenance of the mutation. Protein synthesis in mitochondria isolated from the cybrid, or cytoplasmic hybrid, cells was barely affected by chloramphenicol, in contrast to the inhibitory influence of the drug on mitochondria of the parent teratocarcinoma line. Cells of the cybrid clone resembled teratocarcinoma cells and retained their ability to form diverse tissues in solid tumors produced from subcutaneous grafts. Cells from the tumors were retransplanted and were tested periodically by culture in chloramphenicol; they were found to be stably CAP(R) even after 16 weeks in vivo in the absence of the selective agent. The CAP(R) cybrids were microinjected into blastocysts of another inbred strain and, after transfer to foster mothers, mosaic mice were obtained. They comprised both cybrid- and blastocyst-derived cells in various tissues, as indicated by strain-specific nuclear markers. These results demonstrate successful normal differentiation of the CAP(R) lineage in vivo. Teratocarcinoma cybrids thus offer a practical portal of entry of preselected mitochondrial genes into mice. This will ultimately permit in vivo investigation of maternally transmitted traits, of mitochondrial genetic influences in specialized cells, and of possible roles of cytoplasmic genes in clinical and disease states.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	10
Volume Number	75
Language	English
Publisher	National Academy of Sciences
Publisher Date	1978-01-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Mutation R Factors Teratoma Animals Blastocyst Cell Differentiation Cell Line Chloramphenicol Pharmacology Hybrid Cells Mice Nuclear Transfer Techniques Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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