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Title: Effects of mycoplasma contamination on phenotypic expression of mitochondrial mutants in human cells

Journal Article · · Mol. Cell. Biol.; (United States)
DOI:https://doi.org/10.1128/MCB.1.4.321· OSTI ID:5963475

HeLa cells sensitive to the mitochondrial protein synthesis inhibitors erythromycin (ERY) and chloramphenicol (CAP) and HeLa variants resistant to the effects of these drugs were purposefully infected with drug-sensitive and -resistnat mycoplasma strains. Mycoplasma hyorhinis and the ERY-resistant strain of Mycoplasma orale, MO-ERY/sup r/, did not influence the growth of HeLa and ERY-resistant ERY2301 cells in the presence or absence of ERY. M. hyorhinis also did not affect the growth of HeLa and CAP-resistant Cap-2 cells in the presence or absence of CAP. However, both HeLa and Cap-2 cells infected with the CAP-resistant strain of M. hyorhinis, MH-CAP/sup r/, were more sensitive to the cytotoxix effect of CAP. This maybe due to the glucose dependence of the cells, which was compromised by the increased utilization of glucose by MH-CAP/sup r/ in these infected cell cultures. In vitro protein synthesis by isolated mitochondria was significantly altered by mycoplasma infection of the various cell lines. A substantial number of mycoplasmas copurified with the mitochondria, resulting in up to a sevenfold increase in the incorporation of (/sup 3/H)leucine into the trichloroacetic acid-insoluble material. More importantly, the apparent drug sensitivity or resistance of mitchondrial preparations from mycoplasma-infected cells reflected the drug sensitivity or resistance of the contaminating mycoplasmas. These results illustrate the hazards in interpreting mitochondrial protein synthesis data derived from mycoplasma-infected cell lines, particularly putative mitochondrially encoded mutants resistant to inhibitors of mitochondrial protein synthesis.

Research Organization:
Div. of Biology, California Institute of Technology, Pasadena, CA 91125
OSTI ID:
5963475
Journal Information:
Mol. Cell. Biol.; (United States), Vol. 1:4
Country of Publication:
United States
Language:
English