Generation of trans‐mitochondrial mito‐mice by the introduction of a pathogenic G13997A mtDNA from highly metastatic lung carcinoma cells

M Yokota, H Shitara, O Hashizume, K Ishikawa… - FEBS …, 2010 - Wiley Online Library
M Yokota, H Shitara, O Hashizume, K Ishikawa, K Nakada, R Ishii, C Taya, K Takenaga…
FEBS letters, 2010Wiley Online Library
To investigate the effects of respiration defects on the disease phenotypes, we generated
trans‐mitochondrial mice (mito‐mice) by introducing a mutated G13997A mtDNA, which
specifically induces respiratory complex I defects and metastatic potentials in mouse tumor
cells. First, we obtained ES cells and chimeric mice containing the G13997A mtDNA, and
then we generated mito‐mice carrying the G13997A mtDNA via its female germ line
transmission. The three‐month‐old mito‐mice showed complex I defects and lactate …
To investigate the effects of respiration defects on the disease phenotypes, we generated trans‐mitochondrial mice (mito‐mice) by introducing a mutated G13997A mtDNA, which specifically induces respiratory complex I defects and metastatic potentials in mouse tumor cells. First, we obtained ES cells and chimeric mice containing the G13997A mtDNA, and then we generated mito‐mice carrying the G13997A mtDNA via its female germ line transmission. The three‐month‐old mito‐mice showed complex I defects and lactate overproduction, but showed no other phenotypes related to mitochondrial diseases or tumor formation, suggesting that aging or additional nuclear abnormalities are required for expression of other phenotypes.
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