Figure 39.5 A. Mitochondrial hypervariable D-loop PCR amplicons from monkey, cat and bovine. Lanes 1, 7, 10: 100 bp ladder. Lanes 2-4: M. mulatto. Lanes 5, 6: M. nemestrina. Lanes 8, 9: F. catus; Lane 11: B. taurus. B. DNA chromatogram of M. mulatto mitochondrial control region. C. M. mulatta mitochondrial DNA, D-loop hypervariable region (1600 bp). Unpublished data by Brenner et al.
Since all embryonic stem (ES) cell lines are derived from fertilized oocytes, it is expected that such oocyte defects are also present in these cells, and because virtually all primate (monkey and human) oocytes used in research or
IVF clinics come from females stimulated with gonado-tropins, which may increase mtDNA error frequencies, we must be cautious about heavily investing in research using this source of material.
Several mtDNA mutations appear in somatic tissues at a higher frequency in older than in younger subjects. Some of these mutations are associated with overt pathologies while others are not. A key question is, Do mitochondrial DNA mutations affect oocyte quality and developmental capacity? This raises a related question: because mtDNA mutations accumulate in oocytes with increasing age of the patient, do these errors play a significant role in age-related loss of fertility? Our laboratory has investigated whether there is an age-dependent, oocyte-specific point mutation in the mtDNA control region of human oocytes. Preliminary data showed that a prevalent point mutation at bp position 414 in the mitochondrial genome may preferentially accumulate with age in human oocytes (Barritt et al., 2000).
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