Several studies have evaluated transcript abundance in human skeletal muscle, some of which have implicated mitochondrial impairment in healthy adults. A recent report also indicated that mitochondrial dysfunction was a feature of aging; however, the muscle tissue was harvested from patients undergoing surgery for illnesses that can alter mitochondrial mRNA abundance in skeletal muscle, such as cancer. Another study characterized the “molecular signature of sarcopenia” in healthy young and older adults, but did not report major alterations in the abundance of mitochondrial transcripts. Nevertheless, fibroblasts from patients with FRDA have impaired responses to oxidative insults, whether endogenous or exogenous. FRDA fibroblasts exhibit actin stress fiber abnormalities and are deficient in glutathione. Previous attempts to determine why these cells are hypersensitive to oxidative stress were unsuccessful. Faulty NF-KB-dependent signaling of antioxidant defenses was ruled out. We recently established that human fibroblasts harboring the ATPase 6 NARP mutation activated the Nrf2-dependent Phase II antioxidant pathway. Under basal conditions, the transcription factor Nrf2 is sequestered in the cytosol, where its Neh2 domain binds to the Kelch domain of the Keap1 protein tethered to actin bundles. These bundles, called actin stress fibers, are found in the center of the cytoplasm and periphery of the nucleus. Cul3-dependent ubiquitination of Nrf2 leads to degradation by the proteasome. When oxidative modification of one of the Keap1 cysteines occurs, Nrf2 escapes from this proteolytic pathway. Phosphorylated Nrf2 then translocates to the nucleus, where it dimerizes with a small Maf protein and binds to the cis-acting antioxidant responsive element DNA sequences of Phase II antioxidant genes, activating their transcription. However, it remains to be determined to what extent the results obtained from the artificially-assembled spindles can be applied to the kinetochore-containing meiotic spindles during meiosis. An interesting question that also needs to be addressed in the future is how the kinetochore-dependent and the NVP-BEZ235 kinetochore-independent poleward forces are coordinated during meiosis. It was previously observed in plant cells and insect spermatocytes that microsurgically generated chromosome fragments, which contain no kinetochores, are able to move to spindle poles. However, in these experiments, due to the presence of both intact chromosomes and kinetochore-free chromosome fragments in the same spindle, it was unclear if the chromosome fragments could be “hijacked” by the kinetochore-microtubule generated poleward forces. Another difference is that the previously reported kinetochore-independent poleward movements were observed both at metaphase and anaphase, while the poleward movement of DNA beads described here is tightly coupled with anaphase onset, suggesting that the observed poleward force generation described here is under precise cell cycle control.