This scenario may explain the puzzling relationship between protein aggregation and cell toxicity, in that aggregate formation does not necessarily result in cell death. For example, aggregates have been detected in the dentate nucleus of the HD cerebellum, a brain region unaffected in this disease, and a cellular model has shown a discrepancy between aggregate formation and cell death. In contrast, in both polyQ transgenic mice and Drosophila, interference with aggregate formation has been shown to prolong survival and to ameliorate neuropathology. These results suggest that the process of aggregate formation is necessary for, but does not necessarily result in, cell toxicity. Correspondingly, the genetic gain-of-function of polyQ expansion leads to the nucleation process of aggregate formation, but does not have a direct toxic effect on the cells. Another possibility is that AICAR is derived from FAICAR if the accumulation of dihydrofolate polyglutamates causes the AICART reaction to run L-Ornithine backward, as suggested by the fact that the equilibrium of this reaction actually lies in the direction of AICAR formation. We did not detect strong changes in the gene sets expressed in the MON810 variety DKC6575 and its near-isogenic counterpart; and genes expressed in the GM and/or the non-GM variety did not cluster in a specific, overrepresented GO categories. Even so, up to 140 genes were expressed at different levels in DKC6575 and Tietar immature embryos. This corresponded to about 0.95% and 0.94% maize genes detected as expressed both in DKC6575 and Tietar 20 DAP embryos. This is in accordance with previous reports on transcriptome comparisons of various GM versus noGM plants. mRNA-seq results were further validated by comparing DKC6575 and Tietar embryo transcriptomic profiles using a microarray hybridisation approach with the Agilent platform, questioning around 33,000 genes. Our results show that these six E2F family members have very different effects on cell growth under conditions of limiting mitogenic Doxercalciferol signals.In FSHD cells, the delocalization of FR-MAR would thus result in an increased flexibility of the corresponding chromosomal segment and additional possibilities of interaction for the 4qA/B marker. This may provide an explanation for the FSHD-specific, direct interaction of 4qA/B with the ANT1 and FRG1 gene promoters we observed in FSHD myoblasts.