Hypothesis Volume 1, Issue 7 pp 598—607

Figure 1. A self-stabilizing tensegrity model for DNA-NM interactions in the cell nucleus as a function of age. (A) In a newborn cell NM proteins are in a compacted immature state (brown), thus the NM contact surface is reduced and so a large DNA loop (black) is anchored to two NM segments by means of two MARs that became actual LARs (blue circles) while three potential MARs (yellow circles) cannot attach to the NM due to steric hindrance and lack of enough contact surface. During mitosis biochemical modification of NM proteins (e.g., phosphorylation, red circles) cause disassembly of the NM network leading to disappearance of the cell nucleus. (B) In an adult cell the NM proteins are in a more extended state offering a larger contact surface, thus further potential MARs become actualized as LARs reducing the average DNA loop size and increasing the DNA-NM interactions. Yet phosphorylation of NM proteins leads to nuclear disassembly during mitosis. (C) In a senescent cell the NM proteins are fully extended thus offering enough contact surface for several potential MARs to become actualized as LARs since steric hindrance is further reduced. DNA loops become shorter on average and DNA-NM interactions are significantly more numerous. Phosphorylation of NM proteins during mitosis cannot lead to nuclear disassembly since the DNA-loops keep separate NM segments bound together and stabilized by means of the LARs attached to the NM. Thus the available energy becomes limiting for disassembling the nucleus and the cell cannot enter or perform mitosis.