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The Nuclear Matrix and the Organization of Nuclear DNA
Published in Isaac Bekhor, Carol J. Mirell, C. C. Liew, Progress in Nonhistone Protein Research, 1985
Bert Vogelstein, Donald Small, Sabina Robinson, Barry Nelkin
These studies, and similar ones performed by other investigators, suggested specific models of DNA replication.35,37–40 In these models, each loop of DNA functions as a replicon, the loops being reeled through fixed replication complexes on the nuclear matrix during DNA replication. The idea that DNA moves through replication complexes is certainly not new (e.g., see References 41 to 43). However, such models have several conceptually satisfying features when compared to the more conventional view of mobile enzymes moving along the DNA helix. First, it has been demonstrated that many of the enzymes required for DNA replication may exist as a complex.44–47 Energetically, it would appear less favorable for a large and unwieldy complex to move along a thin DNA helix than the reverse. Second, with fixed site models, new loops of DNA are automatically generated through the DNA synthesis itself, thus intrinsically preserving the ordered arrangement of DNA loops during this period of the cell cycle. Third, an intriguing feature of eukaryotic DNA replication is the fact that once replicated in a given S phase, a replicon origin will not become reactivated until the subsequent S phase.48–50 One explanation for this finding suggested by Blumenthal et al. is that “… such a restriction could result from changes during the cycle … in the chromatin structure.”48 Perhaps this postulated change in the chromatin structure is simply that replicon origins are oriented within loops in such a way that they are only in contact with replication complexes on the nuclear matrix at specific times during the cell cycle. This idea is experimentally testable.
Chaetocin induced chromatin condensation: effect on DNA repair signaling and survival
Published in International Journal of Radiation Biology, 2021
A. Sak, K. Bannik, M. Groneberg, M. Stuschke
First, to exclude that the fraction of CICC cells could be overgrown by proliferation of normal, i.e. non-affected cells, Aphidicolin (Aph) was used to stop the proliferation of the cells. Aph is a reversible inhibitor of eukaryotic DNA replication and arrests cell cycle transition of the cells at the early S phase. The data showed that treatment of cells enriched in the G1 phase of the cell cycle for 20 h with 2 μM Aph arrested more than 80% of the cells in the late G1 early S phase, while untreated cells went through the cell cycle (Figure 3(A)). Proliferation of cells with and without chaetocin treatment significantly ceased after treatment of the cells with Aph (Figure 3(B)). These data clearly showed a significant reduction in the percentage of CICC cells, even in non-proliferating Aph treated cells (Figure 3(C)). Furthermore, the data with human Fibroblasts (hFbs) which have naturally a low proliferation capacity clearly demonstrated that the fraction of cells with CICC also increased in a concentration-dependent manner in hFbs and decreased significantly within 24 h after washout of chaetocin (Figure 3(D)).