This genome reductive system has only hitherto been observed in normal human cell populations, carrying DNA-damage


DNA-damage repair caused nucleotide lesions in Fragile Sites (ref). Thus, a cell in our cell population, but with special type DNA-damage, capable of starting repair during S-period.


This repair slows-down progression of S-period, resulting in un-replicated Late DNA, the satellite DNAs, now variously affected by deletion-type “mutations”


These mutations in their own right, will trigger repair-processes, and the question of stable or unstable solutions, is a real issue for genome/chromosomal instability (GCIN), “demanded” for progression


This aberrant S-period can also affect G2 phase time-wise with consequence deteriorated mitosis program, Cyclin B and CDK-1 with chromatin structured diploid cells directly in G1-phase


G1-phase becomes time-reduced, because of no de-condensation of chromosome structure with diploid cells entering a second S-phase, seemingly not interfered by checkpoint controls


This S-period completed with genome-wide down-load of extra cohesin, forming 4-chromatid diplochromosomes, the chromosomal structural base for the 4n-skewed division-system


Division-consequence: stable/unstable repair of satellite DNA deletion-mutations in diploid offspring cells, a potential mechanism for genome instability-associated genetic/epigenetic variability for tumorigenesis.