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Replication Factories Disentangle Sister Chromatids. The disentanglement is essential for distributing the chromatids into daughter cells after DNA replication. Because sister chromatids after DNA replication hold each other by Cohesin rings, there is the only chance for the disentanglement in DNA replication. Fixing of replication machineries ...
Slipped strand mispairing (SSM, also known as replication slippage) is a mutation process which occurs during DNA replication. It involves denaturation and displacement of the DNA strands, resulting in mispairing of the complementary bases. Slipped strand mispairing is one explanation for the origin and evolution of repetitive DNA sequences. [1]
The process of semiconservative replication for the site of DNA replication is a fork-like DNA structure, the replication fork, where the DNA helix is open, or unwound, exposing unpaired DNA nucleotides for recognition and base pairing for the incorporation of free nucleotides into double-stranded DNA.
The temporal order of replication of all the segments in the genome, called its replication-timing program, can now be easily measured in two different ways. [1] One way simply measures the amount of the different DNA sequences along the length of the chromosome per cell.
The DNA re-replication response is different from the response taken when damage is due to oxygen radical generation. Damage from oxygen radical generations leads to a response from the Myc oncogene, which phosphorylates p53 and H2AX. [16] The ATM/ATR DNA damage network will also respond to cases where there is an overexpression of Cdt1.
During replication DNA polymerase begins to copy the DNA. At some point during the replication process, the polymerase dissociates from the DNA and replication stalls. When the polymerase reattaches to the DNA strand, it aligns the replicating strand to an incorrect position and incidentally copies the same section more than once.
The replication of DNA with a broken sugar-phosphate backbone is most likely facilitated by the homologous recombination proteins that confer resistance to ionizing radiation. The activity of PRR enzymes is regulated by the SOS response in bacteria and may be controlled by the postreplication checkpoint response in eukaryotes.
At the G1/S checkpoint, p53 acts to ensure that the cell is ready for DNA replication, while at the G2/M checkpoint p53 acts to ensure that the cells have properly duplicated their content before entering mitosis. [40] Specifically, when DNA damage is present, ATM and ATR kinases are activated, activating various checkpoint kinases. [41]