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Elevated CDK activity at the end of G1 triggers the firing of the origins and the dismantling of the pre-RCs. High CDK levels, which are maintained until the end of mitosis, inhibit or destroy pre-RC components and prevent the origin from relicensing. A new MCM complex cannot be loaded onto the origin until the pre-RC subunits are reactivated ...
[h] The authors conclude that if replication is defined by a subsequent study finding a sufficiently similar effect size to the original, replication success is not likely even if replications have very large sample sizes. Importantly, this occurs even if replications are direct or exact since heterogeneity nonetheless remains relatively high ...
The replication fork consists of a group of proteins that influence the activity of DNA replication. In order for the replication fork to stall, the cell must possess a certain number of stalled forks and arrest length. The replication fork is specifically paused due to the stalling of helicase and polymerase activity, which are linked together ...
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.
During the replication process, the DNA replication enzymes are not able to copy the ending sequences at the telomere. Those sequences, located at the end of the telomere and chromosome, would hence get lost gradually. Once all of these sequences have been worn out, the useful genetic information in the cell's chromosome would also get lost.
Eukaryotes initiate DNA replication at multiple points in the chromosome, so replication forks meet and terminate at many points in the chromosome. Because eukaryotes have linear chromosomes, DNA replication is unable to reach the very end of the chromosomes. Due to this problem, DNA is lost in each replication cycle from the end of the chromosome.
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]
This is known as the end replication problem. [1] The end replication problem is handled in eukaryotic cells by telomere regions and telomerase. Telomeres extend the 3' end of the parental chromosome beyond the 5' end of the daughter strand. This single-stranded DNA structure can act as an origin of replication that recruits telomerase.