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[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 ...
As the cell divides, the telomeres on the ends of chromosomes shorten. The Hayflick limit is the limit on cell replication imposed by the shortening of telomeres with each division. This end stage is known as cellular senescence. The Hayflick limit has been found to correlate with the length of the telomeric region at the end of chromosomes.
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.
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.
To get substantial re-replication of DNA, regulation of all three components, Cdc6, Mcm2-7 and the ORC has to be prevented. Having multiple mechanisms to prevent re-replication is beneficial because it the regulatory network continues to function even if one of the components fails. [3]
DNA damages cause changes in the structure of the genetic material and prevents the replication mechanism from functioning and performing properly. [1] The DNA damage response (DDR) is a complex signal transduction pathway which recognizes when DNA is damaged and initiates the cellular response to the damage.
The MCM complex is the DNA helicase that opens the helix at the replication origin and unwinds the two strands as the replication forks travel along the DNA. [5] Elevated CDK activity at the end of G1 triggers the firing of the origins and the dismantling of the pre-RCs.
Replication timing is correlated with the expression of genes such that the genetic information being utilized in a cell is generally replicated earlier than the information that is not being used. We also know that the replication-timing program changes during development, along with changes in the expression of genes.