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Lagging strand during DNA replication During DNA replication, DNA polymerase cannot replicate the sequences present at the 3' ends of the parent strands. This is a consequence of its unidirectional mode of DNA synthesis: it can only attach new nucleotides to an existing 3'-end (that is, synthesis progresses 5'-3') and thus it requires a primer ...
Telomerase is a reverse transcriptase enzyme that carries its own RNA molecule (e.g., with the sequence 3′-CCCAAUCCC-5′ in Trypanosoma brucei) [3] which is used as a template when it elongates telomeres. Telomerase is active in gametes and most cancer cells, but is normally absent in most somatic cells.
After around 20 nucleotides, elongation is taken over by Pol ε on the leading strand and Pol δ on the lagging strand. [103] Polymerase δ (Pol δ): Highly processive and has proofreading, 3'->5' exonuclease activity. In vivo, it is the main polymerase involved in both lagging strand and leading strand synthesis. [104]
The lagging strand is the strand of new DNA whose direction of synthesis is opposite to the direction of the growing replication fork. Because of its orientation, replication of the lagging strand is more complicated as compared to that of the leading strand.
The leading strand is continuously synthesized and is elongated during this process to expose the template that is used for the lagging strand (Okazaki fragments). During the process of DNA replication, DNA and RNA primers are removed from the lagging strand of DNA to allow Okazaki fragments to bind to.
This problem makes eukaryotic cells unable to copy the last few bases on the 3' end of the template DNA strand, leading to chromosome—and, therefore, telomere—shortening every S phase. [2] Measurements of telomere lengths across cell types at various ages suggest that this gradual chromosome shortening results in a gradual reduction in ...
The dimerisation of the replicative polymerases solves the problems related to efficient synchronisation of leading and lagging strand synthesis at the replication fork, but the tight spatial-structural coupling of the replicative polymerases, while solving the difficult issue of synchronisation, creates another challenge: dimerisation of the ...
This process alleviates the inhibitory effect of the telomere-associated proteins, and allows Cdc13 (a binding protein on both the lagging strand, and leading strand) to cover telomeric DNA. [15] The binding of cdc13 to DNA suppresses DNA damage checkpoint and allows resection to occur while allowing for telomerase elongation at the DSB ends. [3]