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Finally, post-replication mismatch repair mechanisms monitor the DNA for errors, being capable of distinguishing mismatches in the newly synthesized DNA Strand from the original strand sequence. Together, these three discrimination steps enable replication fidelity of less than one mistake for every 10 9 nucleotides added.
In replicating cells, such as cells lining the colon, errors occur upon replication of past damages in the template strand of DNA or during repair of DNA damages. These errors can give rise to mutations or epigenetic alterations. [6] Both of these types of alteration can be replicated and passed on to subsequent cell generations.
Four classes of mutations are (1) spontaneous mutations (molecular decay), (2) mutations due to error-prone replication bypass of naturally occurring DNA damage (also called error-prone translesion synthesis), (3) errors introduced during DNA repair, and (4) induced mutations caused by mutagens. Scientists may sometimes deliberately introduce ...
Transcription errors in DNA replication. In biology, transcription errors may occur in the process of DNA replication, resulting in genetic mutations. [4]
In order to preserve genetic information during cell division, DNA replication must be completed with high fidelity. In order to achieve this task, eukaryotic cells have proteins in place during certain points in the replication process that are able to detect any errors during DNA replication and are able to preserve genomic integrity.
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]
Gene duplications can arise as products of several types of errors in DNA replication and repair machinery as well as through fortuitous capture by selfish genetic elements. Common sources of gene duplications include ectopic recombination, retrotransposition event, aneuploidy, polyploidy, and replication slippage. [1]
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.