Abstract
All living organisms need to duplicate their genetic information while protecting it from unwanted mutations, which can lead to genetic disorders and cancer development. Inaccuracies during DNA replication are the major cause of genomic instability, as replication forks are prone to stalling and collapse, resulting in DNA damage. The presence of exogenous DNA damaging agents as well as endogenous difficult-to-replicate DNA regions containing DNA–protein complexes, repetitive DNA, secondary DNA structures, or transcribing RNA polymerases, increases the risk of genomic instability and thus threatens cell survival. Therefore, understanding the cellular mechanisms required to preserve the genetic information during S phase is of paramount importance. In this review, we will discuss our current understanding of how cells cope with these natural impediments in order to prevent DNA damage and genomic instability during DNA replication.
Highlights
DNA replication is essential in all living organisms
Aside from the DNA damage events that happen under physiological conditions [1], eukaryotic genomes themselves present a wide range of natural impediments to DNA replication [2]
Pol II) complex replication stress and genomic instability addition, numerous studies have demonstrated that encounters between the replisome andinherent the the transcription process itself could be a source of DNA damage
Summary
DNA replication is essential in all living organisms. It is highly complex and regulated at many levels to ensure accurate and timely duplication of genetic information. Numerous studies have demonstrated that encounters between the replisome and the RNA Another type of natural impediment that occurs during DNA replication is the encounter between replication machinerycause and other enzymatic complexes that operate on theInDNA. Addition, numerous studies have demonstrated that encounters between the replisome andinherent the the transcription process itself could be a source of DNA damage. This is, in part, due to the RNA polymerase II (RNA Pol II) complex cause replication stress and genomic instability [5]. We as will focus on thethe mechanisms that regulate the in transcription andDNA‐binding replication machineries, collisions between two machineries may result coordination betweenrecombination transcription and machineries, as collisions between the two transcription-associated andreplication mutagenesis
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