Postreplication repair
You don't need to be Editor-In-Chief to add or edit content to WikiDoc. You can begin to add to or edit text on this WikiDoc page by clicking on the edit button at the top of this page. Next enter or edit the information that you would like to appear here. Once you are done editing, scroll down and click the Save page button at the bottom of the page.
 |
This article or section is in need of attention from an expert on the subject. WikiProject Biology or the Biology Portal may be able to help recruit one. |
 |
This article may require cleanup to meet Wikipedia's quality standards. Please improve this article if you can. |
| This article is orphaned as few or no other articles link to it. Please help introduce links in articles on related topics. |
Postreplication Repair (PRR)
DNA damage prevents the normal enzymatic synthesis of DNA by the replication fork[1][1][1][1]. At damaged sites in the genome, both prokaryotic and eukaryotic cells utilize a number of postreplication repair (PRR) mechanisms to complete DNA replication. Chemically modified bases can be bypassed by either error-prone[1] or error-free[1] translesion polymerases, or through genetic exchange with the sister chromatid[1]. 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 by the postreplication checkpoint response in eukaryotes[1][1].
The eludication of PRR mechanisms is an active area of molecular biology research, and the terminology is currently in flux. For instance, PRR has recently been referred to as "DNA damage tolerance" to emphasize the instances in which postreplication DNA damage is repaired without removing the original chemical modification to the DNA[1]. While the term PRR has most frequently been used to describe the repair of single-stranded postreplication gaps opposite damaged bases, a more broad usage has been suggested[1]. In this case, the term PRR would encompasses all processes that facilitate the replication of damaged DNA, including those that repair replication-induced double-strand breaks.
References
In this case, the term PRR would encompasses all processes that facilitate the repair of damaged DNA, including those that repair replication-induced double-strand breaks.
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
