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Plos Genetics : Ku Regulates the Non-homologous End Joining Pathway Choice of Dna Double-strand Break Repair in Human Somatic Cells, Volume 6

By Pearson, Christopher E.

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Book Id: WPLBN0003929750
Format Type: PDF eBook :
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Reproduction Date: 2015

Title: Plos Genetics : Ku Regulates the Non-homologous End Joining Pathway Choice of Dna Double-strand Break Repair in Human Somatic Cells, Volume 6  
Author: Pearson, Christopher E.
Volume: Volume 6
Language: English
Subject: Journals, Science, Genetics
Collections: Periodicals: Journal and Magazine Collection (Contemporary), PLoS Genetics
Historic
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Publisher: Plos

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Pearson, C. E. (n.d.). Plos Genetics : Ku Regulates the Non-homologous End Joining Pathway Choice of Dna Double-strand Break Repair in Human Somatic Cells, Volume 6. Retrieved from http://www.nationalpubliclibrary.com/


Description
Description : The repair of DNA double-strand breaks (DSBs) is critical for the maintenance of genomic integrity and viability for all organisms. Mammals have evolved at least two genetically discrete ways to mediate DNA DSB repair : homologous recombination (HR) and non-homologous end joining (NHEJ). In mammalian cells, most DSBs are preferentially repaired by NHEJ. Recent work has demonstrated that NHEJ consists of at least two sub-pathways—the main Ku heterodimerdependent or ‘‘classic’’ NHEJ (C-NHEJ) pathway and an ‘‘alternative’’ NHEJ (A-NHEJ) pathway, which usually generates microhomology-mediated signatures at repair junctions. In our study, recombinant adeno-associated virus knockout vectors were utilized to construct a series of isogenic human somatic cell lines deficient in the core C-NHEJ factors (Ku, DNA-PKcs, XLF, and LIGIV), and the resulting cell lines were characterized for their ability to carry out DNA DSB repair. The absence of DNA-PKcs, XLF, or LIGIV resulted in cell lines that were profoundly impaired in DNA DSB repair activity. Unexpectedly, Ku86- null cells showed wild-type levels of DNA DSB repair activity that was dominated by microhomology joining events indicative of A-NHEJ. Importantly, A-NHEJ DNA DSB repair activity could also be efficiently de-repressed in LIGIV-null and DNA-PKcs-null cells by subsequently reducing the level of Ku70. These studies demonstrate that in human cells C-NHEJ is the major DNA DSB repair pathway and they show that Ku is the critical C-NHEJ factor that regulates DNA NHEJ DSB pathway choice.

 

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