Replication-Independent Endogenous DNA Double-Strand Breaks in Saccharomyces cerevisiae Model

DSpace/Manakin Repository

Replication-Independent Endogenous DNA Double-Strand Breaks in Saccharomyces cerevisiae Model

Citable link to this page

 

 
Title: Replication-Independent Endogenous DNA Double-Strand Breaks in Saccharomyces cerevisiae Model
Author: Thongsroy, Jirapan; Matangkasombut, Oranart; Thongnak, Araya; Rattanatanyong, Prakasit; Jirawatnotai, Siwanon; Mutirangura, Apiwat

Note: Order does not necessarily reflect citation order of authors.

Citation: Thongsroy, Jirapan, Oranart Matangkasombut, Araya Thongnak, Prakasit Rattanatanyong, Siwanon Jirawatnotai, and Apiwat Mutirangura. 2013. “Replication-Independent Endogenous DNA Double-Strand Breaks in Saccharomyces cerevisiae Model.” PLoS ONE 8 (8): e72706. doi:10.1371/journal.pone.0072706. http://dx.doi.org/10.1371/journal.pone.0072706.
Full Text & Related Files:
Abstract: Without exposure to any DNA-damaging agents, non-dividing eukaryotic cells carry endogenous DNA double-strand breaks (EDSBs), or Replication-Independent (RIND)-EDSBs. In human cells, RIND-EDSBs are enriched in the methylated heterochromatic areas of the genome and are repaired by an ATM-dependent non-homologous end-joining pathway (NHEJ). Here, we showed that Saccharomyces cerevisiae similarly possess RIND-EDSBs. Various levels of EDSBs were detected during different phases of the cell cycle, including G0. Using a collection of mutant yeast strains, we investigated various DNA metabolic and DNA repair pathways that might be involved in the maintenance of RIND-EDSB levels. We found that the RIND-EDSB levels increased significantly in yeast strains lacking proteins involved in NHEJ DNA repair and in suppression of heterochromatin formation. RIND-EDSB levels were also upregulated when genes encoding histone deacetylase, endonucleases, topoisomerase, and DNA repair regulators were deleted. In contrast, RIND-EDSB levels were downregulated in the mutants that lack chromatin-condensing proteins, such as the high-mobility group box proteins, and Sir2. Likewise, RIND-EDSB levels were also decreased in human cells lacking HMGB1. Therefore, we conclude that the genomic levels of RIND-EDSBs are evolutionally conserved, dynamically regulated, and may be influenced by genome topology, chromatin structure, and the efficiency of DNA repair systems.
Published Version: doi:10.1371/journal.pone.0072706
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3747138/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:11855846
Downloads of this work:

Show full Dublin Core record

This item appears in the following Collection(s)

 
 

Search DASH


Advanced Search
 
 

Submitters