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PMID:24171103

2017-08-09T20:09:47Z

Xia2017ECGA: New PMID: Page!

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PMID:24171103

2017-08-09T20:09:47Z

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'''Shee, C, Cox, BD, Gu, F, Luengas, EM, Joshi, MC, Chiu, LY, Magnan, D, Halliday, JA, Frisch, RL, Gibson, JL, Nehring, RB, Do, HG, Hernandez, M, Li, L, Herman, C, Hastings, PJ, Bates, D, Harris, RS, Miller, KM and Rosenberg, SM''' (2013) Engineered proteins detect spontaneous DNA breakage in human and bacterial cells. ''Elife'' '''2''':e01222
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!align=left align='left' bgcolor='#CCCCFF' |Abstract
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Spontaneous DNA breaks instigate genomic changes that fuel cancer and evolution, yet direct quantification of double-strand breaks (DSBs) has been limited. Predominant sources of spontaneous DSBs remain elusive. We report synthetic technology for quantifying DSBs using fluorescent-protein fusions of double-strand DNA end-binding protein, Gam of bacteriophage Mu. In Escherichia coli GamGFP forms foci at chromosomal DSBs and pinpoints their subgenomic locations. Spontaneous DSBs occur mostly one per cell, and correspond with generations, supporting replicative models for spontaneous breakage, and providing the first true breakage rates. In mammalian cells GamGFP-labels laser-induced DSBs antagonized by end-binding protein Ku; co-localizes incompletely with DSB marker 53BP1 suggesting superior DSB-specificity; blocks resection; and demonstrates DNA breakage via APOBEC3A cytosine deaminase. We demonstrate directly that some spontaneous DSBs occur outside of S phase. The data illuminate spontaneous DNA breakage in E. coli and human cells and illustrate the versatility of fluorescent-Gam for interrogation of DSBs in living cells. DOI:http://dx.doi.org/10.7554/eLife.01222.001.
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!align=left align='left' bgcolor='#CCCCFF' |Links
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=24171103 PubMed] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3809393 PMC3809393]
Online version:[http://dx.doi.org/10.7554/eLife.01222 10.7554/eLife.01222]
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!align=left align='left' bgcolor='#CCCCFF' |Keywords
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Animals; Bacteriophage mu/chemistry; Chromosomes, Bacterial/chemistry; Chromosomes, Bacterial/metabolism; Cytidine Deaminase/genetics; Cytidine Deaminase/metabolism; DNA/chemistry; DNA/metabolism; DNA Breaks, Double-Stranded; DNA Helicases/genetics; DNA Helicases/metabolism; DNA-Binding Proteins/genetics; DNA-Binding Proteins/metabolism; Escherichia coli/genetics; Escherichia coli/metabolism; Gene Expression Regulation; Genes, Reporter; Green Fluorescent Proteins/genetics; Green Fluorescent Proteins/metabolism; HeLa Cells; Humans; Intracellular Signaling Peptides and Proteins/genetics; Intracellular Signaling Peptides and Proteins/metabolism; Ku Autoantigen; Mice; Protein Engineering/methods; Proteins/genetics; Proteins/metabolism; Recombinant Fusion Proteins/genetics; Recombinant Fusion Proteins/metabolism; Synthetic Biology; Tumor Suppressor p53-Binding Protein 1; Viral Proteins/genetics; Viral Proteins/metabolism

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==Main Points of the Paper ==
{{LitSignificance}}

== Materials and Methods Used ==
{{LitMaterials}}

==Phenotype Annotations==
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!|Phenotype of!!Taxon Information!!Genotype Information (if known)!!Condition Information!!OMP ID!!OMP Term Name!!ECO ID!!ECO Term Name!!Notes!!Status

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==Notes==

==References==
{{RefHelp}}
<references/>

[[Category:Publication]]

PMID:28090586

2017-08-09T16:29:28Z

Xia2017ECGA: Fill PMID: Page!

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{| id="E598b38681ffaa" class=" tableEdit PMID_info_table"

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'''Xia, J, Chen, LT, Mei, Q, Ma, CH, Halliday, JA, Lin, HY, Magnan, D, Pribis, JP, Fitzgerald, DM, Hamilton, HM, Richters, M, Nehring, RB, Shen, X, Li, L, Bates, D, Hastings, PJ, Herman, C, Jayaram, M and Rosenberg, SM''' (2016) Holliday junction trap shows how cells use recombination and a junction-guardian role of RecQ helicase. ''Sci Adv'' '''2''':e1601605
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!align=left align='left' bgcolor='#CCCCFF' |Abstract
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DNA repair by homologous recombination (HR) underpins cell survival and fuels genome instability, cancer, and evolution. However, the main kinds and sources of DNA damage repaired by HR in somatic cells and the roles of important HR proteins remain elusive. We present engineered proteins that trap, map, and quantify Holliday junctions (HJs), a central DNA intermediate in HR, based on catalytically deficient mutant RuvC protein of Escherichia coli. We use RuvCDefGFP (RDG) to map genomic footprints of HR at defined DNA breaks in E. coli and demonstrate genome-scale directionality of double-strand break (DSB) repair along the chromosome. Unexpectedly, most spontaneous HR-HJ foci are instigated, not by DSBs, but rather by single-stranded DNA damage generated by replication. We show that RecQ, the E. coli ortholog of five human cancer proteins, nonredundantly promotes HR-HJ formation in single cells and, in a novel junction-guardian role, also prevents apparent non-HR-HJs promoted by RecA overproduction. We propose that one or more human RecQ orthologs may act similarly in human cancers overexpressing the RecA ortholog RAD51 and find that cancer genome expression data implicate the orthologs BLM and RECQL4 in conjunction with EME1 and GEN1 as probable HJ reducers in such cancers. Our results support RecA-overproducing E. coli as a model of the many human tumors with up-regulated RAD51 and provide the first glimpses of important, previously elusive reaction intermediates in DNA replication and repair in single living cells.
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!align=left align='left' bgcolor='#CCCCFF' |Links
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=28090586 PubMed] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5222578 PMC5222578]
Online version:[http://dx.doi.org/10.1126/sciadv.1601605 10.1126/sciadv.1601605]
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!align=left align='left' bgcolor='#CCCCFF' |Keywords
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==Main Points of the Paper ==
{{LitSignificance}}

== Materials and Methods Used ==
{{LitMaterials}}

==Phenotype Annotations==
{{AnnotationTableHelp}}
<protect>

{| border="2" cellpadding="4" cellspacing="0" style="margin: 1em 1em 1em 0; border: 1px #aaa solid; border-collapse: collapse;" id="L598b386895666" class=" tableEdit Phenotype_Table_2"
|- align='left' bgcolor='#CCCCFF'
!|Phenotype of!!Taxon Information!!Genotype Information (if known)!!Condition Information!!OMP ID!!OMP Term Name!!ECO ID!!ECO Term Name!!Notes!!Status

|- class="tableEdit_footer"
|<div class="tableEdit_editLink plainlinks">[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=d41d8cd98f00b204e9800998ecf8427e.14831.L598b386895666&page=14831&pagename={{FULLPAGENAMEE}}&type=0&template=Phenotype_Table_2 edit table]</div> || || || || || || || || ||
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</protect>

==Notes==

==References==
{{RefHelp}}
<references/>

[[Category:Publication]]

PMID:28090586

2017-08-09T16:29:27Z

Xia2017ECGA: New PMID: Page!

PMID on Demand placeholder