Difference between revisions of "PMID:28090586"
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| + | !align=left align='left' bgcolor='#CCCCFF' |Citation | ||
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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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| + | [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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| + | ==Main Points of the Paper == | ||
| + | {{LitSignificance}} | ||
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| + | == Materials and Methods Used == | ||
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| + | ==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== | ||
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| + | ==References== | ||
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| + | <references/> | ||
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| + | [[Category:Publication]] | ||
Latest revision as of 11:29, 9 August 2017
| Citation |
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 |
|---|---|
| Abstract |
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. |
| Links |
PubMed PMC5222578 Online version:10.1126/sciadv.1601605 |
| Keywords |
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Main Points of the Paper
Please summarize the main points of the paper.
Materials and Methods Used
Please list the materials and methods used in this paper (strains, plasmids, antibodies, etc).
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 |
|---|---|---|---|---|---|---|---|---|---|
Notes
References
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