• Je něco špatně v tomto záznamu ?

Unloading of homologous recombination factors is required for restoring double-stranded DNA at damage repair loci

Y. Vasianovich, V. Altmannova, O. Kotenko, MD. Newton, L. Krejci, S. Makovets,

. 2017 ; 36 (2) : 213-231. [pub] 20161208

Jazyk angličtina Země Anglie, Velká Británie

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/bmc17031236

Cells use homology-dependent DNA repair to mend chromosome breaks and restore broken replication forks, thereby ensuring genome stability and cell survival. DNA break repair via homology-based mechanisms involves nuclease-dependent DNA end resection, which generates long tracts of single-stranded DNA required for checkpoint activation and loading of homologous recombination proteins Rad52/51/55/57. While recruitment of the homologous recombination machinery is well characterized, it is not known how its presence at repair loci is coordinated with downstream re-synthesis of resected DNA We show that Rad51 inhibits recruitment of proliferating cell nuclear antigen (PCNA), the platform for assembly of the DNA replication machinery, and that unloading of Rad51 by Srs2 helicase is required for efficient PCNA loading and restoration of resected DNA As a result, srs2Δ mutants are deficient in DNA repair correlating with extensive DNA processing, but this defect in srs2Δ mutants can be suppressed by inactivation of the resection nuclease Exo1. We propose a model in which during re-synthesis of resected DNA, the replication machinery must catch up with the preceding processing nucleases, in order to close the single-stranded gap and terminate further resection.

Citace poskytuje Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc17031236
003      
CZ-PrNML
005      
20171025115439.0
007      
ta
008      
171025s2017 enk f 000 0|eng||
009      
AR
024    7_
$a 10.15252/embj.201694628 $2 doi
035    __
$a (PubMed)27932447
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a enk
100    1_
$a Vasianovich, Yulia $u Institute of Cell Biology, School of Biological Sciences, University of Edinburgh, Edinburgh, UK.
245    10
$a Unloading of homologous recombination factors is required for restoring double-stranded DNA at damage repair loci / $c Y. Vasianovich, V. Altmannova, O. Kotenko, MD. Newton, L. Krejci, S. Makovets,
520    9_
$a Cells use homology-dependent DNA repair to mend chromosome breaks and restore broken replication forks, thereby ensuring genome stability and cell survival. DNA break repair via homology-based mechanisms involves nuclease-dependent DNA end resection, which generates long tracts of single-stranded DNA required for checkpoint activation and loading of homologous recombination proteins Rad52/51/55/57. While recruitment of the homologous recombination machinery is well characterized, it is not known how its presence at repair loci is coordinated with downstream re-synthesis of resected DNA We show that Rad51 inhibits recruitment of proliferating cell nuclear antigen (PCNA), the platform for assembly of the DNA replication machinery, and that unloading of Rad51 by Srs2 helicase is required for efficient PCNA loading and restoration of resected DNA As a result, srs2Δ mutants are deficient in DNA repair correlating with extensive DNA processing, but this defect in srs2Δ mutants can be suppressed by inactivation of the resection nuclease Exo1. We propose a model in which during re-synthesis of resected DNA, the replication machinery must catch up with the preceding processing nucleases, in order to close the single-stranded gap and terminate further resection.
650    _2
$a DNA $x metabolismus $7 D004247
650    12
$a poškození DNA $7 D004249
650    _2
$a enzymy opravy DNA $x metabolismus $7 D045643
650    12
$a homologní rekombinace $7 D059765
650    _2
$a biologické modely $7 D008954
650    _2
$a proliferační antigen buněčného jádra $x metabolismus $7 D018809
650    _2
$a rekombinasy $x metabolismus $7 D045522
650    12
$a rekombinační oprava DNA $7 D059767
650    _2
$a Saccharomyces cerevisiae $x enzymologie $x genetika $x metabolismus $7 D012441
655    _2
$a časopisecké články $7 D016428
700    1_
$a Altmannová, Veronika $u Department of Biology, Masaryk University, Brno, Czech Republic. International Clinical Research Center, St. Anne's University Hospital in Brno, Brno, Czech Republic. $7 mub2011626283
700    1_
$a Kotenko, Oleksii $u Institute of Cell Biology, School of Biological Sciences, University of Edinburgh, Edinburgh, UK.
700    1_
$a Newton, Matthew D $u Institute of Cell Biology, School of Biological Sciences, University of Edinburgh, Edinburgh, UK.
700    1_
$a Krejci, Lumir $u Department of Biology, Masaryk University, Brno, Czech Republic. International Clinical Research Center, St. Anne's University Hospital in Brno, Brno, Czech Republic. National Centre for Biomolecular Research, Masaryk University, Brno, Czech Republic.
700    1_
$a Makovets, Svetlana $u Institute of Cell Biology, School of Biological Sciences, University of Edinburgh, Edinburgh, UK smakovet@staffmail.ed.ac.uk.
773    0_
$w MED00181668 $t The EMBO journal $x 1460-2075 $g Roč. 36, č. 2 (2017), s. 213-231
856    41
$u https://pubmed.ncbi.nlm.nih.gov/27932447 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y a $z 0
990    __
$a 20171025 $b ABA008
991    __
$a 20171025115521 $b ABA008
999    __
$a ok $b bmc $g 1254829 $s 992263
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2017 $b 36 $c 2 $d 213-231 $e 20161208 $i 1460-2075 $m The EPMA journal $n EPMA J $x MED00181668
LZP    __
$a Pubmed-20171025
Zpět

Najít záznam

Citační ukazatele

Možnosti archivace