Strand invasion by HLTF as a mechanism for template switch in
fork rescue

J 2014

Strand invasion by HLTF as a mechanism for template switch in fork rescue

BURKOVICS, Peter, Marek ŠEBESTA, David BALOGH, Lajos HARACSKA, Lumír KREJČÍ et. al.

Základní údaje

Originální název

Strand invasion by HLTF as a mechanism for template switch in fork rescue

Autoři

BURKOVICS, Peter (348 Maďarsko, domácí), Marek ŠEBESTA (703 Slovensko, domácí), David BALOGH (348 Maďarsko), Lajos HARACSKA (348 Maďarsko) a Lumír KREJČÍ (203 Česká republika, garant, domácí)

Vydání

Nucleic Acids Research, Oxford, Oxford University Press, 2014, 0305-1048

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

Genetika a molekulární biologie

Stát vydavatele

Velká Británie a Severní Irsko

Utajení

není předmětem státního či obchodního tajemství

Impakt faktor

Impact factor: 9.112

Kód RIV

RIV/00216224:14110/14:00073467

Organizační jednotka

Lékařská fakulta

DOI

http://dx.doi.org/10.1093/nar/gkt1040

UT WoS

000331138800030

Klíčová slova anglicky

TRANSLESION DNA-SYNTHESIS; CELL NUCLEAR ANTIGEN; HOMOLOGOUS RECOMBINATION; POSTREPLICATION REPAIR; SACCHAROMYCES-CEREVISIAE; REPLICATION FORK; DAMAGED DNA; UBIQUITIN LIGASE; POLYMERASE IOTA; RAD51 PROTEIN

Štítky

EL OK, podil

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 2. 4. 2014 17:13, Ing. Mgr. Věra Pospíšilíková

Anotace

V originále

Stalling of replication forks at unrepaired DNA lesions can result in discontinuities opposite the damage in the newly synthesized DNA strand. Translesion synthesis or facilitating the copy from the newly synthesized strand of the sister duplex by template switching can overcome such discontinuities. During template switch, a new primer–template junction has to be formed and two mechanisms, including replication fork reversal and D-loop formation have been suggested. Genetic evidence indicates a major role for yeast Rad5 in template switch and that both Rad5 and its human orthologue, Helicase-like transcription factor (HLTF), a potential tumour suppressor can facilitate replication fork reversal. This study demonstrates the ability of HLTF and Rad5 to form a D-loop without requiring ATP binding and/or hydrolysis. We also show that this strand-pairing activity is independent of RAD51 in vitro and is not mechanistically related to that of another member of the SWI/SNF family, RAD54. In addition, the 30-end of the invading strand in the D-loop can serve as a primer and is extended by DNA polymerase. Our data indicate that HLTF is involved in a RAD51-independent Dloop branch of template switch pathway that can promote repair of gaps formed during replication of damaged DNA.

Návaznosti

EE2.3.20.0011, projekt VaV

Název: Centrum výzkumu pluripotentních buněk a nestability genomu

GAP207/12/2323, projekt VaV

Název: Endonuleazová a translokázová aktivita v restričních-modifikáčních komplexéch typu I

Investor: Grantová agentura ČR, Endonuleázová a translokázová aktivita v restrikčních-modifikačních komplexech typu I

GA13-26629S, projekt VaV

Název: SUMO a stability genomu

Investor: Grantová agentura ČR, SUMO a stability genomu

Citovat

BURKOVICS, Peter, Marek ŠEBESTA, David BALOGH, Lajos HARACSKA a Lumír KREJČÍ. Strand invasion by HLTF as a mechanism for template switch in fork rescue. Nucleic Acids Research. Oxford: Oxford University Press, 2014, roč. 42, č. 3, s. 1711-1720. ISSN 0305-1048. Dostupné z: https://dx.doi.org/10.1093/nar/gkt1040.

@article{1160748,
   author = {Burkovics, Peter and Šebesta, Marek and Balogh, David and Haracska, Lajos and Krejčí, Lumír},
   article_location = {Oxford},
   article_number = {3},
   doi = {http://dx.doi.org/10.1093/nar/gkt1040},
   keywords = {TRANSLESION DNA-SYNTHESIS; CELL NUCLEAR ANTIGEN; HOMOLOGOUS RECOMBINATION; POSTREPLICATION REPAIR; SACCHAROMYCES-CEREVISIAE; REPLICATION FORK; DAMAGED DNA; UBIQUITIN LIGASE; POLYMERASE IOTA; RAD51 PROTEIN},
   language = {eng},
   issn = {0305-1048},
   journal = {Nucleic Acids Research},
   title = {Strand invasion by HLTF as a mechanism for template switch in fork rescue},
   volume = {42},
   year = {2014}
}

TY  - JOUR
ID  - 1160748
AU  - Burkovics, Peter - Šebesta, Marek - Balogh, David - Haracska, Lajos - Krejčí, Lumír
PY  - 2014
TI  - Strand invasion by HLTF as a mechanism for template switch in fork rescue
JF  - Nucleic Acids Research
VL  - 42
IS  - 3
SP  - 1711-1720
EP  - 1711-1720
PB  - Oxford University Press
SN  - 03051048
KW  - TRANSLESION DNA-SYNTHESIS
KW  - CELL NUCLEAR ANTIGEN
KW  - HOMOLOGOUS RECOMBINATION
KW  - POSTREPLICATION REPAIR
KW  - SACCHAROMYCES-CEREVISIAE
KW  - REPLICATION FORK
KW  - DAMAGED DNA
KW  - UBIQUITIN LIGASE
KW  - POLYMERASE IOTA
KW  - RAD51 PROTEIN
N2  - Stalling of replication forks at unrepaired DNA lesions can result in discontinuities opposite the damage in the newly synthesized DNA strand. Translesion synthesis or facilitating the copy from the newly synthesized strand of the sister duplex by template switching can overcome such discontinuities. During template switch, a new primer–template junction has to be formed and two mechanisms, including replication fork reversal and D-loop formation have been suggested. Genetic evidence indicates a major role for yeast Rad5 in template switch and that both Rad5 and its human orthologue, Helicase-like transcription factor (HLTF), a potential tumour suppressor can facilitate replication fork reversal. This study demonstrates the ability of HLTF and Rad5 to form a D-loop without requiring ATP binding and/or hydrolysis. We also show that this strand-pairing activity is independent of RAD51 in vitro and is not mechanistically related to that of another member of the SWI/SNF family, RAD54. In addition, the 30-end of the invading strand in the D-loop can serve as a primer and is extended by DNA polymerase. Our data indicate that HLTF is involved in a RAD51-independent Dloop branch of template switch pathway that can promote repair of gaps formed during replication of damaged DNA.
ER  -

BURKOVICS, Peter, Marek ŠEBESTA, David BALOGH, Lajos HARACSKA a Lumír KREJČÍ. Strand invasion by HLTF as a mechanism for template switch in fork rescue. \textit{Nucleic Acids Research}. Oxford: Oxford University Press, 2014, roč.~42, č.~3, s.~1711-1720. ISSN~0305-1048. Dostupné z: https://dx.doi.org/10.1093/nar/gkt1040.

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