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@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 and Lumír KREJČÍ. Strand invasion by HLTF as a mechanism for template switch in fork rescue. \textit{Nucleic Acids Research}. Oxford: Oxford University Press, vol.~42, No~3, p.~1711-1720. ISSN~0305-1048. doi:10.1093/nar/gkt1040. 2014.
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