RECQ1 is required for cellular resistance to replication stress and catalyzes strand exchange on stalled replication fork structures

Popuri, Venkateswarlu; Croteau, Deborah L.; Brosh, Robert M.; Bohr, Vilhelm A.

doi:10.4161/cc.22581

Cited by 47 publications

(60 citation statements)

References 58 publications

(78 reference statements)

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“…35 Loss of RECQ1 helicase results in replication fork collapse and DNA damage response. 36 Interestingly, RECQ1-deficient cells show defective chromosomal condensation due to untimely DNA replication, reminiscent of anaphase ultra-fine DNA bridges in ZNF365-knockdown cells. 19,36 Our identification of MRE11-dependent DNA end resection as an affected step upon ZNF365 loss supports its role in interplay between HR repair and replication fork recovery.…”

Section: Discussionmentioning

confidence: 98%

“…36 Interestingly, RECQ1-deficient cells show defective chromosomal condensation due to untimely DNA replication, reminiscent of anaphase ultra-fine DNA bridges in ZNF365-knockdown cells. 19,36 Our identification of MRE11-dependent DNA end resection as an affected step upon ZNF365 loss supports its role in interplay between HR repair and replication fork recovery. Similarly, DNA2 nuclease mediates replication-coupled repair of DSB at the resection step and interacts with the Faconi anemia interstrand crosslinking (ICL) repair machinery.…”

Section: Discussionmentioning

confidence: 98%

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ZNF365 promotes stalled replication forks recovery to maintain genome stability

et al. 2013

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The ZNF365 locus is associated with breast cancer risk in carriers of mutated BRCA1 and BRCA2, which are important molecules required for DNA damage response. Previously, we demonstrated that ZNF365 is necessary for timely resolution of replication intermediates of genomic fragile sites and, thus, for suppression of genomic instability; however, the mechanism underlying the function of ZNF365 on damaged DNA and stalled replication forks remains unknown. Here, we demonstrate that ZNF365 is induced by DNA double-strand break (DSB) signals, is involved in the homologous recombination (HR) repair pathway, and maintains genome integrity during DNA replication. On the mechanistic level, ZNF365 interacts with poly(ADP-ribose) polymerase (PARP) 1 to tether MRE11 to the DNA end resection site. Loss of ZNF365 results in delayed mitotic progression and exit due to increased replication stress, ultimately leading to cytokinesis failure, re-duplication of centrosomes, and increased aneuploidy. Collectively, these results suggest an HR repair-dependent function of ZNF365 in preventing genomic instability.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 98%

ZNF365 promotes stalled replication forks recovery to maintain genome stability

et al. 2013

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“…We found that RECQL and RECQL5 are expressed at statistically significant decreased levels in CRC when compared to matched normal colonic mucosa ( Figure 2). Although loss of function of RECQL and RECQL5 have not been clearly linked to human disease, there is evidence from studies of mouse models as well as in vitro systems that loss of function of these helicases would likely lead to disease given their role in the maintenance of genomic stability [35,36,[38][39][40][41]. RECQL5 is implicated in DNA replication, transcription, and repair processes, and RECQL5 deficiency is thought to contribute to genomic instability [18,42].…”

Section: Discussionmentioning

confidence: 99%

Altered RecQ Helicase Expression in Sporadic Primary Colorectal Cancers

Lao

Carter

Dzieciatkowski

et al. 2013

Journal of Surgical Research

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Deregulation of DNA repair enzymes occurs in cancers and may create a susceptibility to chemotherapy. Expression levels of DNA repair enzymes have been shown to predict the responsiveness of cancers to certain chemotherapeutic agents. The RECQ helicases repair damaged DNA including damage caused by topoisomerase I inhibitors, such as irinotecan. Altered expression levels of these enzymes in colorectal cancer (CRC) may influence the response of the cancers to irinotecan. Thus, we assessed RECQ helicase (WRN, BLM, RECQL, RECQL4, and RECQL5) expression in primary CRCs, matched normal colon, and CRC cell lines. We found that BLM and RECQL4 mRNA levels are significantly increased in CRC (P = .0011 and P < .0001, respectively), whereas RECQL and RECQL5 are significantly decreased (P = .0103 and P = .0029, respectively). RECQ helicase expression patterns varied between specific molecular subtypes of CRCs. The mRNA and protein expression of the majority of the RECQ helicases was closely correlated, suggesting that altered mRNA expression is the predominant mechanism for deregulated RECQ helicase expression. Immunohistochemistry localized the RECQ helicases to the nucleus. RECQ helicase expression is altered in CRC, suggesting that RECQ helicase expression has potential to identify CRCs that are susceptible to specific chemotherapeutic agents.

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“…The RECQL1 and WRN 3′ to 5′ DNA helicase activities unwind the leading strand of forked DNA substrates, while RECQL4 and RECQL5β only unwind the lagging strand (Popuri et al , 2012a). RECQL1 alone is able to unwind short DNA duplexes (<110 base pairs), whereas it requires the presence of RPA to unwind longer substrates (501 base pairs) (Cui et al , 2003, 2004).…”

Section: Characteristics Of Human Recq Helicasesmentioning

confidence: 99%

“…RECQL1 is thought to stimulate PARP1-mediated DNA replication restart (Berti et al , 2013). Defects in RECQL1 lead to hyper-phosphorylation of RPA32 and activation of CHK1 (Popuri et al , 2012a). DSBs and sister chromatid exchange (SCE) are more pronounced in RECQL1-deficient mouse embryo fibroblasts (Sharma & Brosh, 2007).…”

Section: Characteristics Of Human Recq Helicasesmentioning

confidence: 99%

The role of RecQ helicases in non-homologous end-joining

Keijzers

Maynard

Shamanna

et al. 2014

Critical Reviews in Biochemistry and Molecular Biology

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DNA double-strand breaks are highly toxic DNA lesions that cause genomic instability, if not efficiently repaired. RecQ helicases are a family of highly conserved proteins that maintain genomic stability through their important roles in several DNA repair pathways, including DNA double-strand break repair. Double-strand breaks can be repaired by homologous recombination (HR) using sister chromatids as templates to facilitate precise DNA repair, or by an HR-independent mechanism known as non-homologous end-joining (NHEJ) (error-prone). NHEJ is a non-templated DNA repair process, in which DNA termini are directly ligated. Canonical NHEJ requires DNA-PKcs and Ku70/80, while alternative NHEJ pathways are DNA-PKcs and Ku70/80 independent. This review discusses the role of RecQ helicases in NHEJ, alternative (or back-up) NHEJ (B-NHEJ) and microhomology-mediated end-joining (MMEJ) in V(D)J recombination, class switch recombination and telomere maintenance.

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RECQ1 is required for cellular resistance to replication stress and catalyzes strand exchange on stalled replication fork structures

Cited by 47 publications

References 58 publications

ZNF365 promotes stalled replication forks recovery to maintain genome stability

ZNF365 promotes stalled replication forks recovery to maintain genome stability

Altered RecQ Helicase Expression in Sporadic Primary Colorectal Cancers

The role of RecQ helicases in non-homologous end-joining

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