The ZGRF1 Helicase Promotes Recombinational Repair of Replication-Blocking DNA Damage in Human Cells | Zendy

André Brannvoll | Zendy; Xiaoyu Xue | Zendy; Youngho Kwon | Zendy; Smaragdi Kompocholi | Zendy; Anne Simonsen | Zendy; Keerthana Stine Viswalingam | Zendy; Leticia Gonzalez | Zendy; Ian D. Hickson | Zendy; Vibe H. Oestergaard | Zendy; Hocine W Mankouri | Zendy; Patrick Sung | Zendy; Michael Lisby | Zendy

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The ZGRF1 Helicase Promotes Recombinational Repair of Replication-Blocking DNA Damage in Human Cells

Author(s) -

André Brannvoll,

Xiaoyu Xue,

Youngho Kwon,

Smaragdi Kompocholi,

Anne Simonsen,

Keerthana Stine Viswalingam,

Leticia Gonzalez,

Ian D. Hickson,

Vibe H. Oestergaard,

Hocine W Mankouri,

Patrick Sung,

Michael Lisby

Publication year - 2020

Publication title -

cell reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 6.264

H-Index - 154

eISSN - 2639-1856

pISSN - 2211-1247

DOI - 10.1016/j.celrep.2020.107849

Subject(s) - helicase , homologous recombination , rad51 , dna repair , biology , dna replication , dna damage , control of chromosome duplication , microbiology and biotechnology , postreplication repair , replication protein a , dna , mitosis , genetics , nucleotide excision repair , gene , dna binding protein , rna , transcription factor

Replication-blocking DNA lesions are particularly toxic to proliferating cells because they can lead to chromosome mis-segregation if not repaired prior to mitosis. In this study, we report that ZGRF1 null cells accumulate chromosome aberrations following replication perturbation and show sensitivity to two potent replication-blocking anticancer drugs: mitomycin C and camptothecin. Moreover, ZGRF1 null cells are defective in catalyzing DNA damage-induced sister chromatid exchange despite accumulating excessive FANCD2, RAD51, and γ-H2AX foci upon induction of interstrand DNA crosslinks. Consistent with a direct role in promoting recombinational DNA repair, we show that ZGRF1 is a 5'-to-3' helicase that catalyzes D-loop dissociation and Holliday junction branch migration. Moreover, ZGRF1 physically interacts with RAD51 and stimulates strand exchange catalyzed by RAD51-RAD54. On the basis of these data, we propose that ZGRF1 promotes repair of replication-blocking DNA lesions through stimulation of homologous recombination.

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