Parallel genome-wide screens identify synthetic viable interactions between the BLM helicase complex and Fanconi anemia

Martin Moder, Georgia Velimezi, Michel Owusu, Abdelghani Mazouzi, Marc Wiedner, Joana Ferreira da Silva, Lydia Robinson-Garcia, Fiorella Schischlik, Rastislav Slavkovsky, Robert Kralovics, Michael Schuster, Christoph Bock, Trey Ideker, Stephen P. Jackson, Jörg Menche and Joanna I. Loizou ()
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Martin Moder: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences
Georgia Velimezi: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences
Michel Owusu: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences
Abdelghani Mazouzi: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences
Marc Wiedner: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences
Joana Ferreira da Silva: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences
Lydia Robinson-Garcia: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences
Fiorella Schischlik: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences
Rastislav Slavkovsky: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences
Robert Kralovics: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences
Michael Schuster: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences
Christoph Bock: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences
Trey Ideker: Division of Genetics, University of California San Diego
Stephen P. Jackson: The Wellcome Trust and Cancer Research UK Gurdon Institute, and Department of Biochemistry, University of Cambridge
Jörg Menche: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences
Joanna I. Loizou: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences

Nature Communications, 2017, vol. 8, issue 1, 1-8

Abstract: Abstract Maintenance of genome integrity via repair of DNA damage is a key biological process required to suppress diseases, including Fanconi anemia (FA). We generated loss-of-function human haploid cells for FA complementation group C (FANCC), a gene encoding a component of the FA core complex, and used genome-wide CRISPR libraries as well as insertional mutagenesis to identify synthetic viable (genetic suppressor) interactions for FA. Here we show that loss of the BLM helicase complex suppresses FANCC phenotypes and we confirm this interaction in cells deficient for FA complementation group I and D2 (FANCI and FANCD2) that function as part of the FA I-D2 complex, indicating that this interaction is not limited to the FA core complex, hence demonstrating that systematic genome-wide screening approaches can be used to reveal genetic viable interactions for DNA repair defects.

Date: 2017
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DOI: 10.1038/s41467-017-01439-x

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