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

M. Moder, G. Velimezi, M. Owusu, A. Mazouzi, M. Wiedner, J. Ferreira da Silva, L. Robinson-Garcia, F. Schischlik, R. Slavkovsky, R. Kralovics, M. Schuster, C. Bock, T. Ideker, SP. Jackson, J. Menche, JI. Loizou,

. 2017 ; 8 (1) : 1238. [pub] 20171101

Language English Country England, Great Britain

Document type Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't

Persistent link   https://www.medvik.cz/link/bmc19001120

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.

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$a Maintenance of genome integrity via repair of DNA damage is a key biological process required to suppress diseases, including Fanconi anemia (FA). We generated loss-of-function human haploid cells for FA complementation group C (FANCC), a gene encoding a component of the FA core complex, and used genome-wide CRISPR libraries as well as insertional mutagenesis to identify synthetic viable (genetic suppressor) interactions for FA. Here we show that loss of the BLM helicase complex suppresses FANCC phenotypes and we confirm this interaction in cells deficient for FA complementation group I and D2 (FANCI and FANCD2) that function as part of the FA I-D2 complex, indicating that this interaction is not limited to the FA core complex, hence demonstrating that systematic genome-wide screening approaches can be used to reveal genetic viable interactions for DNA repair defects.
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$a Velimezi, Georgia $u CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14, AKH BT 25.3, 1090, Vienna, Austria.
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$a Schischlik, Fiorella $u CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14, AKH BT 25.3, 1090, Vienna, Austria.
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$a Slavkovsky, Rastislav $u CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14, AKH BT 25.3, 1090, Vienna, Austria. Institute of Molecular and Translational Medicine, Faculty of Medicine and Dentistry, Palacky University Olomouc, Olomouc, Czech Republic.
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$a Kralovics, Robert $u CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14, AKH BT 25.3, 1090, Vienna, Austria.
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$a Bock, Christoph $u CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14, AKH BT 25.3, 1090, Vienna, Austria.
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$a Ideker, Trey $u Department of Medicine, Division of Genetics, University of California San Diego, La Jolla, CA, 92093, USA. Department of Bioengineering, University of California San Diego, La Jolla, CA, 92093, USA. Moores Cancer Center, University of California San Diego, La Jolla, CA, 92093, USA. The Cancer Cell Map Initiative, La Jolla, CA, 92093, USA.
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$a Jackson, Stephen P $u The Wellcome Trust and Cancer Research UK Gurdon Institute, and Department of Biochemistry, University of Cambridge, Cambridge, CB2 1QN, UK. The Wellcome Trust Sanger Institute, Hinxton, Cambridge, CB10 1SA, UK.
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$a Loizou, Joanna I $u CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14, AKH BT 25.3, 1090, Vienna, Austria. jloizou@cemm.oeaw.ac.at.
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