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.

• MeSH
• Cell Line MeSH
• CRISPR-Cas Systems MeSH
• DNA Helicases genetics   MeSH
• Fanconi Anemia genetics   MeSH
• Haploidy MeSH
• HEK293 Cells MeSH
• RecQ Helicases genetics   MeSH
• Mutagenesis, Insertional MeSH
• Humans MeSH
• NAD(P)H Dehydrogenase (Quinone) genetics   MeSH
• DNA Repair genetics   MeSH
• DNA Damage MeSH
• Fanconi Anemia Complementation Group C Protein genetics   MeSH
• Fanconi Anemia Complementation Group D2 Protein genetics   MeSH
• Fanconi Anemia Complementation Group Proteins genetics   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Research Support, N.I.H., Extramural MeSH