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Genetic redundancy has evolved as a way for human cells to survive the loss of genes that are single copy and essential in other organisms, but also allows tumours to survive despite having highly rearranged genomes. In this study we CRISPR screen 1191 gene pairs, including paralogues and known and predicted synthetic lethal interactions to identify 105 gene combinations whose co-disruption results in a loss of cellular fitness. 27 pairs influence fitness across multiple cell lines including the paralogues  FAM50A/FAM50B , two genes of unknown function. Silencing of  FAM50B  occurs across a range of tumour types and in this context disruption of  FAM50A  reduces cellular fitness whilst promoting micronucleus formation and extensive perturbation of transcriptional programmes. Our studies reveal the fitness effects of  FAM50A/FAM50B  in cancer cells.

Combinatorial CRISPR screen identifies fitness effects of gene paralogues