Figure 1. Large-scale functional... | Rockefeller University Press

Figure 1.

$Large-scale functional genetics screens reveal modulators of antimicrotubule drug sensitivity. (A) Schematic showing the workflow for the pooled CRISPR screen. (B) Schematic showing the effects of microtubule drugs (nocodazole and paclitaxel) on microtubule dynamics. (C) The curve illustrating the CRISPR score of fitness conferring and growth enhancer genes upon treatment with either nocodazole or paclitaxel. (D) Scatter plot showing the CRISPR scores in untreated versus nocodazole-treated cell pools. (E) Scatter plot showing the CRISPR scores in untreated versus paclitaxel-treated cell pools. (F) Table showing the CRISPR scores of selected iKO in high concentrations of nocodazole or paclitaxel. (G) Autosomal start and end positions (from GRCH38.p12) of genes (black lines) with CRISPR score >1.5, P < 0.05 in 250 nM nocodazole (suppressors) on chromosome 1 were obtained from BioMart and plotted in R (for illustration of all chromosomes see Fig. S1 B); expected versus observed fractions of hits on between the end of chromosome 1 and KIF2C, or between KIF2C and the centromere. Expected fractions were calculated by assuming an even distribution of hits across the chromosome 1 length. (H) Scatter plot illustrating the differential CRISPR scores across all gene targets in the secondary screen. The differential was calculated between nocodazole and untreated and paclitaxel and untreated K562 cell pools. (I) Scatter plot illustrating the differential CRISPR scores across all gene targets in the secondary screen. The differential was calculated between nocodazole and untreated and paclitaxel and untreated HeLa cell pools.$

Large-scale functional genetics screens reveal modulators of antimicrotubule drug sensitivity. (A) Schematic showing the workflow for the pooled CRISPR screen. (B) Schematic showing the effects of microtubule drugs (nocodazole and paclitaxel) on microtubule dynamics. (C) The curve illustrating the CRISPR score of fitness conferring and growth enhancer genes upon treatment with either nocodazole or paclitaxel. (D) Scatter plot showing the CRISPR scores in untreated versus nocodazole-treated cell pools. (E) Scatter plot showing the CRISPR scores in untreated versus paclitaxel-treated cell pools. (F) Table showing the CRISPR scores of selected iKO in high concentrations of nocodazole or paclitaxel. (G) Autosomal start and end positions (from GRCH38.p12) of genes (black lines) with CRISPR score >1.5, P < 0.05 in 250 nM nocodazole (suppressors) on chromosome 1 were obtained from BioMart and plotted in R (for illustration of all chromosomes see Fig. S1 B); expected versus observed fractions of hits on between the end of chromosome 1 and KIF2C, or between KIF2C and the centromere. Expected fractions were calculated by assuming an even distribution of hits across the chromosome 1 length. (H) Scatter plot illustrating the differential CRISPR scores across all gene targets in the secondary screen. The differential was calculated between nocodazole and untreated and paclitaxel and untreated K562 cell pools. (I) Scatter plot illustrating the differential CRISPR scores across all gene targets in the secondary screen. The differential was calculated between nocodazole and untreated and paclitaxel and untreated HeLa cell pools.

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