Assay scaling for high-throughput editing. (A) Representative low-magnification view of 384-well plate regions showing consistent editing in U-2 OS PEX cells treated with crLIS1, crDYNC1H1, and crPLK1. crLIS1 and crDYNC1H1 activities were assessed by immunostaining for the target proteins, whereas activity of crPLK1 was read out by a reduction in cell number (revealed by Hoechst staining). (B–D) Violin plots (median, bold line; first/third quartile, dashed lines) of frequency of cells depleted for LIS1 (B) or DYNC1H1 (C), or the number of cells (D), after transfection with crLIS1, crDYNC1H1, or crPLK1, respectively. Gating of target-depleted cells was based on the range of the fluorescence signal of NTC cells. Datapoints represent mean per cell intensities aggregated at the well level (minimum of 100 cells from 192 wells per plate) for three individual plates (P).
Figure S3.

Assay scaling for high-throughput editing. (A) Representative low-magnification view of 384-well plate regions showing consistent editing in U-2 OS PEX cells treated with crLIS1, crDYNC1H1, and crPLK1. crLIS1 and crDYNC1H1 activities were assessed by immunostaining for the target proteins, whereas activity of crPLK1 was read out by a reduction in cell number (revealed by Hoechst staining). (B–D) Violin plots (median, bold line; first/third quartile, dashed lines) of frequency of cells depleted for LIS1 (B) or DYNC1H1 (C), or the number of cells (D), after transfection with crLIS1, crDYNC1H1, or crPLK1, respectively. Gating of target-depleted cells was based on the range of the fluorescence signal of NTC cells. Datapoints represent mean per cell intensities aggregated at the well level (minimum of 100 cells from 192 wells per plate) for three individual plates (P).

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