Fig. 5: Genome-wide positive selection of GPI-anchor-synthesis- and N-glycosylation-defective cells in a proaerolysin (PA)-resistance screen. | Nature Communications

Fig. 5: Genome-wide positive selection of GPI-anchor-synthesis- and N-glycosylation-defective cells in a proaerolysin (PA)-resistance screen.

From: Higher resolution pooled genome-wide CRISPR knockout screening in Drosophila cells using integration and anti-CRISPR (IntAC)

Fig. 5: Genome-wide positive selection of GPI-anchor-synthesis- and N-glycosylation-defective cells in a proaerolysin (PA)-resistance screen.

A Schematic of the eukaryotic GPI anchor synthesis pathway highlighting genes shown to be necessary (red) or dispensable/unclear (dark gray/light gray) for human cell sensitivity to aerolysin34,35. B A genome-wide IntAC PA-resistance screen identifies genes in the GPI anchor synthesis (red) and N-glycosylation (brown) pathways, confirming the results of past studies in mammalian cells34,35,36. Plotted values are -Log of MAGeCK25 robust rank aggregation (RRA) scores from two independent replicates of PA treatment compared to sgRNA distribution in a common untreated cell population. C The orthologs of the genes identified in the PA resistance screen from B are placed within the GPI anchor synthesis pathway, highlighting genes that are enriched in the Drosophila IntAC screen (red) versus not enriched or not annotated as conserved (gray or gray strikethrough). Figure adapted from Liu et al. A knockout cell library of GPI biosynthetic genes for functional studies of GPI-anchored proteins, 2021 Communications Biology35 (CC-BY-4.0. http://creativecommons.org/licenses/by/4.0/).

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