Fig. 1: Depletion of C16orf72 is synthetic lethal with disruption of PARPs. | Nature Communications

Fig. 1: Depletion of C16orf72 is synthetic lethal with disruption of PARPs.

From: C16orf72/HAPSTR1/TAPR1 functions with BRCA1/Senataxin to modulate replication-associated R-loops and confer resistance to PARP disruption

Fig. 1

a A genome-wide CRISPR screen identified C16orf72 as one of ten genes whose disruption negatively affected the survival of PARP1/PARP2 double knock-out cells (parp1Δparp2Δ) as compared to wild-type U2OS cells. b Clonogenic survival assay of wild-type U2OS and parp1/2Δ cells treated with siRNA targeting C16orf72. Treatment with non-targeting siRNA (siNT) and siRNA targeting BRCA1 act as negative and positive controls, respectively. c Clonogenic survival assay of wild-type U2OS, PARP1 knock-out (parp1∆), PARP2 knock-out (parp2∆) and PARP1/PARP2 double knock-out (parp1/2∆) cells transfected with siC16orf72. d Clonogenic survival assay of C16orf72 knock-out cells (c16orf72Δ.2) and complemented cells (c16orf72Δ.2 cells expressing Flag-C16orf72) treated with increasing concentration of Olaparib for 9 days. e Clonogenic survival assay of C16orf72 knock-out cells (c16orf72Δ.2) and complemented cells (c16orf72Δ.2 + Flag-C16orf72) treated with increasing concentration of ATRi for 9 days. For all clonogenic survival assay plots, mean values ± SEM of three independent biological repeats shown. Statistical analysis was performed using either a one-way ANOVA with a Bonferroni post-hoc analysis (b, c), or two-way ANOVA (d, e); *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001. Source data are provided as a Source Data file.

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