Fig. 6: Ablation of FAM122A results in reduced proliferation that is rescued by re-expression of FAM122A in a SLiM-dependent manner.

A Western blot analysis of FAM122A CRISPR HEK293 clones (the C8 KO and C17 truncation were selected for further analysis) (n = 3) B Colony formation assays of control (parental and C1) and KOs (C8 and C17). C Ablation of FAM122A in HEK293, T98G cells inhibits proliferation. Cells were seeded in triplicate and the percent confluence was imaged with an Incucyte SX5. Statistical analyses of proliferation curves comparing parental cells to FAM122A knockout cell lines was conducted using a Wilcoxon matched-pairs signed rank test (two-sided). Data are presented as mean values +/− SEM. D A cassette directing the expression of FAM122A WT and SLiM-MT was stably introduced in HEK293 FAM122A KO cells. Expression of FAM122A wildtype but not SLiM mutant rescued the proliferation defect. Statistical analyses of proliferation curves comparing rescues to FAM122A knockout cell lines was conducted using a Friedman’s test (two-sided) of the last 10 measurements. HEK293 vs KO p value < 0.0001 (****), HEK293 WT Clone 1 p value = 0.0436 (*), HEK293 WT Clone 2 p value = 0.0002 (***), HEK293 SLiM MUT Clone 1 p value = 0.2640 (ns). FAM122A WT and SLiM mutant reconstitution are show in separate graphs compared to the same controls to more clearly visualize partial rescue (green curves) vs. absence of rescue with the SLiM mutant (magenta curve). Data are presented as mean values +/− SEM. Source data are provided as a Source Data file.