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. 2021 May 10;12:2594. doi: 10.1038/s41467-021-22813-w

Fig. 5. LRIG1 is necessary to enter in quiescence state.

Fig. 5

a Schematics of Lrig1 gene disruption. b PCR confirming CRISPR-Cas9 (control and parental line). c Flow cytometry plots with the transfected NSCs. d ICC for LRIG1(red) and nuclear counterstaining with DAPI (blue) in sorted populations after transfection. e EdU quantification of the WT and Lrig1 KO NSCs in the different conditions (EGF/FGF2, BMP, and BMP/FGF2) (n = 3). f Quantification of the single-cell colony formation in the WT and Lrig1 KO cells in EGF/FGF2 (n = 3). g Quantification of the number of colonies of deficient and WT NSCs after the treatment with BMP and BMP/FGF2, after to re-exposure to mitogens (n = 3). h Lrig1 KO cells maintain high levels of pEGFR; WB of EGFR total and EGFR-p in WT and Lrig1 KO cells in the different conditions (EGF/FGF2, BMP and BMP/FGF2). Loading control GAPDH. i Quantification of the EdU positive cells in KO and control cells in the different conditions using Gefitinib (n = 3 per condition). j Single-cell colony-forming assay of the deficient and control NSCs using Gefitinib (n = 3 per genotype and condition, 48 single cells plated in each group each time). k Quantification of the colony formation of the WT and Lrig1 KO NSCs in each condition (BMP and BMP/FGF2) using EGFR inhibitor (Gefitinib) (n = 3 per condition). Scale bar in d = 50um. Data are shown as mean ± SEM of the indicated number of the experiments (n) (∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001). Source data are provided as Source Data File.