Extended Data Fig. 9: Human EOMES+ve RL cells are mitotically active UBC progenitors.
From: Failure of human rhombic lip differentiation underlies medulloblastoma formation
a, EOMES and PAX6 expression in the developing human RL at 17 (i) and 19 (ii) PCW. Scale bars: 100 µm. b, EOMES and KI67 expression in the developing human RL at 17 (i) and 19 (ii) PCW. Scale bars as in a. Proliferating EOMES+ve UBC progenitors are common across all developmental timepoints assessed. c, EOMES+ cells in the human RL zones. The RLSVZ contains significantly more EOMES+ cells that the RLVZ. Significance was assessed using an unpaired two-tailed t-test, *** p = 1.048e−18. n = 3 biological repeats, per N = 4 time points; error bars, SEM. d, EOMES and KI67 expression in the developing human RL at the late timepoint 30 PCW. Scale bar as in (a). Proliferating EOMES+ve UBC progenitors can be found across fetal development, though at reduced frequency at later time points as KI67 expression is reduced (Fig. 3c). e, Quantification of the number of EOMES+/KI67+ cells in the human RL across various developmental timepoints. All comparisons to 11 PCW were non-significant using two-tailed unpaired t-tests; 14PCW, p = 0.43; 17PCW, p = 0.65; 19PCW, p = 0.33. n = 3 biological repeats per timepoint; error bars, SEM. EOMES+/KI67+ UBC progenitors are a long-lived and dominant population of the RL, rather than a transient state preceding differentiation. f, Quantification of the number of Eomes+/Ki67+ cells in the mouse RL across various developmental timepoints. Significance was assessed using an unpaired two-tailed t-test, *** p = 0.00015. n = 3 biological repeats per timepoint; error bars, SEM. Eomes+/Ki67+ UBC progenitor cells are a rare population in the mouse RL. g, h, Eomes and Ki67 expression in the mouse RL at E15.5 (g) and E16.5 (h). The RL boundaries are indicated with white dashed lines. Scale bars: 50µm. Eomes+ UBCs are rarely Ki67+. Data presented in a, b, g, h are representative images from three independent experiments with similar results, data in d were not performed in replicates. i, Oncogenic divergence of RLSVZ progenitors from normal initiate G4 MB.
