Correction to: Rp58 and p27kip1 coordinate cell cycle exit and neuronal migration within the embryonic mouse cerebral cortex.

CORRECTION: After publication of the original article [1] it was realised that there were errors in figures 2a,b,f,g, which arose as a result of preparing figures from data collected and analysed at the same time as the work reported in [2] (Supplementary Figure 1 of [2]). An updated Fig. 2 is included with this Correction.

Correction

After publication of the original article [1] it was realised that there were errors in figures 2a,b,f,g, which arose as a result of preparing figures from data collected and analysed at the same time as the work reported in [2] (Supplementary Figure 1 of [2]).

An updated Fig. 2 is included with this Correction.

Fig. 2

p27kip1 restores the defective cell proliferation and radial migration of Rp58 siRNA-treated cortical progenitors. Knockdown of Rp58 leads to a significant reduction in the expression of the cell proliferation marker Ki67. a–d The defective expression of Ki67 in Rp58 siRNA-treated cells could be restored with p27kip1, but not p27kip1(ck-) which is incapable of signalling cell cycle exit owing to a mutation which impairs its cyclin kinase function (e) (F3,8 = 73, p < 0.001, One-way ANOVA, >700 cells counted from 3 independent brains per condition). Similar effects on the co-detection of pHH3, a marker of cell mitosis, were observed (f–k, F2,8 = 20, p = 0.004, One-way ANOVA, >700 cells counted from 3 independent brains per condition). l In addition, suppression of Rp58 by siRNA treatment impaired the migration of GFP-labelled cells, while treatment with either p27kip1 or p27kip1(ck-) promoted the radial migration of Rp58-siRNA treated cells from the VZ/SVZ to the IZ (F2,8 = 12, p < 0.0001, One-way ANOVA, >550 cells counted from 3 independent brains per condition). Scale bar represents 50 μm