Skip to content

Advertisement

Open Access

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

  • Olivier Clément1, 2,
  • Isabel Anne Hemming1, 2,
  • Ivan Enghian Gladwyn-Ng1, 2,
  • Zhengdong Qu3,
  • Shan Shan Li3,
  • Michael Piper4, 5 and
  • Julian Ik-Tsen Heng1, 2, 3, 6Email author
Contributed equally
Neural Development201813:1

https://doi.org/10.1186/s13064-017-0098-x

Received: 9 November 2017

Accepted: 9 November 2017

Published: 11 January 2018

The original article was published in Neural Development 2017 12:8

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.
Figure 1
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

Notes

Declarations

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Authors’ Affiliations

(1)
The Harry Perkins Institute of Medical Research, Perth, Australia
(2)
The Centre for Medical Research, University of Western Australia, Perth, Australia
(3)
EMBL Australia, The Australian Regenerative Medicine Institute, Monash University, Clayton, Australia
(4)
The School of Biomedical Sciences, University of Queensland, Brisbane, Australia
(5)
Queensland Brain Institute, University of Queensland, Brisbane, Australia
(6)
Curtin Health Innovation Research Institute, Curtin University, Bentley, Australia

References

  1. Clément O, Hemming IA, Gladwyn-Ng IE, Qu Z, Li SS, Piper M, et al. Rp58 and p27kip1 coordinate cell cycle exit and neuronal migration within the embryonic mouse cerebral cortex. Neural Dev. 2017;12:8. https://doi.org/10.1186/s13064-017-0084-3.View ArticlePubMedPubMed CentralGoogle Scholar
  2. Heng JI, Qu Z, Ohtaka-Maruyama C, Okado H, Kasai M, Castro D, et al. The zinc finger transcription factor RP58 negatively regulates Rnd2 for the control of neuronal migration during cortical development. Cereb Cortex. 2015;25(3):806–16. https://doi.org/10.1093/cercor/bht277.View ArticlePubMedGoogle Scholar

Copyright

© The Author(s). 2018

Advertisement