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. 2017 Oct 26;7:14077. doi: 10.1038/s41598-017-13688-3

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Effect of Aurora A kinase inhibitor on Mos and Ccnb1 translation in mouse oocytes. (A) The phosphorylation state of CPEB1 during mouse oocyte maturation was monitored by western blot analysis. Extracts from 30 oocytes per lane were fractionated on the SDS PAGE gel, followed by transfer to the PVDF membrane and western blotting. A constant amount of protein application was confirmed by monitoring the amount of tubulin (lower panel). (B) CPEB1 phosphorylation during mouse oocyte in vitro maturation was not affected by Aurora A kinase inhibitor treatment. (C,D) Oocytes were injected with a Mos (C) or Ccnb1 luciferase reporter (D) and matured in the absence or presence of the Aurora A kinase inhibitor, MNL8237. Oocytes were harvested at 6 or 8 h and the accumulation of luciferase was measured. To normalize the amount of injected cRNA, cRNA coding Firefly luciferase was used as a control and the data are expressed as a Renilla/Firefly luciferase ratio. The graphs are the mean ± SEM of three independent experiments. No significant differences between control and treated groups were observed.