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. 2017 Aug 30;7:10007. doi: 10.1038/s41598-017-10270-9

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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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The mtopVIB mutants were defective in DSB formation. (a) A wild-type meiocyte with five bivalents at metaphase I. (b–e) The meiocytes at metaphase I from Atcom1-1 (b), Atrad50-1 (c), Atrad51 (d) and Atmre11 (e) that exhibited chromosome fragmentations. (f–j) The meiocytes at metaphase I from mtopVIB-2 (f), mtopVIB-2 Atcom1-1 (g), mtopVIB-2 Atrad50-1 (h), mtopVIB-2 Atrad51 (i) and mtopVIB-2 Atmre11 (j) had ten univalents, in which no chromosome fragmentation was observed. Bars = 10 μm.