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. 2019 Jun 20;10:774. doi: 10.3389/fpls.2019.00774

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Copyright © 2019 Zelkowski, Zelkowska, Conrad, Hesse, Lermontova, Marzec, Meister, Houben and Schubert.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Mitotic defects (anaphase bridges, laggards) in somatic flower bud nuclei of the A. thaliana nse4 mutants (A). The diagram (B) indicates the frequency (%) of abnormalities in the mutants compared to wild-type. The percentage of abnormalities is clearly increased in the nse4A mutants SALK_057130 and GK-768H08, as well as in the homozygous double mutant GK-768H08/SAIL_296_F02 representing both nse4A and nse4B mutations, respectively. The complementation of the mutation in GK-768H08 clearly decreases the number of abnormalities indicating that they are induced by the dysfunction of the Nse4A gene. The numbers of cells analyzed are indicated above the diagram bars.