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Nat Commun. 2015 Aug 5;6:7889. doi: 10.1038/ncomms8889.

An epigenetic regulator emerges as microtubule minus-end binding and stabilizing factor in mitosis.

Author information

1
1] Cell and Developmental Biology Programme, Centre for Genomic Regulation (CRG), Dr Aiguader 88, 08003 Barcelona, Spain [2] Universitat Pompeu Fabra (UPF), Dr Aiguader 88, 08003 Barcelona, Spain.
2
1] Max Planck Institute of Immunobiology and Epigenetics, Department of Chromatin Regulation, 79108 Freiburg im Breisgau, Germany [2] Faculty of Biology, University of Freiburg, 79104 Freiburg im Breisgau, Germany.
3
1] Cell and Developmental Biology Programme, Centre for Genomic Regulation (CRG), Dr Aiguader 88, 08003 Barcelona, Spain [2] Universitat Pompeu Fabra (UPF), Dr Aiguader 88, 08003 Barcelona, Spain [3] Institució Catalana de Recerca i Estudis Avançats (ICREA), Passeig Lluís Companys 23, 08010 Barcelona, Spain.
4
Max Planck Institute of Immunobiology and Epigenetics, Department of Chromatin Regulation, 79108 Freiburg im Breisgau, Germany.

Abstract

The evolutionary conserved NSL complex is a prominent epigenetic regulator controlling expression of thousands of genes. Here we uncover a novel function of the NSL complex members in mitosis. As the cell enters mitosis, KANSL1 and KANSL3 undergo a marked relocalisation from the chromatin to the mitotic spindle. By stabilizing microtubule minus ends in a RanGTP-dependent manner, they are essential for spindle assembly and chromosome segregation. Moreover, we identify KANSL3 as a microtubule minus-end-binding protein, revealing a new class of mitosis-specific microtubule minus-end regulators. By adopting distinct functions in interphase and mitosis, KANSL proteins provide a link to coordinate the tasks of faithful expression and inheritance of the genome during different phases of the cell cycle.

PMID:
26243146
PMCID:
PMC4918316
DOI:
10.1038/ncomms8889
[Indexed for MEDLINE]
Free PMC Article

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