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Curr Biol. 2014 Nov 3;24(21):2598-605. doi: 10.1016/j.cub.2014.09.045. Epub 2014 Oct 23.

Myo19 ensures symmetric partitioning of mitochondria and coupling of mitochondrial segregation to cell division.

Author information

1
Centre for Clinical Science and Technology, Division of Medicine, University College London, Wolfson House, London NW1 2HE, UK. Electronic address: j.rohn@ucl.ac.uk.
2
MRC Laboratory for Molecular Cell Biology, University College London, London WC1E 6BT, UK.
3
Advanced Light Microscopy Facility, European Molecular Biology Laboratory (EMBL), Meyerhofstrasse 1, 69117 Heidelberg, Germany.
4
Novo Nordisk Foundation Center for Protein Research, Blegdamsvej 3B, 2200 Copenhagen, Denmark.
5
Department of Biology, University of Richmond, Richmond, VA 23173, USA.
6
Department of Cell Biology and Biophysics, European Molecular Biology Laboratory (EMBL), Meyerhofstrasse 1, 69117 Heidelberg, Germany.
7
MRC Laboratory for Molecular Cell Biology, University College London, London WC1E 6BT, UK. Electronic address: b.baum@ucl.ac.uk.

Abstract

During animal cell division, an actin-based ring cleaves the cell into two. Problems with this process can cause chromosome missegregation and defects in cytoplasmic inheritance and the partitioning of organelles, which in turn are associated with human diseases. Although much is known about how chromosome segregation is coupled to cell division, the way organelles coordinate their inheritance during partitioning to daughter cells is less well understood. Here, using a high-content live-imaging small interfering RNA screen, we identify Myosin-XIX (Myo19) as a novel regulator of cell division. Previously, this actin-based motor was shown to control the interphase movement of mitochondria. Our analysis shows that Myo19 is indeed localized to mitochondria and that its silencing leads to defects in the distribution of mitochondria within cells and in mitochondrial partitioning at division. Furthermore, many Myo19 RNAi cells undergo stochastic division failure--a phenotype that can be mimicked using a treatment that blocks mitochondrial fission and rescued by decreasing mitochondrial fusion, implying that mitochondria can physically interfere with cytokinesis. Strikingly, using live imaging we also observe the inappropriate movement of mitochondria to the poles of spindles in cells depleted for Myo19 as they enter anaphase. Since this phenocopies the results of an acute loss of actin filaments in anaphase, these data support a model whereby the Myo19 actin-based motor helps to control mitochondrial movement to ensure their faithful segregation during division. The presence of DNA within mitochondria makes their inheritance an especially important aspect of symmetrical cell division.

PMID:
25447992
PMCID:
PMC4228054
DOI:
10.1016/j.cub.2014.09.045
[Indexed for MEDLINE]
Free PMC Article

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