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J Cell Biol. 2015 Dec 21;211(6):1113-20. doi: 10.1083/jcb.201507006. Epub 2015 Dec 14.

The microtubule catastrophe promoter Sentin delays stable kinetochore-microtubule attachment in oocytes.

Author information

1
Wellcome Trust Centre for Cell Biology, School of Biological Sciences, The University of Edinburgh, Edinburgh EH9 3BF, Scotland, UK.
2
Division of Biological Science, Graduate School of Science, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-8602, Japan.
3
Waksman Institute, Rutgers University, Piscataway, NJ 08854.
4
Wellcome Trust Centre for Cell Biology, School of Biological Sciences, The University of Edinburgh, Edinburgh EH9 3BF, Scotland, UK h.ohkura@ed.ac.uk.

Abstract

The critical step in meiosis is to attach homologous chromosomes to the opposite poles. In mouse oocytes, stable microtubule end-on attachments to kinetochores are not established until hours after spindle assembly, and phosphorylation of kinetochore proteins by Aurora B/C is responsible for the delay. Here we demonstrated that microtubule ends are actively prevented from stable attachment to kinetochores until well after spindle formation in Drosophila melanogaster oocytes. We identified the microtubule catastrophe-promoting complex Sentin-EB1 as a major factor responsible for this delay. Without this activity, microtubule ends precociously form robust attachments to kinetochores in oocytes, leading to a high proportion of homologous kinetochores stably attached to the same pole. Therefore, regulation of microtubule ends provides an alternative novel mechanism to delay stable kinetochore-microtubule attachment in oocytes.

PMID:
26668329
PMCID:
PMC4687879
DOI:
10.1083/jcb.201507006
[Indexed for MEDLINE]
Free PMC Article

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